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labely='50 mV', loc=3, pad=-0.5, borderpad=-1.0, barwidth=2, bbox_to_anchor=Bbox.from_bounds(-0.2, -0.05, 1, 1), +add_scalebar(ax11_spikes, matchx=False, matchy=False, hidex=True, hidey=True, sizex=100, sizey=50, labelx='100\u2009ms', + labely='50\u2009mV', loc=3, pad=-0.5, borderpad=-1.0, barwidth=2, bbox_to_anchor=Bbox.from_bounds(-0.2, -0.05, 1, 1), bbox_transform=ax11_spikes.transAxes) -add_scalebar(ax12_spikes, matchx=False, matchy=False, hidex=True, hidey=True, sizex=100, sizey=50, labelx='100 ms', - labely='50 mV', loc=3, pad=-0.5, borderpad=-1.0, barwidth=2, bbox_to_anchor=Bbox.from_bounds(-0.2, -0.05, 1, 1), +add_scalebar(ax12_spikes, matchx=False, matchy=False, hidex=True, hidey=True, sizex=100, sizey=50, labelx='100\u2009ms', + labely='50\u2009mV', loc=3, pad=-0.5, borderpad=-1.0, barwidth=2, bbox_to_anchor=Bbox.from_bounds(-0.2, -0.05, 1, 1), bbox_transform=ax12_spikes.transAxes) # add subplot labels for i in range(0,len(models)): diff --git a/eNeuro_title_page.docx 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diff --git a/g_table.tex b/g_table.tex index 5a772b6..dc00ce2 100644 --- a/g_table.tex +++ b/g_table.tex @@ -4,27 +4,28 @@ \centering % \begin{tabular}[x]{@{}l@{}} \\ \end{tabular} - \linespread{1.}\selectfont + \linespread{1.5}\selectfont \fontsize{10pt}{12pt}\selectfont{ - \begin{tabular}{c|c|c|c|c|c|c|c|c|c|} + \begin{tabular}{cccccccccc} % in mS/cm^2 - & \begin{tabular}[x]{@{}c@{}} RS\\Pyra-\\midal \end{tabular} & \begin{tabular}[x]{@{}c@{}} RS\\Inhib-\\itory\end{tabular} & FS & \begin{tabular}[x]{@{}c@{}} Cb\\Stellate \end{tabular}& \begin{tabular}[x]{@{}c@{}}Cb\\Stellate\\+\Kv \end{tabular} & \begin{tabular}[x]{@{}c@{}}Cb\\Stellate\\\(\Delta\)\Kv \end{tabular} & STN &\begin{tabular}[x]{@{}c@{}} STN\\+\Kv \end{tabular} &\begin{tabular}[x]{@{}c@{}} STN\\\(\Delta\)\Kv \end{tabular} - \\\Xhline{3\arrayrulewidth} - + \Xhline{1\arrayrulewidth} + & \begin{tabular}[x]{@{}c@{}} RS\\Pyra-\\midal \end{tabular} & \begin{tabular}[x]{@{}c@{}} RS\\Inhib-\\itory\end{tabular} & FS & \begin{tabular}[x]{@{}c@{}} Cb\\Stellate \end{tabular}& \begin{tabular}[x]{@{}c@{}}Cb\\Stellate\\+\Kv \end{tabular} & \begin{tabular}[x]{@{}c@{}}Cb\\Stellate\\\(\Delta\)\Kv \end{tabular} & STN &\begin{tabular}[x]{@{}c@{}} STN\\+\Kv \end{tabular} &\begin{tabular}[x]{@{}c@{}} STN\\\(\Delta\)\Kv \end{tabular} \\ + \Xhline{1\arrayrulewidth} \(g_{Na}\) & 56 & 10 & 58 & 3.4 & 3.4 & 3.4 & 49 & 49 & 49 \\ \(g_{K}\) & 5.4 & 1.89 & 3.51 & 9.0556 & 8.15 &9.0556 & 57 & 56.43 & 57 \\ - \(g_{K_V1.1}\) & 0.6 & 0.21 & 0.39 & - & 0.90556 & 1.50159 & - & 0.57 & 0.5 \\ - \(g_{A}\) & - & - & - & 15.0159 & 15.0159 & - & 5 & 5 & - \\ - \(g_{M}\) & 0.075 & 0.0098 &0.075 & - & - & - & - & - & - \\ - \(g_{L}\) & - & - & - & - & - & - & 5 & 5 & 5 \\ - \(g_{T}\) & - & - & - & 0.45045 & 0.45045 & 0.45045 & 5 & 5 & 5 \\ - \(g_{Ca,K}\) & - & - & - & - & - & - & 1 & 1 & 1 \\ + \(g_{K_V1.1}\) & 0.6 & 0.21 & 0.39 & --- & 0.90556 & 1.50159 & --- & 0.57 & 0.5 \\ + \(g_{A}\) & --- & --- & --- & 15.0159 & 15.0159 & --- & 5 & 5 & --- \\ + \(g_{M}\) & 0.075 & 0.0098 &0.075 & --- & --- & --- & --- & --- & --- \\ + \(g_{L}\) & --- & --- & --- & --- & --- & --- & 5 & 5 & 5 \\ + \(g_{T}\) & --- & --- & --- & 0.45045 & 0.45045 & 0.45045 & 5 & 5 & 5 \\ + \(g_{Ca,K}\) & --- & --- & --- & --- & --- & --- & 1 & 1 & 1 \\ \(g_{Leak}\) &0.0205 & 0.0205 & 0.038 & 0.07407 & 0.07407 & 0.07407 & 0.035 & 0.035 & 0.035 \\%\Xhline{1\arrayrulewidth} - \(\tau_{max_M}\)& 608 & 934 & 502 & - & - & - & - & - & - \\ + \(\tau_{max, M}\)& 608 & 934 & 502 & --- & --- & --- & --- & --- & --- \\ \(C_m\) & 118.44 & 119.99 & 101.71& 177.83 & 177.83 & 177.83 & 118.44& 118.44& 118.44 \\ + \Xhline{1\arrayrulewidth} \end{tabular}} - \caption[Cell properties and conductances of neuronal models]{Cell properties and conductances of regular spiking pyramidal neuron (RS Pyramidal), regular spiking inhibitory neuron (RS Inhibitory), fast spiking neuron (FS), cerebellar stellate cell (Cb Stellate), with additional \(I_{K_V1.1}\) (Cb Stellate \(\Delta\)\Kv) and with \(I_{K_V1.1}\) replacement of \(I_A\) (Cb Stellate \(\Delta\)\Kv), and subthalamic nucleus neuron (STN), with additional \(I_{K_V1.1}\) (STN \(\Delta\)\Kv) and with \(I_{K_V1.1}\) replacement of \(I_A\) (STN \Kv) models. All conductances are given in \(mS/cm^2\). Capacitances (\(C_m\)) and \(\tau_{max_p}\) are given in \(pF\) and \(ms\) respectively.} + \caption[Cell properties and conductances of neuronal models]{Cell properties and conductances of regular spiking pyramidal neuron (RS Pyramidal), regular spiking inhibitory neuron (RS Inhibitory), fast spiking neuron (FS), cerebellar stellate cell (Cb Stellate), with additional \(\textrm{I}_{\textrm{K}_{\textrm{V}}\textrm{1.1}}\) (Cb Stellate \(\Delta\)\Kv) and with \(\textrm{I}_{\textrm{K}_{\textrm{V}}\textrm{1.1}}\) replacement of \(\textrm{I}_\textrm{A}\) (Cb Stellate \(\Delta\)\Kv), and subthalamic nucleus neuron (STN), with additional \(\textrm{I}_{\textrm{K}_{\textrm{V}}\textrm{1.1}}\) (STN \(\Delta\)\Kv) and with \(\textrm{I}_{\textrm{K}_{\textrm{V}}\textrm{1.1}}\) replacement of \(\textrm{I}_{\textrm{A}}\) (STN \Kv) models. All conductances are given in \(\textrm{mS}/\textrm{cm}^2\). Capacitances (\(C_m\)) and \(\tau_{max, M}\) are given in pF and ms respectively.} \label{tab:g} \end{table} \ No newline at end of file diff --git a/manuscript.pdf b/manuscript.pdf index 9e8c62d05c084708b5f1036f6ad860fd4cafbbe0..8d275cd5ad678e98f9f3777de840c9c5f99b6c5c 100644 GIT binary patch delta 704776 zcmagFcOaGT|Hp6dO;+|MarUsu-dpz0EPF;rMu@CqWHyjcHpvVjWR$Fo$jTlWA^P3Y zyZ7hw{eFMH-(R=;oagnru5(@2ea`FgdR{(nqY8_VN&0wba0a(Dp-^%N38vM0E}!CU z$#cu1ry6v=YPW-KQfpC%KyK0}@n1{%{`Kc^NC!(#3U<#l4EKHqx6>Swoc+Z?sm=ZY zccAUhot?QxWU*QCduk)Pa*lvfg`=Ry#x88fwq(8j`{jqXhyB*H9uim$@BT2JG!v5K z_>!|$^-AmXG?>2l%}HVM{v#?(Lzz}5HelI`o_^43Yt;7ZhUNry(b(EA4ouXIY~7=% zUejaFr71*hI`7Q*=;-aUvxywdX7DFf2wc?s&KzMi4X3W!DVc%of=1s#te%?}Yq z7Fj93(9*uVfEMZ$9A2F>Qzz2(nfnP_dn&i3ID@KaGneZuOQ)cI)|L-349a9hLMhV0 zm(>+Z--=g>^0OmEb~~gxQw-+Ftt>QVndG0umydVMiq$M=F}Gi?3|yMFpsgf(j4my`;i2J#Hnw3E`%uFU4YSI;DjuuX zuXaexJYSCVdeI~s&|I83N20eq8THDl-zTmCt~q8omTG*6I=IuAf3lGf*j>FrO~Wjh zw`5y#mQ|xkzjf)Vqj%-bC5CHzcNg%O>@lF9wm0UOiwqL91E1Ali7+pR4xb^eS_IR2 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+\providecommand{\tightlist}{\setlength{\itemsep}{0pt}\setlength{\parskip}{0pt}} \AtBeginDocument{\DeclareGraphicsExtensions{.pdf,.PDF,.eps,.EPS,.png,.PNG,.tif,.TIF,.jpg,.JPG,.jpeg,.JPEG}} \newcommand{\Kv}{\(\textrm{K}_{\textrm{V}}\textrm{1.1}\ \)} \newcommand{\Kvnospace}{\(\textrm{K}_{\textrm{V}}\textrm{1.1}\)} +\newcommand{\IKv}{\(\textrm{I}_{\textrm{K}_{\textrm{V}}\textrm{1.1}}\ \)} \DeclareFloatingEnvironment[fileext=lop]{Extended Data} \newcommand{\beginsupplement}{ @@ -94,65 +96,32 @@ %\textit{It should provide a concise summary of the objectives, methodology (including the species and sex studied), key results, and major conclusions of the study.} Ion channels determine neuronal excitability and disruption in ion channel properties in mutations can result in neurological disorders called channelopathies. Often many mutations are associated with a channelopathy, and determination of the effects of these mutations are generally done at the level of currents. The impact of such mutations on neuronal firing is vital for selecting personalized treatment plans for patients, however whether the effect of a given mutation on firing can simply be inferred from current level effects is unclear. The general impact of the ionic current environment in different neuronal types on the outcome of ion channel mutations is vital to understanding of the impacts of ion channel mutations and effective selection of personalized treatments. -Using a diverse collection of neuronal models, the effects of changes in ion current properties on firing is assessed sytematically and for episodic ataxia type 1 associated \Kv mutations. The effects of ion current property changes or mutations on firing is dependent on the current environment, or cell type, in which such a change occurs in. Characterization of ion channel mutations as loss or gain of function is useful at the level of the ionic current, however the effects of channelopathies on firing is dependent on cell type. To further the efficacy of personalized medicine in channelopathies, the effects of ion channel mutations must be examined in the context of the appropriate cell types. +Using a diverse collection of neuronal models, the effects of changes in ion current properties on firing is assessed systematically and for episodic ataxia type 1 associated \Kv mutations. The effects of ion current property changes or mutations on firing is dependent on the current environment, or cell type, in which such a change occurs in. Characterization of ion channel mutations as loss or gain of function is useful at the level of the ionic current, however the effects of channelopathies on firing is dependent on cell type. To further the efficacy of personalized medicine in channelopathies, the effects of ion channel mutations must be examined in the context of the appropriate cell types. \par\null -\section*{Significant Statement (120 Words Maximum - Currently 105)} +\section*{Significant Statement (120 Words Maximum - Currently 112)} %\textit{The Significance Statement should provide a clear explanation of the importance and relevance of the research in a manner accessible to researchers without specialist knowledge in the field and informed lay readers. The Significance Statement will appear within the paper below the abstract.} -Ion channels determine neuronal excitability and mutations that alter ion channel properties result in neurological disorders called channelopathies. Although the genetic nature of such mutations as well as their effects on the ion channel's biophysical properties are routinely assessed experimentally, determination of the role in altering neuronal firing is more difficult. Computational modelling bridges this gap and demonstrates that the cell type in which a mutation occurs is an important determinant in the effects of firing. As a result, classification of ion channel mutations as loss or gain of function is useful to describe the ionic current but should not be blindly extended to firing. +Ion channels determine neuronal excitability and mutations that alter ion channel properties result in neurological disorders called channelopathies. Although the genetic nature of such mutations as well as their effects on the ion channel's biophysical properties are routinely assessed experimentally, determination of the role in altering neuronal firing is more difficult. Computational modelling bridges this gap and demonstrates that the cell type in which a mutation occurs is an important determinant in the effects of firing. As a result, classification of ion channel mutations as loss or gain of function is useful to describe the ionic current but care should be taken when applying this classification on the level of neuronal firing. \par\null \section*{Introduction (750 Words Maximum - Currently 673)} %\textit{The Introduction should briefly indicate the objectives of the study and provide enough background information to clarify why the study was undertaken and what hypotheses were tested.} Neuronal ion channels are vital in determining neuronal excitability, action potential generation and firing patterns \citep{bernard_channelopathies_2008, carbone_ion_2020}. In particular, the properties and combinations of ion channels and their resulting currents determine the firing properties of the neuron \citep{rutecki_neuronal_1992, pospischil_minimal_2008}. However, ion channel function can be disturb resulting in altered ionic current properties and altered neuronal firing behaviour \citep{carbone_ion_2020}. Ion channel mutations are a common cause of such channelopathies and are often associated with hereditary clinical disorders \citep{bernard_channelopathies_2008, carbone_ion_2020}. The effects of these mutations are frequently determined at a biophysical level, however assessment of the impact of mutations on neuronal firing and excitability is more difficult. Experimentally, transfection of cell cultures or the generation of mutant mice lines are common approaches. Cell culture transfection does not replicate the exact interplay of endogenous currents nor does it take into account the complexity of the nervous system including factors such as expression patterns, intracellular regulation and modulation of ion channels as well as network effects. Transfected currents are characterized in isolation and the role of these isolated currents in the context of other currents in a neuron cannot be definitively inferred. The effects of individual currents \textit{in vivo} also depend on the neuron type they are expressed in and which roles these neurons have in specific circuits. Complex interactions between different cell types \textit{in vivo} are neglected in transfected cell culture. Additionally, transfected currents are not present with the neuron-type specific cellular machinery present \textit{in vivo} and are even transfected in cells of different species. Furthermore, culture conditions can shape ion channel expression \citep{ponce_expression_2018}. + +Ion channel transfection of primary neuronal cultures can overcome some of the limitations of cell culture expression. In transfected neuronal cell cultures firing can more readily be assessed as endogenous currents are present, however the expressed and endogenous versions of the same ion channel are present in the cell \cite{Scalmani2006, Smith2018}. To avoid the confound of both expressed and endogenous current contributing to firing, a drug resistance can be introduced into the ion channel that is transfected and the drug is used to silence the endogenous version of this current \cite{Liu2019}. Although addition of TTX-resistance to \(\textrm{Na}_{\textrm{V}}\) does not alter the gating properties of these channels \cite{Leffler2005}, the relative expression and conductance of the transfected ion channel in relation to endogenous currents can be variable and non-specific blocking of ion channels not affected by the channelopathy may occur. As the firing behaviour and dynamics of neuronal models can be dramatically altered by altering relative current amplitudes \citep{rutecki_neuronal_1992, pospischil_minimal_2008,Kispersky2012, golowasch_failure_2002, barreiro_-current_2012}, primary neuronal cultures provide a useful general indication as to the effects of ion channel mutations but do not provide definitive insight into the effects of a channelopathy on \textit{in vivo} firing. -The generation of mice lines is costly and behavioural characterization of new mice lines is required to assess similarities to patient symptoms. Although the generation of mouse lines is desirable for a clinical disorder characterized by a specific ion channel mutation, this approach becomes impractical for disorders associated with a collection of distinct mutations in a single ion channel. Because of the lack of adequate experimental approaches, a great need is present for the ability to assess the impacts of ion channel mutations on neuronal firing. A more general understanding of the effects of changes in current properties on neuronal firing may help to understand the impacts of ion channel mutations. Specifically, modelling approaches can be used to assess the impacts of current property changes on firing behaviour, bridging the gap between changes in the biophysical properties induced by mutations and clinical symptoms. Conductance-based neuronal models enable insight into the effects of ion channel mutations with specific effects of the resulting ionic current as well as enabling \textit{in silico} assessment of the relative effects of changes in biophysical properties of ionic currents on neuronal firing . The effects of altered voltage-gated potassium channel \Kv function is of particular interest in this study as it gives rise to the \(I_{K_V1.1}\) current and is associated with episodic ataxia type 1. Furthermore, modelling approaches enable predictions of the effects of specific mutation and drug induced biophysical property changes. +The generation of mice lines is costly and behavioural characterization of new mice lines is required to assess similarities to patient symptoms. Although the generation of mouse lines is desirable for a clinical disorder characterized by a specific ion channel mutation, this approach becomes impractical for disorders associated with a collection of distinct mutations in a single ion channel. Because of the lack of adequate experimental approaches, a great need is present for the ability to assess the impacts of ion channel mutations on neuronal firing. A more general understanding of the effects of changes in current properties on neuronal firing may help to understand the impacts of ion channel mutations. Specifically, modelling approaches can be used to assess the impacts of current property changes on firing behaviour, bridging the gap between changes in the biophysical properties induced by mutations and clinical symptoms. Conductance-based neuronal models enable insight into the effects of ion channel mutations with specific effects of the resulting ionic current as well as enabling \textit{in silico} assessment of the relative effects of changes in biophysical properties of ionic currents on neuronal firing . The effects of altered voltage-gated potassium channel \Kv function is of particular interest in this study as it gives rise to the \IKv current and is associated with episodic ataxia type 1. Furthermore, modelling approaches enable predictions of the effects of specific mutation and drug induced biophysical property changes. -\Kv channels, encoded by the \textit{KCNA1} gene, play a role in repolarizing the action potential, neuronal firing patterns, neurotransmitter release, and saltatory conduction \citep{dadamo_episodic_1998} and are expressed throughout the CNS \citep{tsaur_differential_1992, wang_localization_1994, veh_immunohistochemical_1995}. -Altered \Kv channel function as a result of \textit{KCNA1} mutations in humans is associated with episodic ataxia type 1 (EA1) which is characterized by period attacks of ataxia and persistent myokymia \citep{parker_periodic_1946, van_dyke_hereditary_1975}. -Onset of EA1 is before 20 years of age \citep{brunt_familial_1990,rajakulendran_episodic_2007,van_dyke_hereditary_1975, jen_primary_2007} and is associated with a 10 times higher prevalence of epiletic seizures\citep{zuberi_novel_1999}. EA1 significantly impacts patient quality of life \citep{graves_episodic_2014}. +\Kv channels, encoded by the KCNA1 gene, play a role in repolarizing the action potential, neuronal firing patterns, neurotransmitter release, and saltatory conduction \citep{dadamo_episodic_1998} and are expressed throughout the CNS \citep{tsaur_differential_1992, wang_localization_1994, veh_immunohistochemical_1995}. +Altered \Kv channel function as a result of KCNA1 mutations in humans is associated with episodic ataxia type 1 (EA1) which is characterized by period attacks of ataxia and persistent myokymia \citep{parker_periodic_1946, van_dyke_hereditary_1975}. +Onset of EA1 is before 20 years of age \citep{brunt_familial_1990,rajakulendran_episodic_2007,van_dyke_hereditary_1975, jen_primary_2007} and is associated with a 10 times higher prevalence of epileptic seizures\citep{zuberi_novel_1999}. EA1 significantly impacts patient quality of life \citep{graves_episodic_2014}. \Kv null mice have spontaneous seizures without ataxia starting in the third postnatal week although impaired balance has been reported \citep{smart_deletion_1998, zhang_specific_1999} and neuronal hyperexcitability has been demonstrated in these mice \citep{smart_deletion_1998, brew_hyperexcitability_2003}. However, the lack of ataxia in \Kv null mice raises the question if the hyperexcitability seen is representative of the effects of EA1 associated \Kv mutations. Using a diverse set of conductance-based neuronal models we examine the role of current environment on the impact of alterations in channels properties on firing behavior generally and for EA1 associated \Kv mutations. -% \subsection*{Voltage-gated \Kv Potassium Channel} %\textcolor{red}{\textit{KCNA1} and \Kv Ion Channels} -% \Kv channels, encoded by the \textit{KCNA1} gene, play a role in repolarizing the action potential, neuronal firing patterns, neurotransmitter release, and saltatory conduction \citep{dadamo_episodic_1998}. \Kv is expressed throughout the CNS \citep{tsaur_differential_1992, wang_localization_1994} including in the cerebellum where Purkinje cells, granule cells, large Golgi cells, basket cell terminals and deep cerebellar nuclei cells express \Kv \citep{veh_immunohistochemical_1995, tsaur_differential_1992}. Cortical expression of \Kv is strongest in deep and superficial layers \citep{tsaur_differential_1992}. In the periphery, \Kv is expressed in myelinated axons and is reported to be highly expressed at juxtaparanodal regions where they modulate the ability of axons to repetitively fire \citep{mi_differential_1995, rasband_potassium_1998, wang_localization_1994}. - -% % \Kv inactivation/ heterooligomer/trafficking -% \Kv channels do not possess the ball and chain domain responsible for fast inactivation in \textit{Drosophila Shaker} channels and thus have slow inactivation (100s of ms) on their own \citep{glasscock_kv11_2019}. At room temperature when no \Kv fast inactivation is present, the complexing of \Kv with another subunit can confer fast inactivation (10s of ms) to \Kv containing heteromers \citep{glasscock_kv11_2019}. Specifically, \(\textrm{K}_{\textrm{V}}\beta\)1 \citep{rettig_inactivation_1994} and \(\textrm{K}_{\textrm{V}}1.4\) \(\alpha\) \citep{stuhmer_molecular_1989} subunits can confer fast inactivation to \Kv containing channels. Interestingly it has been reported that \(\textrm{K}_{\textrm{V}}\beta\)2 subunits may inhibit the \(\textrm{K}_{\textrm{V}}\beta\)1 induced rapid inactivation, adding further complexity as \(\textrm{K}_{\textrm{V}}\beta\)1 and \(\textrm{K}_{\textrm{V}}\beta\)2 have overlapping expression patterns in mammals \citep{xu_kv2_1997}. However, \Kv inactivation is temperature dependent and at more physiological temperatures (35\(^{\circ}\)C) than typical measurement temperatures (room temperature), fast inactivation is seen in \Kv channels \citep{ranjan_kinetic_2019}. %also \citep{sutachan_effects_2005} at room temp - -% Heteromeric \Kv channels such as those found \textit{in vivo} with \(\textrm{K}_{\textrm{V}}1.2\), \(\textrm{K}_{\textrm{V}}1.4\) and \(\textrm{K}_{\textrm{V}}1.6\) \citep{wang__1999, roeper_nip_1998, coleman_subunit_1999}, have different biophysical properties than homomeric \Kv channels \citep{ruppersberg_heteromultimeric_1990, isacoff_evidence_1990,rettig_inactivation_1994}. -% \(\textrm{K}_{\textrm{V}}\beta\)2 plays a role in \(\textrm{K}_{\textrm{V}}1\) channel trafficking and expression in the cell membrane \citep{shi_efficacy_2016, campomanes_kv_2002, manganas_identification_2001} and in phosphorylation of \Kv increases cell membrane \Kv \citep{jonas_regulation_1996}. - -% Altered \Kv channel function as a result of \textit{KCNA1} mutations in humans is associated with type 1 episodic ataxia where patient have episodes of discoordination as well as with epilepsy and elevated muscle activity \citep{van_dyke_hereditary_1975, jen_primary_2007}. - -% \Kv knock-out or null mice have spontaneous seizures without ataxia starting in the third postnatal week although impaired balance has been reported \citep{smart_deletion_1998, zhang_specific_1999}. \Kv null mice show incoordination after a cold water swim not correlated with seizures or with cold-induced muscle hyperexitability (neuromyotonia; \cite{zhou_temperature-sensitive_1998}). Increased neuronal excitability is present in \Kv null mice as evident by the reduction seizure latency after exposure to a convulsant agent \citep{smart_deletion_1998} and increased neuronal firing rates \citep{brew_hyperexcitability_2003}. Nerve excitability is likewise increased in \Kv null mice with repetitive firing observed \citep{smart_deletion_1998, zhou_temperature-sensitive_1998}. The increased action potential arrival in basket cell terminals results in increased neurotransmitter in \Kv null mice \citep{zhang_specific_1999}. Heterozygous mice show vulnerability to seizures intermediate to that of wild type and null mice suggesting that a 50\% reduction in \Kv is sufficient to affect neuronal excitability \citep{smart_deletion_1998, rho_developmental_1999}. - -% \Kv null mice are a model for sudden unexpected death in epilepsy as about half die suddenly in postnatal weeks 3-5 with several having seizures preceding death \citep{smart_deletion_1998, mishra_scn2a_2017}. Interestingly, in these mice a heterozygous deletion of the SCN2A gene encoding the \(\textrm{Na}_{\textrm{V}}\textrm{1.2}\ \) sodium channel increases survival two-fold and decreases seizure duration \citep{mishra_scn2a_2017} suggesting that reduction in sodium currents may in part be able to compensate for reductions in \Kv currents. Missense mutations in the CACNA1A gene encoding for P/Q-type calcium channels causes absence seizures, however in double mutant mice with missense Cacna1a and knocked out \textit{KCNA1} phenotypes associated with each mutation are attenuated \citep{glasscock_masking_2007}. It is suggested that the increase in excitability induced by lack of KCNA1 expression and impaired synaptic transmission caused by CACNA1A mutation may result in an intermediate level of excitability in the large population of neurons expressing both genes \citep{glasscock_masking_2007}. Therefore, loss of \Kv function and the associated increased excitability may be compensated for by alterations in other currents. - -% \Kv channels do not possess the ball and chain domain responsible for fast inactivation in \textit{Drosophila Shaker} channels and thus have slow inactivation (100s of ms) on their own \citep{glasscock_kv11_2019}. At room temperature when no \Kv fast inactivation is present, the complexing of \Kv with another subunit can confer fast inactivation (10s of ms) to \Kv containing heteromers \citep{glasscock_kv11_2019}. Specifically, \(\textrm{K}_{\textrm{V}}\beta\)1 \citep{rettig_inactivation_1994} and \(\textrm{K}_{\textrm{V}}1.4\) \(\alpha\) \citep{stuhmer_molecular_1989} subunits can confer fast inactivation to \Kv containing channels. Interestingly it has been reported that \(\textrm{K}_{\textrm{V}}\beta\)2 subunits may inhibit the \(\textrm{K}_{\textrm{V}}\beta\)1 induced rapid inactivation, adding further complexity as \(\textrm{K}_{\textrm{V}}\beta\)1 and \(\textrm{K}_{\textrm{V}}\beta\)2 have overlapping expression patterns in mammals \citep{xu_kv2_1997}. However, \Kv inactivation is temperature dependent and at more physiological temperatures (35\(^{\circ}\)C) than typical measurement temperatures (room temperature), fast inactivation is seen in \Kv channels \citep{ranjan_kinetic_2019}. %also \citep{sutachan_effects_2005} at room temp - -% Heteromeric \Kv channels such as those found \textit{in vivo} with \(\textrm{K}_{\textrm{V}}1.2\), \(\textrm{K}_{\textrm{V}}1.4\) and \(\textrm{K}_{\textrm{V}}1.6\) \citep{wang__1999, roeper_nip_1998, coleman_subunit_1999}, have different biophysical properties than homomeric \Kv channels \citep{ruppersberg_heteromultimeric_1990, isacoff_evidence_1990,rettig_inactivation_1994}. \(\textrm{K}_{\textrm{V}}\beta\)2 plays a role in \(\textrm{K}_{\textrm{V}}1\) channel trafficking and expression in the cell membrane \citep{shi_efficacy_2016, campomanes_kv_2002, manganas_identification_2001} and in phosphorylation of \Kv increases cell membrane \Kv \citep{jonas_regulation_1996}. - -%where patients have episodes of discoordination as well as with epilepsy and elevated muscle activity \citep{van_dyke_hereditary_1975, jen_primary_2007}. - %symptoms -%EA1 is characterized by period attacks of ataxia and persistent myokymia \citep{parker_periodic_1946, van_dyke_hereditary_1975}. -%Onset of EA1 is before 20 years of age \citep{brunt_familial_1990,rajakulendran_episodic_2007,van_dyke_hereditary_1975, jen_primary_2007} and is associated with a 10 times higher prevalence of epiletic seizures\citep{zuberi_novel_1999}. EA1 significantly impacts patient quality of life \citep{graves_episodic_2014}. -%\Kv null mice show incoordination after a cold water swim not correlated with seizures or with cold-induced muscle hyperexitability (neuromyotonia; \cite{zhou_temperature-sensitive_1998}). -%Increased neuronal excitability is present in \Kv null mice as evident by the reduction seizure latency after exposure to a convulsant agent \citep{smart_deletion_1998} and increased neuronal firing rates \citep{brew_hyperexcitability_2003}. -%Nerve excitability is likewise increased in \Kv null mice with repetitive firing observed \citep{smart_deletion_1998, zhou_temperature-sensitive_1998}. -%The increased action potential arrival in basket cell terminals results in increased neurotransmitter in \Kv null mice \citep{zhang_specific_1999}. -%Heterozygous mice show vulnerability to seizures intermediate to that of wild type and null mice suggesting that a 50\% reduction in \Kv is sufficient to affect neuronal excitability \citep{smart_deletion_1998, rho_developmental_1999}. - -% \Kv null mice are a model for sudden unexpected death in epilepsy as about half die suddenly in postnatal weeks 3-5 with several having seizures preceding death \citep{smart_deletion_1998, mishra_scn2a_2017}. Interestingly, in these mice a heterozygous deletion of the SCN2A gene encoding the \(\textrm{Na}_{\textrm{V}}\textrm{1.2}\ \) sodium channel increases survival two-fold and decreases seizure duration \citep{mishra_scn2a_2017} suggesting that reduction in sodium currents may in part be able to compensate for reductions in \Kv currents. Missense mutations in the CACNA1A gene encoding for P/Q-type calcium channels causes absence seizures, however in double mutant mice with missense Cacna1a and knocked out \textit{KCNA1} phenotypes associated with each mutation are attenuated \citep{glasscock_masking_2007}. It is suggested that the increase in excitability induced by lack of KCNA1 expression and impaired synaptic transmission caused by CACNA1A mutation may result in an intermediate level of excitability in the large population of neurons expressing both genes \citep{glasscock_masking_2007}. -%Therefore, loss of \Kv function and the associated increased excitability may be compensated for by alterations in other currents. - -% Myokymia consists of spontaneous involuntary muscle contractions that produce a rippling quality in the bodies of patients with this episodic ataxia \citep{rajakulendran_episodic_2007, van_dyke_hereditary_1975}. -% EA1 has an age of onset earlier than age 20 and attack frequencies that often decline with age \citep{brunt_familial_1990,rajakulendran_episodic_2007,van_dyke_hereditary_1975, jen_primary_2007}. -% Episodic attacks can be triggered by shock, sudden movement, physical or emotional stress, and chemical stressors \citep{rajakulendran_episodic_2007, brunt_familial_1990,van_dyke_hereditary_1975} and impact quality of life \citep{graves_episodic_2014}. EA1 patients sometimes have preceding sensory warnings of impending attacks \citep{van_dyke_hereditary_1975, brunt_familial_1990}. Epileptic seizures can occur with EA1 \citep{rajakulendran_episodic_2007, jen_primary_2007} with epilepsy being 10 times more prevalent in individuals with EA1 than individuals without EA1 \citep{zuberi_novel_1999}. \par\null @@ -166,12 +135,21 @@ All modelling and simulation was done in parallel with custom written Python 3.8 % Linux 3.10.0-123.e17.x86_64. \subsection*{Different Cell Models} - A group of neuronal models representing the major classes of cortical and thalamic neurons including regular spiking pyramidal (RS pyramidal), regular spiking inhibitory (RS inhibitory), and fast spiking (FS) cells were used \citep{pospischil_minimal_2008}. To each of these models, a \Kv current (\(I_{K_V1.1}\); \cite{ranjan_kinetic_2019}) was added. A cerebellar stellate cell model from \cite{alexander_cerebellar_2019} is used (Cb Stellate). This model was also used with a \Kv current (\(I_{K_V1.1}\); \cite{ranjan_kinetic_2019}) in addition to the A-type potassium current (Cb stellate +\Kv) or replacing the A-type potassium current (Cb stellate \(\Delta\)\Kv). A subthalamic nucleus neuron model as described by \cite{otsuka_conductance-based_2004} are used (STN) and with a \Kv current (\(I_{K_V1.1}\); \cite{ranjan_kinetic_2019}) in addition to the A-type potassium current (STN +\Kv) or replacing the A-type potassium current (STN \(\Delta\)\Kv). The properties and conductances of each model are detailed in \Cref{tab:g} and the gating properties are unaltered from the original models. The properties of \(I_{K_V1.1}\) were fitted to the mean wild type biophysical parameters of \Kv \citep{lauxmann_therapeutic_2021}. + A group of neuronal models representing the major classes of cortical and thalamic neurons including regular spiking pyramidal (RS pyramidal), regular spiking inhibitory (RS inhibitory), and fast spiking (FS) cells were used \citep{pospischil_minimal_2008}. To each of these models, a \Kv current (\IKv); \cite{ranjan_kinetic_2019}) was added. A cerebellar stellate cell model from \cite{alexander_cerebellar_2019} is used (Cb stellate). This model was also used with a \Kv current (\IKv; \cite{ranjan_kinetic_2019}) in addition to the A-type potassium current (Cb stellate +\Kv) or replacing the A-type potassium current (Cb stellate \(\Delta\)\Kv). A subthalamic nucleus neuron model as described by \cite{otsuka_conductance-based_2004} are used (STN) and with a \Kv current (\IKv; \cite{ranjan_kinetic_2019}) in addition to the A-type potassium current (STN +\Kv) or replacing the A-type potassium current (STN \(\Delta\)\Kv). The properties and conductances of each model are detailed in \Cref{tab:g} and the gating properties are unaltered from the original Cb stellate and STN models. For comparability to typical electrophysiological data fitting reported and for ease of further gating curve manipulations, a Boltzmann function + + \begin{equation}\label{eqn:Boltz} + x_\infty = {\left(\frac{1-a}{1+{exp[{\frac{V-V_{1/2}}{k}}]}} +a\right)^j} + \end{equation} + +with slope \(k\), voltage for half-maximal activation or inactivation (\(V_{1/2}\)), exponent \(j\), and persistent current \(0 \leq a \leq 1\) were fitted for the RS pyramidal, RS inhibitory and FS models \cite{pospischil_minimal_2008}. The properties of \IKv were fitted to the mean wild type biophysical parameters of \Kv \citep{lauxmann_therapeutic_2021}. + \input{g_table} + +\input{gating_table} \subsection*{Firing Frequency Analysis} - The membrane responses to 200 equidistant two second long current steps were simulated using the forward-Euler method with a \(\Delta t = 0.01\)ms from steady state. Current steps ranged from 0 to 1 \(nA\) for all models except for the RS inhibitory neuron models where a range of 0 to 0.35 \(nA\) was used to ensure repetitive firing across the range of input currents. For each current step, action potentials were detected as peaks with at least 50 mV prominence and a minimum interspike interval of 1 ms. The interspike interval was computed and used to determine the instantaneous firing frequencies elicited by the current step. The steady-state firing frequency were defined as the mean firing frequency in 0.5 seconds after the first action potential in the last second of the current step respectively and was used to construct frequency-current (fI) curves. + The membrane responses to 200 equidistant two second long current steps were simulated using the forward-Euler method with a \(\Delta \textrm{t} = 0.01\) ms from steady state. Current steps ranged from 0 to 1 nA for all models except for the RS inhibitory neuron models where a range of 0 to 0.35 nA was used to ensure repetitive firing across the range of input currents. For each current step, action potentials were detected as peaks with at least 50 mV prominence and a minimum interspike interval of 1 ms. The interspike interval was computed and used to determine the instantaneous firing frequencies elicited by the current step. The steady-state firing frequency were defined as the mean firing frequency in 0.5 seconds after the first action potential in the last second of the current step respectively and was used to construct frequency-current (fI) curves. The smallest current at which steady state firing occurs was identified and the current step interval preceding the occurrence of steady state firing was simulated at higher resolution (100 current steps) to determine the current at which steady state firing began. Firing was simulated with 100 current steps from this current upwards for 1/5 of the overall current range. Over this range a fI curve was constructed and the integral, or area under the curve (AUC), of the fI curve over this interval was computed with the composite trapezoidal rule and used as a measure of firing rate independent from rheobase. @@ -184,21 +162,20 @@ All modelling and simulation was done in parallel with custom written Python 3.8 % Sensitivity analyses enable investigation into how different sources of uncertainty in a model result in uncertainty in model outputs \citep{saltelli_sensitivity_2002} and provide information on the relative impact of model inputs \citep{saltelli_why_2019}. We recently used a one-factor-at-a-time (OFAT) sensitivity analysis approach to evaluate the relative impacts of currents on neuronal firing and developed a scoring system for SCN8A mutations that correlated (p = 0.0077, r = 0.64) with the clinical severity of epilepsy in patients with these mutations \citep{johannesen_genotype-phenotype_2021}. This was done in an isolated neuronal model and suggests that even with disregard of network level effects of mutations, the single cell level outcomes of mutations are relevant to disease phenotypes. OFAT sensitivity analyses indicate which factors have or do not have influence, with uninfluential factors never detected as relevant \citep{saltelli_how_2010}. OFAT sensitivity analyses can be used to screen factors that are influential on model outcomes and provide a mechanism by which factors and their relative influence can be easily identified and used in predictive applications. - - Current properties of currents common to all models (\(I_{Na}\), \(I_K\), \(I_A\)/\(I_{K_V1.1}\), and \(I_{Leak}\)) were systematically altered in a one-factor-at-a-time sensitivity analysis for all models. The gating curves for each current were shifted (\(\Delta V_{1/2}\)) from -10 to 10 mV in increments of 1 mV. The slope (\(k\)) of the gating curves were altered from half to twice the initial slope. Similarly, the maximal current conductance (\(g\)) was also scaled from half to twice the initial value. For both slope and conductance alterations, alterations consisted of 21 steps spaced equally on a \(log_2\) scale. + Current properties of currents common to all models (\(\textrm{I}_{\textrm{Na}}\), \(\textrm{I}_{\textrm{K}}\), \(\textrm{I}_{\textrm{A}}\)/\IKv, and \(\textrm{I}_{Leak}\)) were systematically altered in a one-factor-at-a-time sensitivity analysis for all models. The gating curves for each current were shifted (\(\Delta V_{1/2}\)) from -10 to 10 mV in increments of 1 mV. The slope (\(k\)) of the gating curves were altered from half to twice the initial slope. Similarly, the maximal current conductance (\(g\)) was also scaled from half to twice the initial value. For both slope and conductance alterations, alterations consisted of 21 steps spaced equally on a \(\textrm{log}_2\) scale. \subsection*{Model Comparison} Changes in rheobase (\(\Delta rheobase\)) are calculated in relation to the original model rheobase. The contrast of each AUC value (\(AUC_i\)) was computed in comparison to the AUC of the unaltered wild type model (\(AUC_{wt}\)) \begin{equation}\label{eqn:AUC_contrast} AUC_{contrast} = \frac{AUC_i - AUC_{wt}}{AUC_{wt}} \end{equation} - % Correlation across alterations within models + To assess whether the effects of a given alteration on \(AUC_{contrast}\) or \(\Delta rheobase\) are robust across models, the correlation between \(AUC_{contrast}\) or \(\Delta rheobase\) and the magnitude of current property alteration was computed for each alteration in each model and compared across alteration types. The Kendall's \(\tau\) coefficient, a non-parametric rank correlation, is used to describe the relationship between the magnitude of the alteration and AUC or rheobase values. A Kendall \(\tau\) value of -1 or 1 is indicative of monotonically decreasing and increasing relationships respectively. - \subsection*{\textit{KCNA1}/\Kv Mutations}\label{subsec:mut} - Known episodic ataxia type 1 associated \textit{KCNA1} mutations and their electrophysiological characterization reviewed in \cite{lauxmann_therapeutic_2021}. The mutation-induced changes in \(I_{K_V1.1}\) amplitude and activation slope (\(k\)) were normalized to wild type measurements and changes in activation \(V_{1/2}\) were used relative to wild type measurements. The effects of a mutation were also applied to \(I_A\) when present as both potassium currents display prominent inactivation. In all cases, the mutation effects were applied to half of the \(I_{K_V1.1}\) or \(I_A\) under the assumption that the heterozygous mutation results in 50\% of channels carrying the mutation. Frequency-current curves for each mutation in each model were obtained through simulation and used to characterize firing behaviour as described above. For each model the differences in mutation AUC to wild type AUC were normalized by wild type AUC (\(AUC_{contrast}\)) and mutation rheobases are compared to wild type rheobase values (\(\Delta rheobase\)). Pairwise Kendall rank correlations (Kendall \(\tau\)) are used to compare the the correlation in the effects of \Kv mutations on AUC and rheobase between models. + \subsection*{KCNA1/\Kv Mutations}\label{subsec:mut} + Known episodic ataxia type 1 associated KCNA1 mutations and their electrophysiological characterization reviewed in \cite{lauxmann_therapeutic_2021}. The mutation-induced changes in \IKv amplitude and activation slope (\(k\)) were normalized to wild type measurements and changes in activation \(V_{1/2}\) were used relative to wild type measurements. The effects of a mutation were also applied to \(\textrm{I}_{\textrm{A}}\) when present as both potassium currents display prominent inactivation. In all cases, the mutation effects were applied to half of the \Kv or \(\textrm{I}_{\textrm{A}}\) under the assumption that the heterozygous mutation results in 50\% of channels carrying the mutation. Frequency-current curves for each mutation in each model were obtained through simulation and used to characterize firing behaviour as described above. For each model the differences in mutation AUC to wild type AUC were normalized by wild type AUC (\(AUC_{contrast}\)) and mutation rheobases are compared to wild type rheobase values (\(\Delta rheobase\)). Pairwise Kendall rank correlations (Kendall \(\tau\)) are used to compare the the correlation in the effects of \Kv mutations on AUC and rheobase between models. @@ -211,18 +188,22 @@ The code/software described in the paper is freely available online at [URL reda % \textit{The results section should clearly and succinctly present the experimental findings. Only results essential to establish the main points of the work should be included.\\ % Authors must provide detailed information for each analysis performed, including population size, definition of the population (e.g., number of individual measurements, number of animals, number of slices, number of times treatment was applied, etc.), and specific p values (not > or <), followed by a superscript lowercase letter referring to the statistical table provided at the end of the results section. Numerical data must be depicted in the figures with box plots.} +To examine the role of cell specific current environments on the impact of altered ion channel properties on firing behaviour a set of neuronal models is used and properties of channels common across models are altered systematically one at a time. The effects of a set of episodic ataxia type 1 associated \Kv mutations on firing was then examined across different neuronal models with different current environments. + \subsection*{Firing Characterization} -\begin{figure}[ht!]%described +\begin{figure}[ht!] \centering \includegraphics[width=0.5\linewidth]{Figures/firing_characterization.pdf} \linespread{1.}\selectfont - \caption[]{Characterization of firing with AUC and rheobase. (A) The area under the curve (AUC) of the repetitive firing frequency-current (fI) curve. (B) Changes in firing as characterized by \(\Delta\)AUC and \(\Delta\)rheobase occupy 4 quadrants separated by no changes in AUC and rheobase. Representative schematic fI curves in blue with respect to a reference fI curve (black) depict the general changes associated with each quadrant.} + \caption[]{Characterization of firing with AUC and rheobase. (A) The area under the curve (AUC) of the repetitive firing frequency-current (fI) curve. (B) +Changes in firing as characterized by \(\Delta\)AUC and \(\Delta\)rheobase occupy 4 quadrants separated by no changes in AUC and rheobase. Representative schematic fI curves in blue with respect to a reference fI curve (black) depict the general changes associated with each quadrant.} \label{fig:firing_characterizaton} \end{figure} -The quantification of the fI curve using the AUC is seen in \Cref{fig:firing_characterizaton}A. The characterization of firing with AUC and rheobase is seen in \Cref{fig:firing_characterizaton}B, where the upper left quadrant (+\(\Delta\)AUC and -\(\Delta\)rheobase) indicate an increase in firing, whereas the bottom right quadrant (-\(\Delta\)AUC and +\(\Delta\)rheobase) is indicative of decreased firing. In the lower left and upper right quadrants, the effects on firing are more nuance and cannot easily be described as a gain or loss of excitability. -\begin{figure}[ht!]%described +Neuronal firing is a complex phenomenon and classification of firing is needed for comparability across cell types. Here we focus on the classification of two aspects of firing: rheobase (smallest injected current at which the cell fires an action potential) and the initial shape of the frequency-current (fI) curve. The quantification of the inital shape of the fI curve using by computing the area under the curve (AUC) is a measure of the initial firing at currents above rheobase (\Cref{fig:firing_characterizaton}A). The characterization of firing with AUC and rheobase enables determination of general increases or decreases in firing based on current-firing relationships, with the upper left quadrant (+\(\Delta\)AUC and -\(\Delta\)rheobase) indicate an increase in firing, whereas the bottom right quadrant (-\(\Delta\)AUC and +\(\Delta\)rheobase) is indicative of decreased firing (\Cref{fig:firing_characterizaton}B). In the lower left and upper right quadrants, the effects on firing are more nuance and cannot easily be described as a gain or loss of excitability. + +\begin{figure}[ht!] \centering \includegraphics[width=\linewidth]{Figures/diversity_in_firing.pdf} \linespread{1.}\selectfont @@ -231,13 +212,13 @@ The quantification of the fI curve using the AUC is seen in \Cref{fig:firing_cha \end{figure} -The diversity in the neuronal models used is seen in \Cref{fig:diversity_in_firing}. Considerable variability is seen across neuronal models both in representative spike trains and their fI curves. The models chosen all fire repetitively and do not exhibit bursting. Some models, such as Cb stellate and RS inhibitory models, display type I firing whereas others such as Cb stellate \(\Delta\)\Kvnospace and STN models have type II firing. Other models lie on a continuum between these prototypical firing classifications. Most neuronal models exhibit hysteresis with ascending and descending ramps eliciting spikes with different thresholds as shown by the green and red markers in \Cref{fig:diversity_in_firing} respectively. +Considerable diversity is present in the set of neuronal models used as evident in the variability seen across neuronal models both in representative spike trains and their fI curves (\Cref{fig:diversity_in_firing}). The models chosen all fire repetitively and do not exhibit bursting. Some models, such as Cb stellate and RS inhibitory models, display type I firing whereas others such as Cb stellate \(\Delta\)\Kvnospace and STN models have type II firing. Type I firing is characterized by continuous fI curve (i.e. firing rate is continuous) generated through a saddle-node on invariant cycle bifurcation and type II firing is characterized by a discontinuity in the fI curve (i.e. a jump occurs from no firing to firing at a certain frequency) due to a Hopf bifurcation \cite{ERMENTROUT2002, ermentrout_type_1996}. Other models lie on a continuum between these prototypical firing classifications. Most neuronal models exhibit hysteresis with ascending and descending ramps eliciting spikes with different thresholds, however STN +\Kv, STN \(\Delta\)\Kv, Cb stellate \(\Delta\)\Kv have large hysteresis (\Cref{fig:diversity_in_firing}). \subsection*{Sensitivity analysis} -A one-factor-a-time sensitivity analysis enables the comparison of a given alteration in current parameters across models. The effect of changes in gating \(V_{1/2}\) and slope factor k as well as the current conductance on AUC is shown in \Cref{fig:AUC_correlation} A, B and C respectively. Heterogeneity in the correlation between gating and conductance changes and AUC occurs across models for most currents. In these cases some of the models display non-monotonic relationships \\(i.e. \( |\)Kendall \(\tau | \neq\) 1). However, shifts in A current activation \(V_{1/2}\), changes in \Kv activation \(V_{1/2}\) and slope, and changes in A current conductance display consistent monotonic relationships across models. +A one-factor-a-time sensitivity analysis enables the comparison of a given alteration in current parameters across models. Changes in gating \(V_{1/2}\) and slope factor k as well as the current conductance affect AUC (\Cref{fig:AUC_correlation} A, B and C). Heterogeneity in the correlation between gating and conductance changes and AUC occurs across models for most currents. In these cases some of the models display non-monotonic relationships \\(i.e. \( |\)Kendall \(\tau | \neq\) 1). However, shifts in A current activation \(V_{1/2}\), changes in \Kv activation \(V_{1/2}\) and slope, and changes in A current conductance display consistent monotonic relationships across models. -\begin{figure}[ht!]%described +\begin{figure}[ht!] \centering \includegraphics[width=\linewidth]{Figures/AUC_correlation.pdf} \linespread{1.}\selectfont @@ -247,11 +228,10 @@ A one-factor-a-time sensitivity analysis enables the comparison of a given alter -The effect of changes in gating \(V_{1/2}\) and slope factor k as well as the current conductance on rheobase is shown in \Cref{fig:rheobase_correlation} A, B and C respectively. -Shifts in half activation of gating properties are similarly correlated with rheobase across models, however Kendall \(\tau\) values departing from -1 indicate non-monotonic relationships between K current \(V_{1/2}\) and rheobase in some models (\Cref{fig:rheobase_correlation}A) -Changes in Na current inactivation, \Kv current inactivation and A current activation have affect rheobase with positive and negative correlations in different models (\Cref{fig:rheobase_correlation}B). Departures from monotonic relationships occur in some models as a result of K current activation, \Kv current inactivation and A current activation in some models. Current conductance magnitude alterations affect rheobase similarly across models (\Cref{fig:rheobase_correlation}C). -\begin{figure}[ht!]%described +Alterations in gating \(V_{1/2}\) and slope factor k as well as the current conductance also play a role in determining rheobase (\Cref{fig:rheobase_correlation} A, B and C). Shifts in half activation of gating properties are similarly correlated with rheobase across models, however Kendall \(\tau\) values departing from -1 indicate non-monotonic relationships between K current \(V_{1/2}\) and rheobase in some models (\Cref{fig:rheobase_correlation}A). Changes in Na current inactivation, \Kv current inactivation and A current activation have affect rheobase with positive and negative correlations in different models (\Cref{fig:rheobase_correlation}B). Departures from monotonic relationships occur in some models as a result of K current activation, \Kv current inactivation and A current activation in some models. Current conductance magnitude alterations affect rheobase similarly across models (\Cref{fig:rheobase_correlation}C). + +\begin{figure}[ht!] \centering \includegraphics[width=\linewidth]{Figures/rheobase_correlation.pdf} \linespread{1.}\selectfont @@ -260,8 +240,8 @@ Changes in Na current inactivation, \Kv current inactivation and A current activ \end{figure} \subsection*{\Kv} -The changes in AUC and rheobase from wild-type values for reported episodic ataxia type 1 (EA1) associated \Kv mutations are seen in every model containing \Kv in \Cref{fig:simulation_model_comparision}A-I. Pairwise non-parametric Kendall \(\tau\) rank correlations between the simulated effects of these \Kv mutations on rheobase and AUC in different models are seen in \Cref{fig:simulation_model_comparision} J and K respectively. The effects of EA1 associated \Kv mutations on rheobase are highly correlated across models. The effects of the \Kv mutations on AUC are more heterogenous as reflected by both weak and strong positive and negative correlations between models \Cref{fig:simulation_model_comparision}K -\begin{figure}[ht!]%described +The changes in AUC and rheobase from wild-type values for reported episodic ataxia type 1 (EA1) associated \Kv mutations are heterogenous across models containing \Kv, but generally show decreases in rheobase (\Cref{fig:simulation_model_comparision}A-I). Pairwise non-parametric Kendall \(\tau\) rank correlations between the simulated effects of these \Kv mutations on rheobase are highly correlated across models (\Cref{fig:simulation_model_comparision}J). However, the effects of the \Kv mutations on AUC are more heterogenous as reflected by both weak and strong positive and negative pairwise correlations between models (\Cref{fig:simulation_model_comparision}K). +\begin{figure}[ht!] \centering \includegraphics[width=\linewidth]{Figures/simulation_model_comparison.pdf} \linespread{1.}\selectfont @@ -270,34 +250,34 @@ The changes in AUC and rheobase from wild-type values for reported episodic atax \end{figure} -\section*{Discussion (3000 Words Maximum - Currently 1559)} +\section*{Discussion (3000 Words Maximum - Currently 1780)} % \textit{The discussion section should include a brief statement of the principal findings, a discussion of the validity of the observations, a discussion of the findings in light of other published work dealing with the same or closely related subjects, and a statement of the possible significance of the work. Extensive discussion of the literature is discouraged.}\\ Using a set of diverse conductance-based neuronal models, the effects of changes to current properties and conductances on firing were determined to be heterogenous for the AUC of the steady state fI curve but more homogenous for rheobase. For a known channelopathy, episodic ataxia type 1 associated \Kv mutations, the effects on rheobase is consistent across cell types, whereas the effect on AUC is cell type dependent. \subsection*{Validity of Neuronal Models} -The \Kv model from \cite{ranjan_kinetic_2019} is based on expression of only \Kv in CHO cells and represents the biophysical properties of \Kv homotetramers and not heteromers. Thus the \Kv model used here neglects the complex reality of these channels \textit{in vivo} including their expression as heteromers and the altered biophyiscal properties of these heteromers \citep{wang__1999, roeper_nip_1998, coleman_subunit_1999, ruppersberg_heteromultimeric_1990, isacoff_evidence_1990, rettig_inactivation_1994}. Furthermore, dynamic modulation of \Kv channels, although physiologically relevant, is neglected here. For example, \(\textrm{K}_{\textrm{V}}\beta\)2 plays a role in \(K_V1\) channel trafficking and cell membrane expression \citep{shi_efficacy_2016, campomanes_kv_2002, manganas_identification_2001} and \Kv phosphorylation increases cell membrane \Kv \citep{jonas_regulation_1996}. It should be noted that the discrete classification of potassium currents into delayed rectifier and A-type is likely not biological, but rather highlights the characteristics of a spectrum of potassium channel inactivation that arises in part due to additional factors such as heteromer composition \citep{stuhmer_molecular_1989, glasscock_kv11_2019}, non-pore forming subunits (e.g. \(\textrm{K}_{\textrm{V}}\beta\) subunits) \citep{rettig_inactivation_1994, xu_kv2_1997}, and temperature \citep{ranjan_kinetic_2019} modulating channel properties. +The \Kv model from \cite{ranjan_kinetic_2019} is based on expression of only \Kv in CHO cells and represents the biophysical properties of \Kv homotetramers and not heteromers. Thus the \Kv model used here neglects the complex reality of these channels \textit{in vivo} including their expression as heteromers and the altered biophyiscal properties of these heteromers \citep{wang__1999, roeper_nip_1998, coleman_subunit_1999, ruppersberg_heteromultimeric_1990, isacoff_evidence_1990, rettig_inactivation_1994}. Furthermore, dynamic modulation of \Kv channels, although physiologically relevant, is neglected here. For example, \(\textrm{K}_{\textrm{V}}\upbeta\)2 plays a role in \(\textrm{K}_{\textrm{V}}\textrm{1}\) channel trafficking and cell membrane expression \citep{shi_efficacy_2016, campomanes_kv_2002, manganas_identification_2001} and \Kv phosphorylation increases cell membrane \Kv \citep{jonas_regulation_1996}. It should be noted that the discrete classification of potassium currents into delayed rectifier and A-type is likely not biological, but rather highlights the characteristics of a spectrum of potassium channel inactivation that arises in part due to additional factors such as heteromer composition \citep{stuhmer_molecular_1989, glasscock_kv11_2019}, non-pore forming subunits (e.g. \(\textrm{K}_{\textrm{V}}\upbeta\) subunits) \citep{rettig_inactivation_1994, xu_kv2_1997}, and temperature \citep{ranjan_kinetic_2019} modulating channel properties. -Additionally, the single-compartment model does not take into consideration differential effects on neuronal compartments (i.e. axon, soma, dendrites), possible different spatial cellular distribution of channel expression across and within these neuronal compartments or across CNS regions nor does it consider different channel types (e.g \(\textrm{Na}_{\textrm{V}}\text{1.1}\) vs \(\textrm{Na}_{\textrm{V}}\text{1.8}\)). More realistic models would consist of multiple compartments, take more currents into account and take the spatial distribution of channels into account, however these models are more computationally expensive, require current specific models and knowledge of the distribution of conductances across the cell. Despite these limitations, each of the models can reproduce physiological firing behaviour of the neurons they represent \citep{pospischil_minimal_2008, alexander_cerebellar_2019, otsuka_conductance-based_2004} and capture key aspects of the dynamics of these cell types. +Additionally, the single-compartment model does not take into consideration differential effects on neuronal compartments (i.e. axon, soma, dendrites), possible different spatial cellular distribution of channel expression across and within these neuronal compartments or across CNS regions nor does it consider different channel types (e.g \(\textrm{Na}_{\textrm{V}}\text{1.1}\) vs \(\textrm{Na}_{\textrm{V}}\text{1.8}\)). More realistic models would consist of multiple compartments, take more currents into account and take the spatial distribution of channels into account, however these models are more computationally expensive, require current specific models and knowledge of the distribution of conductances across the cell. Despite these limitations, each of the models can reproduce physiological firing behaviour of the neurons they represent \citep{pospischil_minimal_2008, alexander_cerebellar_2019, otsuka_conductance-based_2004} and capture key aspects of the dynamics of these cell types. The firing characterization was performed on adapted firing and as such currents that cause adaptation are neglected in our analysis. \subsection*{Current Environments Determine the Effect of Ion Channel Mutations} -One-factor-at-a-time (OFAT) sensitivity analyses such as the one performed here are predicated on assumptions of model linearity, and cannot account for interactions between factors \citep{czitrom_one-factor-at--time_1999, saltelli_how_2010}. OFAT approaches are local and not global (i.e. always in reference to a baseline point in the parameter space) and therefore cannot be generalized to the global parameter space unless linearity and additivity are met \citep{saltelli_how_2010}. The local space around the wild type neuron is explored with an OFAT sensitivity analysis without taking interactions between parameters into account. Comparisons between the effects of changes in similar parameters across different models can be made at the wild type locale indicative of experimentally observed neuronal behaviour. In this case, the role of deviations in the ionic current properties from their wild type in multiple neuronal models presented here provides a starting point for understanding the general role of these current properties in neurons. However, a more global approach would provide a more holistic understanding of the parameter space and provide insight into interactions between properties. +One-factor-at-a-time (OFAT) sensitivity analyses such as the one performed here are predicated on assumptions of model linearity, and cannot account for interactions between factors \citep{czitrom_one-factor-at--time_1999, saltelli_how_2010}. OFAT approaches are local and not global (i.e. always in reference to a baseline point in the parameter space) and therefore cannot be generalized to the global parameter space unless linearity is met \citep{saltelli_how_2010}. The local space around the wild type neuron is explored with an OFAT sensitivity analysis without taking interactions between parameters into account. Comparisons between the effects of changes in similar parameters across different models can be made at the wild type locale indicative of experimentally observed neuronal behaviour. In this case, the role of deviations in the ionic current properties from their wild type in multiple neuronal models presented here provides a starting point for understanding the general role of these current properties in neurons. However, a more global approach would provide a more holistic understanding of the parameter space and provide insight into interactions between properties. + +Characterization of the effects of a parameter on firing with non-parametric Kendall \(\tau\) correlations takes into account the sign and monotonicity of the correlation. In other words Kendall \(\tau\) coefficients provide information as to whether changing a parameter is positively or negatively correlated with AUC or rheobase as well as the extent to which this correlation is positive or negative across the parameter range examined. Therefore, Kendall \(\tau\) coefficients provide general information as to the sensitivity of different models to a change in a given current property, however more nuanced difference between the sensitivities of models to current property changes, such as the slope of the relationship between parameter change and firing are not included in our analysis. % The inter-model differences seen with the OFAT sensitivity analysis highlight the need for cell specific models. The observed dependence of neuronal firing on voltage-gated sodium channels and delayed-rectifier potassium channels is known \citep{verma_computational_2020, arhem_channel_2006} and substantiated by OFAT analysis across models. It is suggested that variability in these currents may underlie within cell population variability in neuronal firing behaviour \citep{verma_computational_2020}. Although increases in low-voltage activated inward currents are generally accepted to increase firing rates and outward currents to decrease firing rates \citep{nowacki_sensitivity_2011}, this was not always observed in AUC. The heterogeneity in outcomes of model OFAT analysis, especialy with AUC, suggest that the effects of changes in current properties are neuronal dependent and the current environment encompassing the relative conductances, gating \(V_{1/2}\) positions, and gating slopes of other currents plays an important role in modulating firing behaviour and in determining the outcome of a current property change such as a mutation. -Although, to our knowldege, no comprehensive evaluation of how current environment and cell type affect the outcome of ion channel mutations, comparisons between the effects of such mutations in certain cells have been reported. For instance, mutations in the SCN1A gene encoding \(\textrm{Na}_{\textrm{V}}\textrm{1.1}\) result in epileptic phenotypes by selective hypoexcitability of inhibitory but not excitatory neurons in the cortex resulting in circuit hyperexcitability \citep{Hedrich14874}. Additionallly, the L858H mutation in \(\textrm{Na}_\textrm{V}\textrm{1.7}\), associated with erythermyalgia, has been shown to cause hypoexcitability in sympathetic ganglion neurons and hyperexcitability in dorsal root ganglion neurons \citep{Waxman2007, Rush2006}. The differential effects of L858H \(\textrm{Na}_\textrm{V}\textrm{1.7}\) on firing is dependent on the presence or absence of another sodium channel \(\textrm{Na}_\textrm{V}\textrm{1.8}\) \citep{Waxman2007, Rush2006}. In a modelling study, it was found that altering the sodium conductance in 2 stomatogastric ganglion neuron models from a population models decreases rheobase in both models, however the initial slope of the fI curves (proportional to AUC) is increased in one model and decreased in the other suggesting that the magnitude of other currents in these models (such as \(K_d\)) determines the effect of a change in sodium current \citep{Kispersky2012}. These findings, in concert with our findings suggest that the current environment in which a channelopathy occurs is vital in determining the outcomes of the channelopathy on firing. +Although, to our knowledge, no comprehensive evaluation of how current environment and cell type affect the outcome of ion channel mutations, comparisons between the effects of such mutations in certain cells have been reported. For instance, mutations in the SCN1A gene encoding \(\textrm{Na}_{\textrm{V}}\textrm{1.1}\) result in epileptic phenotypes by selective hypoexcitability of inhibitory but not excitatory neurons in the cortex resulting in circuit hyperexcitability \citep{Hedrich14874}. In CA3 of the hippocampus, mutation of \(\textrm{Na}_{\textrm{V}}\textrm{1.6}\) similarly results in increased excitability of pyramidal neurons and decreased excitability of parvalbumin positive interneurons \cite{makinson_scn1a_2016}. Additionally, the L858H mutation in \(\textrm{Na}_\textrm{V}\textrm{1.7}\), associated with erythermyalgia, has been shown to cause hypoexcitability in sympathetic ganglion neurons and hyperexcitability in dorsal root ganglion neurons \citep{Waxman2007, Rush2006}. The differential effects of L858H \(\textrm{Na}_\textrm{V}\textrm{1.7}\) on firing is dependent on the presence or absence of another sodium channel \(\textrm{Na}_\textrm{V}\textrm{1.8}\) \citep{Waxman2007, Rush2006}. In a modelling study, it was found that altering the sodium conductance in 2 stomatogastric ganglion neuron models from a population models decreases rheobase in both models, however the initial slope of the fI curves (proportional to AUC) is increased in one model and decreased in the other suggesting that the magnitude of other currents in these models (such as \(\textrm{K}_\textrm{d}\)) determines the effect of a change in sodium current \citep{Kispersky2012}. These findings, in concert with our findings suggest that the current environment in which a channelopathy occurs is vital in determining the outcomes of the channelopathy on firing. -Cell type specific differences in current properties are important in the effects of ion channel mutations, however within a cell type heterogeneity in channel expression levels exists and it is often desirable to generate a population of neuronal models and to screen them for plausibility to biological data in order to capture neuronal population diversity \citep{marder_multiple_2011}. -The models used here are generated by characterization of current gating properties and by fitting of maximal conductances to experimental data. This practice of fixing maximal conductances based on experimental data is limiting as it does not reproduce the variability in channel expression and neuronal firing behaviour of a heterogeneous neuron population \citep{verma_computational_2020}. For example, a model derived from the mean conductances in a sub-population of stomatogastric ganglion "one-spike bursting" neurons fires 3 spikes instead of 1 per burst due to an L shaped distribution of sodium and potassium conductances \citep{golowasch_failure_2002}. +Cell type specific differences in current properties are important in the effects of ion channel mutations, however within a cell type heterogeneity in channel expression levels exists and it is often desirable to generate a population of neuronal models and to screen them for plausibility to biological data in order to capture neuronal population diversity \citep{marder_multiple_2011}. The models we used here are originally generated by characterization of current gating properties and by fitting of maximal conductances to experimental data \citep{pospischil_minimal_2008, ranjan_kinetic_2019, alexander_cerebellar_2019, otsuka_conductance-based_2004}. This practice of fixing maximal conductances based on experimental data is limiting as it does not reproduce the variability in channel expression and neuronal firing behaviour of a heterogeneous neuron population \citep{verma_computational_2020}. For example, a model derived from the mean conductances in a sub-population of stomatogastric ganglion "one-spike bursting" neurons fires 3 spikes instead of 1 per burst due to an L shaped distribution of sodium and potassium conductances \citep{golowasch_failure_2002}. Multiple sets of current conductances can give rise to the same patterns of activity also termed degeneracy and differences in neuronal dynamics may only be evident with perturbations \citep{marder_multiple_2011, goaillard_ion_2021}. Variability in ion channel expression often correlates with the expression of other ion channels \citep{goaillard_ion_2021} and neurons whose behaviour is similar may possess correlated variability across different ion channels resulting in stability in neuronal phenotype \citep{lamb_correlated_2013, soofi_co-variation_2012, taylor_how_2009}. The variability of ion currents and degeneracy of neurons may account, at least in part, for the observation that the effect of toxins within a neuronal type is frequently not constant \citep{khaliq_relative_2006, puopolo_roles_2007, ransdell_neurons_2013}. -\subsection*{Effects of \textit{KCNA1} Mutations} -Moderate changes in delayed rectifier potassium currents change the bifurcation structure of Hodgkin Huxley model, with changes analogous to those seen with \Kv mutations resulting in increased excitability due to reduced thresholds for repetitive firing \citep{hafez_altered_2020}. Although the Hodgkin Huxley delayed rectifier lacks inactivation, the increases in excitability seen are in line with both score-based and simulation-based predictions of the outcomes of \textit{KCNA1} mutations. Recently, \cite{zhao_common_2020} predicted \textit{in silico} that the depolarizing shifts seen as a result of \textit{KCNA1} mutations broaden action potentials and interfere negatively with high frequency action potential firing. However, comparability of firing rates is lacking in this study. Furthermore the increased excitability seen experimentally with \Kv null mice \citep{smart_deletion_1998, zhou_temperature-sensitive_1998}, with pharmacological \Kv block \citep{chi_manipulation_2007, morales-villagran_protection_1996}, by \cite{hafez_altered_2020} and with score-based and simulation-based predictions of \textit{KCNA1} mutations are contrary to the claims of \cite{zhao_common_2020}. LOF \textit{KCNA1} mutations generally increase neuronal excitability, however the different effects of \textit{KCNA1} mutations across models on AUC are indicative that a certain cell type specific complexity exists. - -Different current properties, such as the difference in \(I_A\) and \(I_{K_V1.1}\) in the Cb stellate and STN model families alter the impact of \textit{KCNA1} mutations on firing highlighting that knowledge of the biophysical properties of a current and its neuronal expression is vital for holistic understanding of the effects of a given ion channel mutation both at a single cell and network level. +\subsection*{Effects of KCNA1 Mutations} +Moderate changes in delayed rectifier potassium currents change the bifurcation structure of Hodgkin Huxley model, with changes analogous to those seen with \Kv mutations resulting in increased excitability due to reduced thresholds for repetitive firing \citep{hafez_altered_2020}. Although the Hodgkin Huxley delayed rectifier lacks inactivation, the increases in excitability seen are in line with both score-based and simulation-based predictions of the outcomes of \textit{KCNA1} mutations. LOF KCNA1 mutations generally increase neuronal excitability, however the different effects of KCNA1 mutations across models on AUC are indicative that a certain cell type specific complexity exists. Increased excitability seen experimentally with \Kv null mice \citep{smart_deletion_1998, zhou_temperature-sensitive_1998}, with pharmacological \Kv block \citep{chi_manipulation_2007, morales-villagran_protection_1996}, by \cite{hafez_altered_2020} and with simulation-based predictions of KCNA1 mutations. Contrary to these results, \cite{zhao_common_2020} predicted \textit{in silico} that the depolarizing shifts seen as a result of KCNA1 mutations broaden action potentials and interfere negatively with high frequency action potential firing, however comparability of firing rates is lacking in this study. +Different current properties, such as the difference in \(\textrm{I}_\textrm{A}\) and \IKv in the Cb stellate and STN model families alter the impact of KCNA1 mutations on firing highlighting that knowledge of the biophysical properties of a current and its neuronal expression is vital for holistic understanding of the effects of a given ion channel mutation both at a single cell and network level. \subsection*{Loss or Gain of Function Characterizations Do Not Fully Capture Ion Channel Mutation Effects on Firing} -The effects of changes in current properties depend in part on the neuronal model in which they occur and can be seen in the variance of correlations (especially in AUC) across models for a given current property change. Therefore, relative conductances and gating properties of currents in the current environment in which an alteration in current properties occurs plays an important role in determining the outcome on firing. The use of loss of function (LOF) and gain of function (GOF) is useful at the level of ion channels and whether a mutation results in more or less ionic current, however the extension of this thinking onto whether mutations induce LOF or GOF at the level of neuronal firing based on the ionic current LOF/GOF is problematic due to the dependency of neuronal firing changes on the current environment. Thus the direct leap from current level LOF/GOF characterizations to effects on firing without experimental or modelling-based evidence, although tempting, should be refrained from and viewed with caution when reported. This is especially relevant in the recent development of personalized medicine for channelopathies, where a patients specific channelopathy is identified and used to tailor treatments \citep{Weber2017, Ackerman2013, Helbig2020, Gnecchi2021}. However, the effects of specific ion channel mutations are often characterized in expression systems and classified as LOF or GOF to aid in treatment decisions \citep{johannesen_genotype-phenotype_2021, Brunklaus2022, Musto2020}. However, this approach must be used with caution and the cell type which expressed the mutant ion channel must be taken into account. Experimental assessment of the effects of a patients specific ion channel mutation \textit{in vivo} is not feasible at a large scale due to time and cost constraints, modelling of the effects of patient specific channelopathies is a desirable approach. +The effects of changes in current properties depend in part on the neuronal model in which they occur and can be seen in the variance of correlations (especially in AUC) across models for a given current property change. Therefore, relative conductances and gating properties of currents in the current environment in which an alteration in current properties occurs plays an important role in determining the outcome on firing. The use of loss of function (LOF) and gain of function (GOF) is useful at the level of ion channels and whether a mutation results in more or less ionic current, however the extension of this thinking onto whether mutations induce LOF or GOF at the level of neuronal firing based on the ionic current LOF/GOF is problematic due to the dependency of neuronal firing changes on the current environment. Thus the direct leap from current level LOF/GOF characterizations to effects on firing without experimental or modelling-based evidence, although tempting, should be refrained from and viewed with caution when reported. This is especially relevant in the recent development of personalized medicine for channelopathies, where a patients specific channelopathy is identified and used to tailor treatments \citep{Weber2017, Ackerman2013, Helbig2020, Gnecchi2021}. However, the effects of specific ion channel mutations are often characterized in expression systems and classified as LOF or GOF to aid in treatment decisions \citep{johannesen_genotype-phenotype_2021, Brunklaus2022, Musto2020}. Interestingly, both LOF and GOF \(\textrm{Na}_{\textrm{V}}\textrm{1.1}\) mutations can benefit from treatment with sodium channel blockers \citep{johannesen_genotype-phenotype_2021}, suggesting that the relationship between effects at the level of ion channels and effects at the level of firing and therapeutics is not linear or evident without further contextual information. Therefore, this approach must be used with caution and the cell type which expressed the mutant ion channel must be taken into account. Experimental assessment of the effects of a patients specific ion channel mutation \textit{in vivo} is not feasible at a large scale due to time and cost constraints, modelling of the effects of patient specific channelopathies is a desirable approach. Accordingly, for accurate modelling and predictions of the effects of mutations on neuronal firing, information as to the type of neurons containing the affected channel, and the properties of the affected and all currents in the affected neuronal type is needed. When modelling approaches are sought out to overcome the limitations of experimental approaches, care must be taken to account for model dependency and the generation of relevant cell-type or cell specific populations of models should be standard in assessing the effects of mutations in specific neurons. \par\null diff --git a/ref.bib b/ref.bib index 8ba7279..1e0b8f3 100644 --- a/ref.bib +++ b/ref.bib @@ -1,5242 +1,1300 @@ - -@Article{Musto2020, - author = {Musto, Elisa and Gardella, Elena and Møller, Rikke S.}, - journal = {European Journal of Paediatric Neurology}, - title = {Recent advances in treatment of epilepsy-related sodium channelopathies}, - year = {2020}, - issn = {1090-3798}, - month = jan, - pages = {123--128}, - volume = {24}, - abstract = {Voltage-gated sodium channels (VGSCs) play a crucial role in generation of action potentials. Pathogenic variants in the five human brain expressed VGSC genes, SCN1A, SCN2A, SCN3A, SCN8A and SCN1B have been associated with a spectrum of epilepsy phenotypes and neurodevelopmental disorders. In the last decade, next generation sequencing techniques have revolutionized the way we diagnose these channelopathies, which is paving the way towards precision medicine. Knowing the functional effect (Loss-of-function versus Gain-of-function) of a variant is not only important for understanding the underlying pathophysiology, but it is particularly crucial to orient therapeutic decisions. Here we provide a review of the literature dealing with treatment options in epilepsy-related sodium channelopathies, including the current and emerging medications.}, - doi = {10.1016/j.ejpn.2019.12.009}, - file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S1090379819304295/pdfft?md5=b62b2d62314c96f68a012a8a5c17a268&pid=1-s2.0-S1090379819304295-main.pdf&isDTMRedir=Y:application/pdf}, - groups = {Jan}, - keywords = {Epilepsy, SCN1A, SCN2A, SCN8A, SCN1B}, - language = {en}, - series = {Epilepsy \& {Neurodevelopmental} {Disorders}}, - url = {https://www.sciencedirect.com/science/article/pii/S1090379819304295}, - urldate = {2022-03-03}, -} - - -@Article{Brunklaus2022, - author = {Brunklaus, Andreas and Feng, Tony and Brünger, Tobias and Perez-Palma, Eduardo and Heyne, Henrike and Matthews, Emma and Semsarian, Christopher and Symonds, Joseph D. and Zuberi, Sameer M. and Lal, Dennis and Schorge, Stephanie}, - journal = {Brain}, - title = {Gene variant effects across sodium channelopathies predict function and guide precision therapy}, - year = {2022}, - issn = {0006-8950}, - month = jan, - pages = {awac006}, - abstract = {Pathogenic variants in the voltage-gated sodium channel gene family (SCNs) lead to early onset epilepsies, neurodevelopmental disorders, skeletal muscle channelopathies, peripheral neuropathies and cardiac arrhythmias. Disease-associated variants have diverse functional effects ranging from complete loss-of-function to marked gain-of-function. Therapeutic strategy is likely to depend on functional effect. Experimental studies offer important insights into channel function, but are resource intensive and only performed in a minority of cases. Given the evolutionarily conserved nature of the sodium channel genes we investigated whether similarities in biophysical properties between different voltage-gated sodium channels can predict function and inform precision treatment across sodium channelopathies. We performed a systematic literature search identifying functionally assessed variants in any of the nine voltage-gated sodium channel genes until 28 April 2021. We included missense variants that had been electrophysiologically characterised in mammalian cells in whole-cell patch-clamp recordings. We performed an alignment of linear protein sequences of all sodium channel genes and correlated variants by their overall functional effect on biophysical properties. Of 951 identified records, 437 sodium channel-variants met our inclusion criteria and were reviewed for functional properties. Of these, 141 variants were epilepsy-associated (SCN1/2/3/8A), 79 had a neuromuscular phenotype (SCN4/9/10/11A), 149 were associated with a cardiac phenotype (SCN5/10A) and 68 (16\%) were considered benign. We detected 38 missense variant pairs with an identical disease-associated variant in a different sodium channel gene. 35 out of 38 of those pairs resulted in similar functional consequences indicating up to 92\% biophysical agreement between corresponding sodium channel variants (odds ratio = 11.3; 95\% CI = 2.8 to 66.9; P \< 0.001). Pathogenic missense variants were clustered in specific functional domains, whereas population variants were significantly more frequent across non conserved domains (odds ratio = 18.6; 95\% CI = 10.9 to 34.4; P \< 0.001). Pore-loop regions were frequently associated with loss-of-function (LoF) variants, whereas inactivation sites were associated with gain-of-function (GoF; odds ratio = 42.1, 95\% CI = 14.5 to 122.4; P \< 0.001), whilst variants occurring in voltage-sensing regions comprised a range of gain- and loss-of-function effects. Our findings suggest that biophysical characterisation of variants in one SCN-gene can predict channel function across different SCN-genes where experimental data are not available. The collected data represent the first GoF versus LoF topological map of SCN proteins indicating shared patterns of biophysical effects aiding variant analysis and guiding precision therapy. We integrated our findings into a free online webtool to facilitate functional sodium channel gene variant interpretation (http://SCN-viewer.broadinstitute.org).}, - doi = {10.1093/brain/awac006}, - file = {:Brunklaus2022 - Gene Variant Effects across Sodium Channelopathies Predict Function and Guide Precision Therapy.pdf:PDF}, - groups = {Jan}, - url = {https://doi.org/10.1093/brain/awac006}, - urldate = {2022-03-06}, -} - -@Article{Weber2017, - author = {Weber, Yvonne G. and Biskup, Saskia and Helbig, Katherine L. and Von Spiczak, Sarah and Lerche, Holger}, - journal = {Expert Review of Molecular Diagnostics}, - title = {The role of genetic testing in epilepsy diagnosis and management}, - year = {2017}, - issn = {1473-7159}, - month = aug, - number = {8}, - pages = {739--750}, - volume = {17}, - abstract = {Introduction: Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. More than 500 epilepsy-associated genes have been described in the literature. Most of these genes play an important role in neuronal excitability, cortical development or synaptic transmission. A growing number of genetic variations have implications on diagnosis and prognostic or therapeutic advice in terms of a personalized medicine.Area covered: The review presents the different forms of genetic epilepsies with respect to their underlying genetic and functional pathophysiology and aims to give advice for recommended genetic testing. Moreover, it discusses ethical and legal guidelines, costs and technical limitations which should be considered.Expert commentary: Genetic testing is an important component in the diagnosis and treatment of many forms of epilepsy.}, - doi = {10.1080/14737159.2017.1335598}, - file = {Full Text PDF:https\://www.tandfonline.com/doi/pdf/10.1080/14737159.2017.1335598:application/pdf}, - groups = {Jan}, - keywords = {Genetic counseling, next generation sequencing, microarray analysis, exome, genome, idiopathic, personalized medicine, precision medicine, metabolic epilepsies, genetic epilepsies}, - pmid = {28548558}, - publisher = {Taylor \& Francis}, - url = {https://doi.org/10.1080/14737159.2017.1335598}, - urldate = {2022-03-06}, -} - - -@Article{Helbig2020, - author = {Helbig, Ingo and Ellis, Colin A.}, - journal = {Neuropharmacology}, - title = {Personalized medicine in genetic epilepsies – possibilities, challenges, and new frontiers}, - year = {2020}, - issn = {0028-3908}, - month = aug, - pages = {107970}, - volume = {172}, - abstract = {Identifying the optimal treatment based on specific characteristics of each patient is the main promise of precision medicine. In the field of epilepsy, the identification of more than 100 causative genes provides the enticing possibility of treatments targeted to specific disease etiologies. These conditions include classical examples, such as the use of vitamin B6 in antiquitin deficiency or the ketogenic diet in GLUT1 deficiency, where the disease mechanism can be directly addressed by the selection of a specific therapeutic compound. For epilepsies caused by channelopathies there have been advances in understanding how the selection of existing medications can be targeted to the functional consequences of genetic alterations. We discuss the examples of the use of sodium channel blockers such as phenytoin and oxcarbazepine in the sodium channelopathies, quinidine in KCNT1-related epilepsies, and strategies in GRIN-related epilepsies as examples of epilepsy precision medicine. Assessing the clinical response to targeted treatments of these conditions has been complicated by genetic and phenotypic heterogeneity, as well as by various neurological and non-neurological comorbidities. Moving forward, the development of standardized outcome measures will be critical to successful precision medicine trials in complex and heterogeneous disorders like the epilepsies. Finally, we address new frontiers in epilepsy precision medicine, including the need to match the growing volume of genetic data with high-throughput functional assays to assess the functional consequences of genetic variants and the ability to extract clinical data at large scale from electronic medical records and apply quantitative methods based on standardized phenotyping language.}, - doi = {10.1016/j.neuropharm.2020.107970}, - file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S0028390820300368/pdfft?md5=dcf89311714033043a9f22309af19b83&pid=1-s2.0-S0028390820300368-main.pdf&isDTMRedir=Y:application/pdf}, - groups = {Jan}, - keywords = {Epilepsy, Neurogenetics, Precision medicine, Electronic medical records, Human phenotype ontology}, - language = {en}, - url = {https://www.sciencedirect.com/science/article/pii/S0028390820300368}, - urldate = {2022-03-06}, -} - -@Article{Ackerman2013, - author = {Ackerman, Michael J. and Marcou, Cherisse A. and Tester, David J.}, - journal = {Revista Española de Cardiología (English Edition)}, - title = {Personalized {Medicine}: {Genetic} {Diagnosis} for {Inherited} {Cardiomyopathies}/{Channelopathies}}, - year = {2013}, - issn = {1885-5857}, - month = apr, - number = {4}, - pages = {298--307}, - volume = {66}, - abstract = {Major advances in the field of molecular genetics have expanded our ability to identify genetic substrates underlying the pathogenesis of various disorders that follow Mendelian inheritance patterns. Included among these disorders are the potentially lethal and heritable channelopathies and cardiomyopathies for which the underlying genetic basis has been identified and is now better understood. Clinical and genetic heterogeneity are hallmark features of these disorders, with thousands of gene mutations being implicated within these divergent cardiovascular diseases. Genetic testing for several of these heritable channelopathies and cardiomyopathies has matured from discovery to research-based genetic testing to clinically/commercially available diagnostic tests. The purpose of this review is to provide the reader with a basic understanding of human medical genetics and genetic testing in the context of cardiovascular diseases of the heart. We review the state of clinical genetic testing for the more common channelopathies and cardiomyopathies, discuss some of the pertinent issues that arise from genetic testing, and discuss the future of personalized medicine in cardiovascular disease. Resumen Se han producido avances importantes en el campo de la genética molecular que han ampliado nuestra capacidad de identificar sustratos genéticos subyacentes a la patogenia de diversos trastornos que siguen patrones de herencia mendeliana. Entre estos trastornos, se encuentran las canalopatías y miocardiopatías hereditarias y potencialmente mortales con base genética subyacente identificada y que ahora se conoce mejor. La heterogeneidad clínica y genética es una característica distintiva de estos trastornos, con miles de mutaciones génicas involucradas en estas enfermedades cardiovasculares divergentes. Las pruebas genéticas en varias de estas canalopatías y miocardiopatías hereditarias han alcanzado ya la fase de madurez, tras evolucionar desde su descubrimiento a las pruebas genéticas para investigación y las pruebas diagnósticas disponibles para uso clínico/comercial. El objetivo de esta revisión es proporcionar al lector un conocimiento básico de la genética médica humana y las pruebas genéticas existentes en el contexto de las enfermedades cardiovasculares que afectan al corazón. Revisamos el estado actual de las pruebas genéticas clínicas para las canalopatías y miocardiopatías más frecuentes, tratamos asuntos pertinentes que surgen de utilizar pruebas genéticas y sobre el futuro de la medicina personalizada en las enfermedades cardiovasculares.}, - doi = {10.1016/j.rec.2012.12.010}, - file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S1885585713000376/pdfft?md5=c6c96ffe659f2463a28e50b927b90d06&pid=1-s2.0-S1885585713000376-main.pdf&isDTMRedir=Y:application/pdf}, - groups = {Jan}, - keywords = {Genetics, Ion channels, Cardiomyopathy, Channelopathies, Genética, Canales iónicos, Miocardiopatía, Canalopatías}, - language = {en}, - shorttitle = {Personalized {Medicine}}, - url = {https://www.sciencedirect.com/science/article/pii/S1885585713000376}, - urldate = {2022-03-06}, -} - - -@Article{Gnecchi2021, - author = {Gnecchi, Massimiliano and Sala, Luca and Schwartz, Peter J}, - journal = {European Heart Journal}, - title = {Precision {Medicine} and cardiac channelopathies: when dreams meet reality}, - year = {2021}, - issn = {0195-668X}, - month = may, - number = {17}, - pages = {1661--1675}, - volume = {42}, - abstract = {Precision Medicine (PM) is an innovative approach that, by relying on large populations’ datasets, patients’ genetics and characteristics, and advanced technologies, aims at improving risk stratification and at identifying patient-specific management through targeted diagnostic and therapeutic strategies. Cardiac channelopathies are being progressively involved in the evolution brought by PM and some of them are benefiting from these novel approaches, especially the long QT syndrome. Here, we have explored the main layers that should be considered when developing a PM approach for cardiac channelopathies, with a focus on modern in vitro strategies based on patient-specific human-induced pluripotent stem cells and on in silico models. PM is where scientists and clinicians must meet and integrate their expertise to improve medical care in an innovative way but without losing common sense. We have indeed tried to provide the cardiologist’s point of view by comparing state-of-the-art techniques and approaches, including revolutionary discoveries, to current practice. This point matters because the new approaches may, or may not, exceed the efficacy and safety of established therapies. Thus, our own eagerness to implement the most recent translational strategies for cardiac channelopathies must be tempered by an objective assessment to verify whether the PM approaches are indeed making a difference for the patients. We believe that PM may shape the diagnosis and treatment of cardiac channelopathies for years to come. Nonetheless, its potential superiority over standard therapies should be constantly monitored and assessed before translating intellectually rewarding new discoveries into clinical practice.}, - doi = {10.1093/eurheartj/ehab007}, - file = {:Gnecchi2021 - Precision Medicine and Cardiac Channelopathies_ When Dreams Meet Reality.pdf:PDF}, - groups = {Jan}, - shorttitle = {Precision {Medicine} and cardiac channelopathies}, - url = {https://doi.org/10.1093/eurheartj/ehab007}, - urldate = {2022-03-06}, -} - - -@Article{Rush2006, - author = {Rush, Anthony M. and Dib-Hajj, Sulayman D. and Liu, Shujun and Cummins, Theodore R. and Black, Joel A. and Waxman, Stephen G.}, - journal = {Proceedings of the National Academy of Sciences}, - title = {A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons}, - year = {2006}, - month = may, - number = {21}, - pages = {8245--8250}, - volume = {103}, - doi = {10.1073/pnas.0602813103}, - file = {Full Text PDF:https\://www.pnas.org/doi/pdf/10.1073/pnas.0602813103:application/pdf}, - groups = {Jan}, - publisher = {Proceedings of the National Academy of Sciences}, - url = {https://www.pnas.org/doi/10.1073/pnas.0602813103}, - urldate = {2022-03-05}, -} - - -@Article{Waxman2007, - author = {Waxman, Stephen G.}, - journal = {Nature Neuroscience}, - title = {Channel, neuronal and clinical function in sodium channelopathies: from genotype to phenotype}, - year = {2007}, - issn = {1546-1726}, - month = apr, - number = {4}, - pages = {405--409}, - volume = {10}, - abstract = {What is the relationship between sodium channel function, neuronal function and clinical status in channelopathies of the nervous system? Given the central role of sodium channels in the generation of neuronal activity, channelopathies involving sodium channels might be expected to cause either enhanced sodium channel function and neuronal hyperexcitability associated with positive clinical manifestations such as seizures, or attenuated channel function and neuronal hypoexcitability associated with negative clinical manifestations such as paralysis. In this article, I review observations showing that changes in neuronal function and clinical status associated with channelopathies are not necessarily predictable solely from the altered physiological properties of the mutated channel itself. I discuss evidence showing that cell background acts as a filter that can strongly influence the effects of ion channel mutations.}, - copyright = {2007 Nature Publishing Group}, - doi = {10.1038/nn1857}, - file = {Full Text PDF:https\://www.nature.com/articles/nn1857.pdf:application/pdf}, - groups = {Jan}, - keywords = {Biomedicine, general, Neurosciences, Behavioral Sciences, Biological Techniques, Neurobiology, Animal Genetics and Genomics}, - language = {en}, - publisher = {Nature Publishing Group}, - shorttitle = {Channel, neuronal and clinical function in sodium channelopathies}, - url = {https://www.nature.com/articles/nn1857}, - urldate = {2022-03-03}, -} - - -@Article{Kispersky2012, - author = {Kispersky, Tilman J. and Caplan, Jonathan S. and Marder, Eve}, - journal = {Journal of Neuroscience}, - title = {Increase in {Sodium} {Conductance} {Decreases} {Firing} {Rate} and {Gain} in {Model} {Neurons}}, - year = {2012}, - issn = {0270-6474, 1529-2401}, - month = aug, - number = {32}, - pages = {10995--11004}, - volume = {32}, - abstract = {We studied the effects of increased sodium conductance on firing rate and gain in two populations of conductance-based, single-compartment model neurons. The first population consisted of 1000 model neurons with differing values of seven voltage-dependent conductances. In many of these models, increasing the sodium conductance threefold unexpectedly reduced the firing rate and divisively scaled the gain at high input current. In the second population, consisting of 1000 simplified model neurons, we found that enhanced sodium conductance changed the frequency–current (FI) curve in two computationally distinct ways, depending on the firing rate. In these models, increased sodium conductance produced a subtractive shift in the FI curve at low firing rates because the additional sodium conductance allowed the neuron to respond more strongly to equivalent input current. In contrast, at high input current, the increase in sodium conductance resulted in a divisive change in the gain because the increased conductance produced a proportionally larger activation of the delayed rectifier potassium conductance. The control and sodium-enhanced FI curves intersect at a point that delimits two regions in which the same biophysical manipulation produces two fundamentally different changes to the model neuron's computational properties. This suggests a potentially difficult problem for homeostatic regulation of intrinsic excitability.}, - chapter = {Articles}, - copyright = {Copyright © 2012 the authors 0270-6474/12/3210995-10\$15.00/0}, - doi = {10.1523/JNEUROSCI.2045-12.2012}, - file = {Full Text PDF:https\://www.jneurosci.org/content/jneuro/32/32/10995.full.pdf:application/pdf;PubMed entry:http\://www.ncbi.nlm.nih.gov/pubmed/22875933:text/html}, - groups = {Jan}, - language = {en}, - pmid = {22875933}, - publisher = {Society for Neuroscience}, - url = {https://www.jneurosci.org/content/32/32/10995}, - urldate = {2022-03-05}, -} - - -@article {Hedrich14874, - author = {Hedrich, Ulrike B.S. and Liautard, Camille and Kirschenbaum, Daniel and Pofahl, Martin and Lavigne, Jennifer and Liu, Yuanyuan and Theiss, Stephan and Slotta, Johannes and Escayg, Andrew and Dihn{\'e}, Marcel and Beck, Heinz and Mantegazza, Massimo and Lerche, Holger}, - title = {Impaired Action Potential Initiation in GABAergic Interneurons Causes Hyperexcitable Networks in an Epileptic Mouse Model Carrying a Human NaV1.1 Mutation}, - volume = {34}, - number = {45}, - pages = {14874--14889}, - year = {2014}, - doi = {10.1523/JNEUROSCI.0721-14.2014}, - publisher = {Society for Neuroscience}, - abstract = {Mutations in SCN1A and other ion channel genes can cause different epileptic phenotypes, but the precise mechanisms underlying the development of hyperexcitable networks are largely unknown. Here, we present a multisystem analysis of an SCN1A mouse model carrying the NaV1.1-R1648H mutation, which causes febrile seizures and epilepsy in humans. We found a ubiquitous hypoexcitability of interneurons in thalamus, cortex, and hippocampus, without detectable changes in excitatory neurons. Interestingly, somatic Na+ channels in interneurons and persistent Na+ currents were not significantly changed. Instead, the key mechanism of interneuron dysfunction was a deficit of action potential initiation at the axon initial segment that was identified by analyzing action potential firing. This deficit increased with the duration of firing periods, suggesting that increased slow inactivation, as recorded for recombinant mutated channels, could play an important role. The deficit in interneuron firing caused reduced action potential-driven inhibition of excitatory neurons as revealed by less frequent spontaneous but not miniature IPSCs. Multiple approaches indicated increased spontaneous thalamocortical and hippocampal network activity in mutant mice, as follows: (1) more synchronous and higher-frequency firing was recorded in primary neuronal cultures plated on multielectrode arrays; (2) thalamocortical slices examined by field potential recordings revealed spontaneous activities and pathological high-frequency oscillations; and (3) multineuron Ca2+ imaging in hippocampal slices showed increased spontaneous neuronal activity. Thus, an interneuron-specific generalized defect in action potential initiation causes multisystem disinhibition and network hyperexcitability, which can well explain the occurrence of seizures in the studied mouse model and in patients carrying this mutation.}, - issn = {0270-6474}, - URL = {https://www.jneurosci.org/content/34/45/14874}, - eprint = {https://www.jneurosci.org/content/34/45/14874.full.pdf}, - journal = {Journal of Neuroscience} -} - -@article{pospischil_minimal_2008, - title = {Minimal {Hodgkin}–{Huxley} type models for different classes of cortical and thalamic neurons}, - volume = {99}, - issn = {1432-0770}, - url = {https://doi.org/10.1007/s00422-008-0263-8}, - doi = {10.1007/s00422-008-0263-8}, - abstract = {We review here the development of Hodgkin–Huxley (HH) type models of cerebral cortex and thalamic neurons for network simulations. The intrinsic electrophysiological properties of cortical neurons were analyzed from several preparations, and we selected the four most prominent electrophysiological classes of neurons. These four classes are “fast spiking” “regular spiking” “intrinsically bursting” and “low-threshold spike” cells. For each class, we fit “minimal” HH type models to experimental data. The models contain the minimal set of voltage-dependent currents to account for the data. To obtain models as generic as possible, we used data from different preparations in vivo and in vitro, such as rat somatosensory cortex and thalamus, guinea-pig visual and frontal cortex, ferret visual cortex, cat visual cortex and cat association cortex. For two cell classes, we used automatic fitting procedures applied to several cells, which revealed substantial cell-to-cell variability within each class. The selection of such cellular models constitutes a necessary step towards building network simulations of the thalamocortical system with realistic cellular dynamical properties.}, - language = {en}, - number = {4}, - urldate = {2020-09-23}, - journal = {Biological Cybernetics}, - author = {Pospischil, Martin and Toledo-Rodriguez, Maria and Monier, Cyril and Piwkowska, Zuzanna and Bal, Thierry and Frégnac, Yves and Markram, Henry and Destexhe, Alain}, - month = nov, - year = {2008}, - pages = {427--441}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SGVJJSXF\\Pospischil et al. - 2008 - Minimal Hodgkin–Huxley type models for different c.pdf:application/pdf}, -} - -@article{hodgkin_quantitative_1952, - title = {A quantitative description of membrane current and its application to conduction and excitation in nerve}, - volume = {117}, - copyright = {© 1952 The Physiological Society}, - issn = {1469-7793}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1952.sp004764}, - doi = {10.1113/jphysiol.1952.sp004764}, - language = {en}, - number = {4}, - urldate = {2020-10-22}, - journal = {The Journal of Physiology}, - author = {Hodgkin, A. L. and Huxley, A. F.}, - year = {1952}, - pages = {500--544}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\IL6EB629\\Hodgkin and Huxley - 1952 - A quantitative description of membrane current and.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8RHYLPCA\\jphysiol.1952.html:text/html}, -} - -@article{barreiro_-current_2012, - title = {A-current and type {I}/type {II} transition determine collective spiking from common input}, - volume = {108}, - issn = {0022-3077}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544951/}, - doi = {10.1152/jn.00928.2011}, - abstract = {The mechanisms and impact of correlated, or synchronous, firing among pairs and groups of neurons are under intense investigation throughout the nervous system. A ubiquitous circuit feature that can give rise to such correlations consists of overlapping, or common, inputs to pairs and populations of cells, leading to common spike train responses. Here, we use computational tools to study how the transfer of common input currents into common spike outputs is modulated by the physiology of the recipient cells. We focus on a key conductance, gA, for the A-type potassium current, which drives neurons between “type II” excitability (low gA), and “type I” excitability (high gA). Regardless of gA, cells transform common input fluctuations into a tendency to spike nearly simultaneously. However, this process is more pronounced at low gA values. Thus, for a given level of common input, type II neurons produce spikes that are relatively more correlated over short time scales. Over long time scales, the trend reverses, with type II neurons producing relatively less correlated spike trains. This is because these cells' increased tendency for simultaneous spiking is balanced by an anticorrelation of spikes at larger time lags. These findings extend and interpret prior findings for phase oscillators to conductance-based neuron models that cover both oscillatory (superthreshold) and subthreshold firing regimes. We demonstrate a novel implication for neural signal processing: downstream cells with long time constants are selectively driven by type I cell populations upstream and those with short time constants by type II cell populations. Our results are established via high-throughput numerical simulations and explained via the cells' filtering properties and nonlinear dynamics.}, - number = {6}, - urldate = {2020-10-27}, - journal = {Journal of Neurophysiology}, - author = {Barreiro, Andrea K. and Thilo, Evan L. and Shea-Brown, Eric}, - month = sep, - year = {2012}, - pages = {1631--1645}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4CWLP49S\\Barreiro et al. - 2012 - A-current and type Itype II transition determine .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B37GK9MB\\jn.00928.html:text/html;Submitted Version:C\:\\Users\\nilsk\\Zotero\\storage\\GRCRXMAN\\Barreiro et al. - 2012 - A-current and type Itype II transition determine .pdf:application/pdf}, -} - -@article{alonso_visualization_2019, - title = {Visualization of currents in neural models with similar behavior and different conductance densities}, - volume = {8}, - issn = {2050-084X}, - url = {https://doi.org/10.7554/eLife.42722}, - doi = {10.7554/eLife.42722}, - abstract = {Conductance-based models of neural activity produce large amounts of data that can be hard to visualize and interpret. We introduce visualization methods to display the dynamics of the ionic currents and to display the models’ response to perturbations. To visualize the currents’ dynamics, we compute the percent contribution of each current and display them over time using stacked-area plots. The waveform of the membrane potential and the contribution of each current change as the models are perturbed. To represent these changes over a range of the perturbation control parameter, we compute and display the distributions of these waveforms. We illustrate these procedures in six examples of bursting model neurons with similar activity but that differ as much as threefold in their conductance densities. These visualization methods provide heuristic insight into why individual neurons or networks with similar behavior can respond widely differently to perturbations.}, - urldate = {2020-11-07}, - journal = {eLife}, - author = {Alonso, Leandro M and Marder, Eve}, - editor = {Westbrook, Gary L and Skinner, Frances K and Lankarany, Milad and Britton, Oliver}, - month = jan, - year = {2019}, - keywords = {ionic channels, Ca++ channels, conductance-based, K+ channels, Na+ channels, neuronal oscillators}, - pages = {e42722}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Z3Z84VN6\\Alonso and Marder - 2019 - Visualization of currents in neural models with si.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\IBZZZ3LU\\Alonso and Marder - 2019 - Visualization of currents in neural models with si.pdf:application/pdf}, -} - -@article{ranjan_kinetic_2019, - title = {A {Kinetic} {Map} of the {Homomeric} {Voltage}-{Gated} {Potassium} {Channel} ({Kv}) {Family}}, - volume = {13}, - issn = {1662-5102}, - url = {https://www.frontiersin.org/articles/10.3389/fncel.2019.00358/full}, - doi = {10.3389/fncel.2019.00358}, - abstract = {The voltage-gated potassium (Kv) channels, encoded by 40 genes, repolarize all electrically excitable cells, including plant, cardiac and neuronal cells. Although these genes were fully sequenced decades ago, a comprehensive kinetic characterization of all Kv channels is still missing, especially near physiological temperature. Here, we present a standardized kinetic map of the 40 homomeric Kv channels systematically characterized at 15°C, 25°C and 35°C. Importantly, the Kv kinetics at 35°C differ significantly from commonly reported kinetics, usually performed at room temperature. We observed voltage-dependent Q10 for all active Kv channels and inherent heterogeneity in kinetics for some of them. Kinetic properties are consistent across different host cell lines and conserved across mouse, rat and human. All electrophysiology data from all Kv channels are made available through public website (Channelpedia). This dataset provides a solid foundation for exploring kinetics of heteromeric channels, roles of auxiliary subunits, kinetic modulation, and for building accurate Kv models.}, - language = {English}, - urldate = {2021-02-16}, - journal = {Frontiers in Cellular Neuroscience}, - author = {Ranjan, Rajnish and Logette, Emmanuelle and Marani, Michela and Herzog, Mirjia and Tâche, Valérie and Scantamburlo, Enrico and Buchillier, Valérie and Markram, Henry}, - year = {2019}, - keywords = {Kinetics, automated patch clamp electrophysiology, CHO - Chinese hamster ovary, ion channel, Kv}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JP3ET4D5\\Ranjan et al. - 2019 - A Kinetic Map of the Homomeric Voltage-Gated Potas.pdf:application/pdf}, -} - -@article{hao_kv11_2013, - title = {Kv1.1 {Channels} {Act} as {Mechanical} {Brake} in the {Senses} of {Touch} and {Pain}}, - volume = {77}, - issn = {0896-6273}, - url = {https://www.sciencedirect.com/science/article/pii/S0896627313000433}, - doi = {10.1016/j.neuron.2012.12.035}, - abstract = {Molecular determinants of threshold sensitivity of mammalian mechanoreceptors are unknown. Here, we identify a mechanosensitive (MS) K+ current (IKmech) that governs mechanical threshold and adaptation of distinct populations of mechanoreceptors. Toxin profiling and transgenic mouse studies indicate that IKmech is carried by Kv1.1-Kv1.2 heteromers. Mechanosensitivity is attributed to Kv1.1 subunits, through facilitation of voltage-dependent open probability. IKmech is expressed in high-threshold C-mechano-nociceptors (C-HTMRs) and Aβ-mechanoreceptors, but not in low-threshold C-mechanoreceptors. IKmech opposes depolarization induced by slow/ultraslow MS cation currents in C-HTMRs, thereby shifting mechanical threshold for firing to higher values. However, due to kinetics mismatch with rapidly-adapting MS cation currents, IKmech tunes firing adaptation but not mechanical threshold in Aβ-mechanoreceptors. Expression of Kv1.1 dominant negative or inhibition of Kv1.1/IKmech caused severe mechanical allodynia but not heat hyperalgesia. By balancing the activity of excitatory mechanotransducers, Kv1.1 acts as a mechanosensitive brake that regulates mechanical sensitivity of fibers associated with mechanical perception.}, - language = {en}, - number = {5}, - urldate = {2021-02-18}, - journal = {Neuron}, - author = {Hao, Jizhe and Padilla, Françoise and Dandonneau, Mathieu and Lavebratt, Catharina and Lesage, Florian and Noël, Jacques and Delmas, Patrick}, - month = mar, - year = {2013}, - pages = {899--914}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KU2TJYCD\\Hao et al. - 2013 - Kv1.1 Channels Act as Mechanical Brake in the Sens.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4H5395VP\\S0896627313000433.html:text/html}, -} - -@article{bretschneider_expression_1999, - title = {Expression in mammalian cells and electrophysiological characterization of two mutant {Kv1}.1 channels causing episodic ataxia type 1 ({EA}-1)}, - volume = {11}, - issn = {1460-9568}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1460-9568.1999.00659.x}, - doi = {https://doi.org/10.1046/j.1460-9568.1999.00659.x}, - abstract = {Episodic ataxia type 1 (EA-1) is a rare neurological disorder and was the first ionic channel disease to be associated with defects in a potassium channel. Until now 10 different point mutations in the KCNA1-gene have been reported to cause this disorder. We have investigated the functional consequences of two mutations leading to amino acid substitutions in the first and sixth transmembrane segments of a Kv1.1 channel subunit, by means of the patch-clamp technique; we injected cRNA coding for, respectively, F184C and V408A mutant Kv1.1 channels into mammalian cells and compared the resulting currents with those in the wild-type. The expression levels of F184C and V408A mutant channels relative to that of the wild-type was 38 and 68\%, respectively. Since the single-channel conductance of the F184C mutant was similar to that of the wild-type (12 pS) without an apparent change in the maximum open probability, we conclude that the lower expression level in the F184C mutant channels is due to a reduced number of functional channels on the cell surface. F184C activated slower, and at more depolarized potentials, and deactivated faster compared with the wild-type. V408A channels deactivated and inactivated faster compared with the wild-type. Studies with different extracellular cations and tetraethylammonium gave no indication that the pore structure was changed in the mutant channels. Acetazolamide, that is helpful in some patients suffering from EA-1, was without effect on Kv1.1 wild-type or mutant channels. This study confirms and extends earlier studies on the functional consequences of Kv1.1 mutations associated with EA-1, in an attempt to understand the pathophysiology of the disease.}, - language = {en}, - number = {7}, - urldate = {2021-02-18}, - journal = {European Journal of Neuroscience}, - author = {Bretschneider, Frank and Wrisch, Anja and Lehmann‐Horn, Frank and Grissmer, Stephan}, - year = {1999}, - keywords = {electrophysiology, EA1-associated mutations in Kv1.1, episodic ataxia type 1, Kv1.1, voltage-gated potassium channels}, - pages = {2403--2412}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4PSE9CXT\\Bretschneider et al. - 1999 - Expression in mammalian cells and electrophysiolog.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YBK787AZ\\Bretschneider et al. - 1999 - Expression in mammalian cells and electrophysiolog.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\52GFR3PH\\Bretschneider et al. - 1999 - Expression in mammalian cells and electrophysiolog.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\U2SZ44J4\\j.1460-9568.1999.00659.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EMLTGVWF\\j.1460-9568.1999.00659.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\6G55CUXX\\j.1460-9568.1999.00659.html:text/html}, -} - -@article{cox_molecular_2005, - title = {Molecular determinants of voltage-gated potassium currents in vascular smooth muscle}, - volume = {42}, - issn = {1559-0283}, - url = {https://doi.org/10.1385/CBB:42:2:167}, - doi = {10.1385/CBB:42:2:167}, - abstract = {Voltage-gated K+ channels (Kv) play an important role in regulating contraction of vascular smooth muscle cells (VSMC) through their effects on membrane potential and on voltage-gated Ca2+ channel activity. Kv channels are tetrameric structures consisting of four identical or closely related pore-forming α subunits that may be associated with accessory subunits. More than 30 different gene products that contribute to Kv channel complexes have been identified to date, some of which are subject to alternative splicing. Consequently, there is an enormous potential diversity in the molecular composition and properties of possible Kv channel complexes. Electrophysiologic measurements of K+ currents in VSMC suggest the presence of multiple Kv channel assemblies including: (1) rapidly inactivating, 4-aminopyridine-sensitive, (2) slowly inactivating, tetraethylammonium-insensitive, and (3) noninactivating, tetraethylammonium-sensitive components. Based on electrophysiological and expression studies, it is likely that the latter two components are represented by a heteromultimeric complex of Kv1.2 with either Kv1.4 or Kv1.5 and a Kvβ1 subunit, and by at least Kv2.1, respectively. The identity of the first A-type current component, however, is not clear at this time. The relative abundance of these current components appears to vary in VSMC from different anatomical sites, from animals of different ages, and perhaps in VSMC within specific vascular segments. Expression of numerous Kv α and β subunits has been demonstrated in VSMC at both the gene and protein level. However, the number of expressed subunits appears to be much larger than the number of apparent Kv current components. It remains unclear if all of these transcripts are expressed in VSCM or in other cell types in the tissue, or if expression patterns are homogenous or heterogeneous in VSMC at a given site.}, - language = {en}, - number = {2}, - urldate = {2021-02-18}, - journal = {Cell Biochemistry and Biophysics}, - author = {Cox, Robert H.}, - month = apr, - year = {2005}, - pages = {167--195}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\A9XXRS4N\\Cox - 2005 - Molecular determinants of voltage-gated potassium .pdf:application/pdf}, -} - -@article{sutachan_effects_2005, - title = {Effects of {Kv1}.1 channel glycosylation on {C}-type inactivation and simulated action potentials}, - volume = {1058}, - issn = {0006-8993}, - url = {https://www.sciencedirect.com/science/article/pii/S0006899305011170}, - doi = {10.1016/j.brainres.2005.07.050}, - abstract = {Kv1.1 channels are brain glycoproteins that play an important role in repolarization of action potentials. In previous work, we showed that lack of N-glycosylation, particularly lack of sialylation, of Kv1.1 affected its macroscopic gating properties and slowed activation and C-type inactivation kinetics and produced a depolarized shift in the steady-state activation curve. In our current study, we used single channel analysis to investigate voltage-independent C-type inactivation in both Kv1.1 and Kv1.1N207Q, a glycosylation mutant. Both channels underwent brief and long-lived closures, and the lifetime and frequency of the long-lived closed states were voltage-independent and similar for both channels. We found that, as in macroscopic measurements, Kv1.1N207Q exhibited a ∼8 mV positive shift in its single channel fractional open time (fo) and a shallower fo–voltage slope compared with Kv1.1. Data suggested that C-type inactivation reflected the equilibration time with at least two slow voltage-independent long-lived closed states that followed the rapid activation process. In addition, data simulation indicated that the C-type inactivation process reflected the equilibration time between the open state and at least two long-lived closed states. Moreover, the faster macroscopic current decay in Kv1.1 mostly reflected a slower equilibration time in these channels as compared with Kv1.1N207Q. Finally, action potential simulations indicated that the N207Q mutation broaden the action potential and decreased the interspike interval. The shape of the action potential was not significantly affected by C-type inactivation, however, for a given channel, C-type inactivation increased the interspike interval. Data and simulations suggested that excitable cells could use differences in K+ channel glycosylation degree as an additional mechanism to increase channel functional diversity which could modify cell excitability.}, - language = {en}, - number = {1}, - urldate = {2021-02-18}, - journal = {Brain Research}, - author = {Sutachan, Jhon J. and Watanabe, Itaru and Zhu, Jing and Gottschalk, Allan and Recio-Pinto, Esperanza and Thornhill, William B.}, - month = oct, - year = {2005}, - keywords = {Action potential simulation, Glycosylation, Single K channel}, - pages = {30--43}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RJTNHW27\\Sutachan et al. - 2005 - Effects of Kv1.1 channel glycosylation on C-type i.pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\76YI92LW\\Sutachan et al. - 2005 - Effects of Kv1.1 channel glycosylation on C-type i.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2YNIJV5A\\S0006899305011170.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9VBBBXMV\\S0006899305011170.html:text/html}, -} - -@article{ori_dynamic_2020, - title = {Dynamic clamp constructed phase diagram for the {Hodgkin} and {Huxley} model of excitability}, - volume = {117}, - copyright = {Copyright © 2020 the Author(s). Published by PNAS.. https://creativecommons.org/licenses/by-nc-nd/4.0/This open access article is distributed under Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND).}, - issn = {0027-8424, 1091-6490}, - url = {https://www.pnas.org/content/117/7/3575}, - doi = {10.1073/pnas.1916514117}, - abstract = {Excitability—a threshold-governed transient in transmembrane voltage—is a fundamental physiological process that controls the function of the heart, endocrine, muscles, and neuronal tissues. The 1950s Hodgkin and Huxley explicit formulation provides a mathematical framework for understanding excitability, as the consequence of the properties of voltage-gated sodium and potassium channels. The Hodgkin–Huxley model is more sensitive to parametric variations of protein densities and kinetics than biological systems whose excitability is apparently more robust. It is generally assumed that the model’s sensitivity reflects missing functional relations between its parameters or other components present in biological systems. Here we experimentally assembled excitable membranes using the dynamic clamp and voltage-gated potassium ionic channels (Kv1.3) expressed in Xenopus oocytes. We take advantage of a theoretically derived phase diagram, where the phenomenon of excitability is reduced to two dimensions defined as combinations of the Hodgkin–Huxley model parameters, to examine functional relations in the parameter space. Moreover, we demonstrate activity dependence and hysteretic dynamics over the phase diagram due to the impacts of complex slow inactivation kinetics. The results suggest that maintenance of excitability amid parametric variation is a low-dimensional, physiologically tenable control process. In the context of model construction, the results point to a potentially significant gap between high-dimensional models that capture the full measure of complexity displayed by ion channel function and the lower dimensionality that captures physiological function.}, - language = {en}, - number = {7}, - urldate = {2021-03-01}, - journal = {Proceedings of the National Academy of Sciences}, - author = {Ori, Hillel and Hazan, Hananel and Marder, Eve and Marom, Shimon}, - month = feb, - year = {2020}, - keywords = {excitability, potassium channels, dynamic clamp, sodium channels, slow inactivation}, - pages = {3575--3582}, - file = {Dynamic clamp constructed phase diagram for the Hodgkin and Huxley model of excitability | PNAS:C\:\\Users\\nilsk\\Zotero\\storage\\TGHVIBW9\\tab-figures-data.html:text/html;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4LIRPQI5\\Ori et al. - 2020 - Dynamic clamp constructed phase diagram for the Ho.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ACDMHUHD\\3575.html:text/html}, -} - -@article{peng_differential_2007, - title = {Differential {Contributions} of {Shaker} and {Shab} {K}+ {Currents} to {Neuronal} {Firing} {Patterns} in {Drosophila}}, - volume = {97}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.01012.2006}, - doi = {10.1152/jn.01012.2006}, - abstract = {Different K+ currents participate in generating neuronal firing patterns. The Drosophila embryonic “giant” neuron culture system has facilitated current- and voltage-clamp recordings to correlate distinct excitability patterns with the underlying K+ currents and to delineate the mutational effects of identified K+ channels. Mutations of Sh and Shab K+ channels removed part of inactivating IA and sustained IK, respectively, and the remaining IA and IK revealed the properties of their counterparts, e.g., Shal and Shaw channels. Neuronal subsets displaying the delayed, tonic, adaptive, and damping spike patterns were characterized by different profiles of K+ current voltage dependence and kinetics and by differential mutational effects. Shab channels regulated membrane repolarization and repetitive firing over hundreds of milliseconds, and Shab neurons showed a gradual decline in repolarization during current injection and their spike activities became limited to high-frequency, damping firing. In contrast, Sh channels acted on events within tens of milliseconds, and Sh mutations broadened spikes and reduced firing rates without eliminating any categories of firing patterns. However, removing both Sh and Shal IA by 4-aminopyridine converted the delayed to damping firing pattern, demonstrating their actions in regulating spike initiation. Specific blockade of Shab IK by quinidine mimicked the Shab phenotypes and converted tonic firing to a damping pattern. These conversions suggest a hierarchy of complexity in K+ current interactions underlying different firing patterns. Different lineage-defined neuronal subsets, identifiable by employing the GAL4-UAS system, displayed different profiles of spike properties and K+ current compositions, providing opportunities for mutational analysis in functionally specialized neurons.}, - number = {1}, - urldate = {2021-03-29}, - journal = {Journal of Neurophysiology}, - author = {Peng, I-Feng and Wu, Chun-Fang}, - month = jan, - year = {2007}, - pages = {780--794}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\VLK3QXXX\\Peng and Wu - 2007 - Differential Contributions of Shaker and Shab K+ C.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\YTQXM9JY\\jn.01012.html:text/html}, -} - -@article{otsuka_conductance-based_2004, - title = {Conductance-{Based} {Model} of the {Voltage}-{Dependent} {Generation} of a {Plateau} {Potential} in {Subthalamic} {Neurons}}, - volume = {92}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00508.2003}, - doi = {10.1152/jn.00508.2003}, - abstract = {Because the subthalamic nucleus (STN) acts as a driving force of the basal ganglia, it is important to know how the activities of STN neurons are regulated. Previously, we have reported that a subset of STN neurons generates a plateau potential in a voltage-dependent manner. These plateau potentials can be evoked only when the cell is hyperpolarized. Here, to examine the mechanism of the voltage-dependent generation of the plateau potential in STN neurons, we constructed a conductance-based model of the plateau-generating STN neuron based on experimental observations and compared simulation results with recordings in slices. The model consists of a single compartment containing a Na+ current, a delayed-rectifier K+ current, an A-type K+ current, an L-like long-lasting Ca2+ current, a T-type Ca2+ current, a Ca2+-dependent K+ current, and a leak current. Our simulation results showed that a plateau potential in the model could be induced in a voltage-dependent manner that depended on the inactivation properties of L-like long-lasting Ca2+ current. The model could also reproduce the generation of a plateau potential as a rebound potential after termination of hyperpolarizing current injection. In addition, we tested the stability of simulated plateau potentials against inhibitory perturbation and found that the model showed similar properties observed for the plateau potentials of STN neurons in slices. The effects of K+ channel blockade by TEA and intracellular Ca2+ ion chelation by BAPTA on the plateau duration were also tested in the model and were found to match experimental observations. Thus our STN neuron model could qualitatively reproduce a number of experimental observations on plateau potentials. Our results suggest that the inactivation of L-type Ca2+ channels plays an important role in the voltage-dependent generation of the plateau potential.}, - number = {1}, - urldate = {2021-03-31}, - journal = {Journal of Neurophysiology}, - author = {Otsuka, Takeshi and Abe, Takafumi and Tsukagawa, Takahisa and Song, Wen-Jie}, - month = jul, - year = {2004}, - pages = {255--264}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YYMYAXMJ\\Otsuka et al. - 2004 - Conductance-Based Model of the Voltage-Dependent G.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\NIZRIRNC\\jn.00508.html:text/html}, -} - -@article{chen_kv4_2020, - title = {Kv4 channel expression and kinetics in {GABAergic} and non-{GABAergic} {rNST} neurons}, - volume = {124}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00396.2020}, - doi = {10.1152/jn.00396.2020}, - abstract = {The rostral nucleus of the solitary tract (rNST) serves as the first central relay in the gustatory system. In addition to synaptic interactions, central processing is also influenced by the ion channel composition of individual neurons. For example, voltage-gated K+ channels such as outward K+ current (IA) can modify the integrative properties of neurons. IA currents are prevalent in rNST projection cells but are also found to a lesser extent in GABAergic interneurons. However, characterization of the kinetic properties of IA, the molecular basis of these currents, as well as the consequences of IA on spiking properties of identified rNST cells is lacking. Here, we show that IA in rNST GABAergic (G+) and non-GABAergic (G−) neurons share a common molecular basis. In both cell types, there was a reduction in IA following treatment with the specific Kv4 channel blocker AmmTx3. However, the kinetics of activation and inactivation of IA in the two cell types were different with G− neurons having significantly more negative half-maximal activation and inactivation values. Likewise, under current clamp, G− cells had significantly longer delays to spike initiation in response to a depolarizing stimulus preceded by a hyperpolarizing prepulse. Computational modeling and dynamic clamp suggest that differences in the activation half-maximum may account for the differences in delay. We further observed evidence for a window current under both voltage clamp and current clamp protocols. We speculate that the location of Kv4.3 channels on dendrites, together with a window current for IA at rest, serves to regulate excitatory afferent inputs.NEW \& NOTEWORTHY Here, we demonstrate that the transient outward K+ current IA occurs in both GABAergic and non-GABAergic neurons via Kv4.3 channels in the rostral (gustatory) solitary nucleus. Although found in both cell types, IA is more prevalent in non-GABAergic cells; a larger conductance at more negative potentials leads to a greater impact on spike initiation compared with GABAergic neurons. An IA window current further suggests that IA can regulate excitatory afferent input to the nucleus.}, - number = {6}, - urldate = {2021-03-31}, - journal = {Journal of Neurophysiology}, - author = {Chen, Z. and Boxwell, A. and Conte, C. and Haas, T. and Harley, A. and Terman, D. H. and Travers, S. P. and Travers, J. B.}, - month = sep, - year = {2020}, - pages = {1727--1742}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\N7BGVPDD\\Chen et al. - 2020 - Kv4 channel expression and kinetics in GABAergic a.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\66YFHCQG\\jn.00396.html:text/html}, -} - -@article{dadamo_kv11_2020, - title = {Kv1.1 {Channelopathies}: {Pathophysiological} {Mechanisms} and {Therapeutic} {Approaches}}, - volume = {21}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - shorttitle = {Kv1.1 {Channelopathies}}, - url = {https://www.mdpi.com/1422-0067/21/8/2935}, - doi = {10.3390/ijms21082935}, - abstract = {Kv1.1 belongs to the Shaker subfamily of voltage-gated potassium channels and acts as a critical regulator of neuronal excitability in the central and peripheral nervous systems. KCNA1 is the only gene that has been associated with episodic ataxia type 1 (EA1), an autosomal dominant disorder characterized by ataxia and myokymia and for which different and variable phenotypes have now been reported. The iterative characterization of channel defects at the molecular, network, and organismal levels contributed to elucidating the functional consequences of KCNA1 mutations and to demonstrate that ataxic attacks and neuromyotonia result from cerebellum and motor nerve alterations. Dysfunctions of the Kv1.1 channel have been also associated with epilepsy and kcna1 knock-out mouse is considered a model of sudden unexpected death in epilepsy. The tissue-specific association of Kv1.1 with other Kv1 members, auxiliary and interacting subunits amplifies Kv1.1 physiological roles and expands the pathogenesis of Kv1.1-associated diseases. In line with the current knowledge, Kv1.1 has been proposed as a novel and promising target for the treatment of brain disorders characterized by hyperexcitability, in the attempt to overcome limited response and side effects of available therapies. This review recounts past and current studies clarifying the roles of Kv1.1 in and beyond the nervous system and its contribution to EA1 and seizure susceptibility as well as its wide pharmacological potential.}, - language = {en}, - number = {8}, - urldate = {2021-03-31}, - journal = {International Journal of Molecular Sciences}, - author = {D’Adamo, Maria Cristina and Liantonio, Antonella and Rolland, Jean-Francois and Pessia, Mauro and Imbrici, Paola}, - month = jan, - year = {2020}, - keywords = {epilepsy, episodic ataxia type 1, acetazolamide, ataxic mouse, channel modulators, knock-out mouse, Kv1.1 potassium channel, sodium channel blockers, SUDEP}, - pages = {2935}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\C8R932BF\\D’Adamo et al. - 2020 - Kv1.1 Channelopathies Pathophysiological Mechanis.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\D3GRYNZI\\2935.html:text/html}, -} - -@article{farjami_bursting_2020, - title = {Bursting in cerebellar stellate cells induced by pharmacological agents: {Non}-sequential spike adding}, - volume = {16}, - issn = {1553-7358}, - shorttitle = {Bursting in cerebellar stellate cells induced by pharmacological agents}, - url = {https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1008463}, - doi = {10.1371/journal.pcbi.1008463}, - abstract = {Cerebellar stellate cells (CSCs) are spontaneously active, tonically firing (5-30 Hz), inhibitory interneurons that synapse onto Purkinje cells. We previously analyzed the excitability properties of CSCs, focusing on four key features: type I excitability, non-monotonic first-spike latency, switching in responsiveness and runup (i.e., temporal increase in excitability during whole-cell configuration). In this study, we extend this analysis by using whole-cell configuration to show that these neurons can also burst when treated with certain pharmacological agents separately or jointly. Indeed, treatment with 4-Aminopyridine (4-AP), a partial blocker of delayed rectifier and A-type K+ channels, at low doses induces a bursting profile in CSCs significantly different than that produced at high doses or when it is applied at low doses but with cadmium (Cd2+), a blocker of high voltage-activated (HVA) Ca2+ channels. By expanding a previously revised Hodgkin–Huxley type model, through the inclusion of Ca2+-activated K+ (K(Ca)) and HVA currents, we explain how these bursts are generated and what their underlying dynamics are. Specifically, we demonstrate that the expanded model preserves the four excitability features of CSCs, as well as captures their bursting patterns induced by 4-AP and Cd2+. Model investigation reveals that 4-AP is potentiating HVA, inducing square-wave bursting at low doses and pseudo-plateau bursting at high doses, whereas Cd2+ is potentiating K(Ca), inducing pseudo-plateau bursting when applied in combination with low doses of 4-AP. Using bifurcation analysis, we show that spike adding in square-wave bursts is non-sequential when gradually changing HVA and K(Ca) maximum conductances, delayed Hopf is responsible for generating the plateau segment within the active phase of pseudo-plateau bursts, and bursting can become “chaotic” when HVA and K(Ca) maximum conductances are made low and high, respectively. These results highlight the secondary effects of the drugs applied and suggest that CSCs have all the ingredients needed for bursting.}, - language = {en}, - number = {12}, - urldate = {2021-04-13}, - journal = {PLOS Computational Biology}, - author = {Farjami, Saeed and Alexander, Ryan P. D. and Bowie, Derek and Khadra, Anmar}, - month = dec, - year = {2020}, - keywords = {Neurons, Behavior, Action potentials, Membrane potential, Bifurcation theory, Ionic current, Olives, Purkinje cells}, - pages = {e1008463}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GB9G63K3\\Farjami et al. - 2020 - Bursting in cerebellar stellate cells induced by p.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2RTIJXUS\\Farjami et al. - 2020 - Bursting in cerebellar stellate cells induced by p.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\3M5IN63W\\article.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FQKJLX3T\\article.html:text/html}, -} - -@article{alexander_cerebellar_2019, - title = {Cerebellar {Stellate} {Cell} {Excitability} {Is} {Coordinated} by {Shifts} in the {Gating} {Behavior} of {Voltage}-{Gated} {Na}+ and {A}-{Type} {K}+ {Channels}}, - volume = {6}, - copyright = {Copyright © 2019 Alexander et al.. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.}, - issn = {2373-2822}, - url = {https://www.eneuro.org/content/6/3/ENEURO.0126-19.2019}, - doi = {10.1523/ENEURO.0126-19.2019}, - abstract = {Neuronal excitability in the vertebrate brain is governed by the coordinated activity of both ligand- and voltage-gated ion channels. In the cerebellum, spontaneous action potential (AP) firing of inhibitory stellate cells (SCs) is variable, typically operating within the 5- to 30-Hz frequency range. AP frequency is shaped by the activity of somatodendritic A-type K+ channels and the inhibitory effect of GABAergic transmission. An added complication, however, is that whole-cell recording from SCs induces a time-dependent and sustained increase in membrane excitability making it difficult to define the full range of firing rates. Here, we show that whole-cell recording in cerebellar SCs of both male and female mice augments firing rates by reducing the membrane potential at which APs are initiated. AP threshold is lowered due to a hyperpolarizing shift in the gating behavior of voltage-gated Na+ channels. Whole-cell recording also elicits a hyperpolarizing shift in the gating behavior of A-type K+ channels which contributes to increased firing rates. Hodgkin–Huxley modeling and pharmacological experiments reveal that gating shifts in A-type K+ channel activity do not impact AP threshold, but rather promote channel inactivation which removes restraint on the upper limit of firing rates. Taken together, our work reveals an unappreciated impact of voltage-gated Na+ channels that work in coordination with A-type K+ channels to regulate the firing frequency of cerebellar SCs.}, - language = {en}, - number = {3}, - urldate = {2021-04-13}, - journal = {eNeuro}, - author = {Alexander, Ryan P. D. and Mitry, John and Sareen, Vasu and Khadra, Anmar and Bowie, Derek}, - month = may, - year = {2019}, - keywords = {cerebellum, action potential, A-type potassium channel, computational modeling, sodium channel, stellate cell}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FJT2PTDH\\Alexander et al. - 2019 - Cerebellar Stellate Cell Excitability Is Coordinat.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GQVXJ8F2\\ENEURO.0126-19.html:text/html}, -} - -@article{druckmann_novel_2007, - title = {A novel multiple objective optimization framework for constraining conductance-based neuron models by experimental data}, - volume = {1}, - issn = {1662-453X}, - url = {https://www.frontiersin.org/articles/10.3389/neuro.01.1.1.001.2007/full}, - doi = {10.3389/neuro.01.1.1.001.2007}, - abstract = {We present a novel framework for automatically constraining parameters of compartmental models of neurons, given a large set of experimentally measured responses of these neurons. In experiments, intrinsic noise gives rise to a large variability (e.g., in firing pattern) in the voltage responses to repetitions of the exact same input. Thus, the common approach of fitting models by attempting to perfectly replicate, point by point, a single chosen trace out of the spectrum of variable responses does not seem to do justice to the data. In addition, finding a single error function that faithfully characterizes the distance between two spiking traces is not a trivial pursuit. To address these issues, one can adopt a multiple objective optimization approach that allows the use of several error functions jointly.When more than one error function is available, the comparison between experimental voltage traces and model response can be performed on the basis of individual features of interest (e.g., spike rate, spike width). Each feature can be compared between model and experimental mean, in units of its experimental variability, thereby incorporating into the fitting this variability. We demonstrate the success of this approach, when used in conjunction with genetic algorithm optimization, in generating an excellent fit between model behavior and the firing pattern of two distinct electrical classes of cortical interneurons, accommodating and fast-spiking. We argue that the multiple, diverse models generated by this method could serve as the building blocks for the realistic simulation of large neuronal networks.}, - language = {English}, - urldate = {2021-04-19}, - journal = {Frontiers in Neuroscience}, - author = {Druckmann, Shaul and Banitt, Yoav and Gidon, Albert A. and Schürmann, Felix and Markram, Henry and Segev, Idan}, - year = {2007}, - keywords = {compartmental model, cortical interneurons, firing pattern, multi-objective optimization, noisy neurons}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7WLDNUKV\\Druckmann et al. - 2007 - A novel multiple objective optimization framework .pdf:application/pdf}, -} - -@article{de_schutter_active_1994, - title = {An active membrane model of the cerebellar {Purkinje} cell. {I}. {Simulation} of current clamps in slice}, - volume = {71}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/abs/10.1152/jn.1994.71.1.375}, - doi = {10.1152/jn.1994.71.1.375}, - abstract = {1. A detailed compartmental model of a cerebellar Purkinje cell with active dendritic membrane was constructed. The model was based on anatomic reconstructions of single Purkinje cells and included 10 different types of voltage-dependent channels described by Hodgkin-Huxley equations, derived from Purkinje cell-specific voltage-clamp data where available. These channels included a fast and persistent Na+ channel, three voltage-dependent K+ channels, T-type and P-type Ca2+ channels, and two types of Ca(2+)-activated K+ channels. 2. The ionic channels were distributed differentially over three zones of the model, with Na+ channels in the soma, fast K+ channels in the soma and main dendrite, and Ca2+ channels and Ca(2+)-activated K+ channels in the entire dendrite. Channel densities in the model were varied until it could reproduce Purkinje cell responses to current injections in the soma or dendrite, as observed in slice recordings. 3. As in real Purkinje cells, the model generated two types of spiking behavior. In response to small current injections the model fired exclusively fast somatic spikes. These somatic spikes were caused by Na+ channels and repolarized by the delayed rectifier. When higher-amplitude current injections were given, sodium spiking increased in frequency until the model generated large dendritic Ca2+ spikes. Analysis of membrane currents underlying this behavior showed that these Ca2+ spikes were caused by the P-type Ca2+ channel and repolarized by the BK-type Ca(2+)-activated K+ channel. As in pharmacological blocking experiments, removal of Na+ channels abolished the fast spikes and removal of Ca2+ channels removed Ca2+ spiking. 4. In addition to spiking behavior, the model also produced slow plateau potentials in both the dendrite and soma. These longer-duration potentials occurred in response to both short and prolonged current steps. Analysis of the model demonstrated that the plateau potentials in the soma were caused by the window current component of the fast Na+ current, which was much larger than the current through the persistent Na+ channels. Plateau potentials in the dendrite were carried by the same P-type Ca2+ channel that was also responsible for Ca2+ spike generation. The P channel could participate in both model functions because of the low-threshold K2-type Ca(2+)-activated K+ channel, which dynamically changed the threshold for dendritic spike generation through a negative feedback loop with the activation kinetics of the P-type Ca2+ channel. 5. These model responses were robust to changes in the densities of all of the ionic channels.(ABSTRACT TRUNCATED AT 400 WORDS)}, - number = {1}, - urldate = {2021-04-20}, - journal = {Journal of Neurophysiology}, - author = {De Schutter, E. and Bower, J. M.}, - month = jan, - year = {1994}, - pages = {375--400}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JV3HCPKG\\De Schutter and Bower - 1994 - An active membrane model of the cerebellar Purkinj.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\LMMQ7PG5\\jn.1994.71.1.html:text/html}, -} - -@article{wang_adaptation_2003, - title = {Adaptation and {Temporal} {Decorrelation} by {Single} {Neurons} in the {Primary} {Visual} {Cortex}}, - volume = {89}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00242.2003}, - doi = {10.1152/jn.00242.2003}, - abstract = {Limiting redundancy in the real-world sensory inputs is of obvious benefit for efficient neural coding, but little is known about how this may be accomplished by biophysical neural mechanisms. One possible cellular mechanism is through adaptation to relatively constant inputs. Recent investigations in primary visual (V1) cortical neurons have demonstrated that adaptation to prolonged changes in stimulus contrast is mediated in part through intrinsic ionic currents, a Ca2+-activated K+ current (IKCa) and especially a Na+-activated K+ current (IKNa). The present study was designed to test the hypothesis that the activation of adaptation ionic currents may provide a cellular mechanism for temporal decorrelation in V1. A conductance-based neuron model was simulated, which included an IKCa and an IKNa. We show that the model neuron reproduces the adaptive behavior of V1 neurons in response to high contrast inputs. When the stimulus is stochastic with 1/f2 or 1/f-type temporal correlations, these autocorrelations are greatly reduced in the output spike train of the model neuron. The IKCa is effective at reducing positive temporal correlations at approximately 100-ms time scale, while a slower adaptation mediated by IKNa is effective in reducing temporal correlations over the range of 1–20 s. Intracellular injection of stochastic currents into layer 2/3 and 4 (pyramidal and stellate) neurons in ferret primary visual cortical slices revealed neuronal responses that exhibited temporal decorrelation in similarity with the model. Enhancing the slow afterhyperpolarization resulted in a strengthening of the decorrelation effect. These results demonstrate the intrinsic membrane properties of neocortical neurons provide a mechanism for decorrelation of sensory inputs.}, - number = {6}, - urldate = {2021-04-20}, - journal = {Journal of Neurophysiology}, - author = {Wang, Xiao-Jing and Liu, Yinghui and Sanchez-Vives, Maria V. and McCormick, David A.}, - month = jun, - year = {2003}, - pages = {3279--3293}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JG3N5CEA\\Wang et al. - 2003 - Adaptation and Temporal Decorrelation by Single Ne.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\X8C5BBPY\\jn.00242.html:text/html}, -} - -@article{destexhe_impact_1999, - title = {Impact of {Network} {Activity} on the {Integrative} {Properties} of {Neocortical} {Pyramidal} {Neurons} {In} {Vivo}}, - volume = {81}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.1999.81.4.1531}, - doi = {10.1152/jn.1999.81.4.1531}, - abstract = {Impact of network activity on the integrative properties of neocortical pyramidal neurons in vivo. During wakefulness, neocortical neurons are subjected to an intense synaptic bombardment. To assess the consequences of this background activity for the integrative properties of pyramidal neurons, we constrained biophysical models with in vivo intracellular data obtained in anesthetized cats during periods of intense network activity similar to that observed in the waking state. In pyramidal cells of the parietal cortex (area 5–7), synaptic activity was responsible for an approximately fivefold decrease in input resistance (Rin), a more depolarized membrane potential (Vm), and a marked increase in the amplitude of Vm fluctuations, as determined by comparing the same cells before and after microperfusion of tetrodotoxin (TTX). The model was constrained by measurements ofRin, by the average value and standard deviation of the Vm measured from epochs of intense synaptic activity recorded with KAc or KCl-filled pipettes as well as the values measured in the same cells after TTX. To reproduce all experimental results, the simulated synaptic activity had to be of relatively high frequency (1–5 Hz) at excitatory and inhibitory synapses. In addition, synaptic inputs had to be significantly correlated (correlation coefficient ∼0.1) to reproduce the amplitude of Vm fluctuations recorded experimentally. The presence of voltage-dependent K+ currents, estimated from current-voltage relations after TTX, affected these parameters by {\textless}10\%. The model predicts that the conductance due to synaptic activity is 7–30 times larger than the somatic leak conductance to be consistent with the approximately fivefold change inRin. The impact of this massive increase in conductance on dendritic attenuation was investigated for passive neurons and neurons with voltage-dependent Na+/K+ currents in soma and dendrites. In passive neurons, correlated synaptic bombardment had a major influence on dendritic attenuation. The electrotonic attenuation of simulated synaptic inputs was enhanced greatly in the presence of synaptic bombardment, with distal synapses having minimal effects at the soma. Similarly, in the presence of dendritic voltage-dependent currents, the convergence of hundreds of synaptic inputs was required to evoke action potentials reliably. In this case, however, dendritic voltage-dependent currents minimized the variability due to input location, with distal apical synapses being as effective as synapses on basal dendrites. In conclusion, this combination of intracellular and computational data suggests that, during low-amplitude fast electroencephalographic activity, neocortical neurons are bombarded continuously by correlated synaptic inputs at high frequency, which significantly affect their integrative properties. A series of predictions are suggested to test this model.}, - number = {4}, - urldate = {2021-04-20}, - journal = {Journal of Neurophysiology}, - author = {Destexhe, Alain and Paré, Denis}, - month = apr, - year = {1999}, - pages = {1531--1547}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\89J98TST\\Destexhe and Paré - 1999 - Impact of Network Activity on the Integrative Prop.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GGIRPN8W\\jn.1999.81.4.html:text/html}, -} - -@article{zona_riluzole_1998, - title = {Riluzole interacts with voltage-activated sodium and potassium currents in cultured rat cortical neurons}, - volume = {85}, - issn = {0306-4522}, - url = {https://www.sciencedirect.com/science/article/pii/S0306452297006040}, - doi = {10.1016/S0306-4522(97)00604-0}, - abstract = {The actions of the neuroprotective and anticonvulsant agent riluzole on voltage-activated currents were studied in primary cultures of rat cortical neurons by using whole-cell patch-clamp recording techniques. Isolated Na+, Ca2+ and K+ currents were generated in these cells by depolarizing commands from a holding potential of −80mV. Riluzole (10–300μM) reversibly reduced in a dose-dependent manner the inward Na+ currents with an IC50 of 51μM in all the tested neurons (n=29). This drug also shifted the steady-state inactivation curve of the sodium current towards more negative values (about 20mV, n=15) while it did not change significantly the decay phase of the Na+ current. Furthermore, riluzole (100 and 300μM; n=5 and n=3, respectively) did not modulate the inward Ca2+ currents evoked by depolarizing steps on cortical cells. An additional concentration-dependent effect of riluzole was observed on the outward potassium currents. In fact, while the amplitude of the peak of the outward current (IA) was not changed significantly, the amplitude of the late component of the outward K+ current (Iss) was markedly decreased during the perfusion of riluzole (IC50=88μM; n=16). It is concluded that riluzole modulates the Na+- and the late K+-dependent currents in cortical neurons. Both phenomena may explain, at least in part, the anticonvulsant and neuroprotective properties of this compound.}, - language = {en}, - number = {3}, - urldate = {2021-04-27}, - journal = {Neuroscience}, - author = {Zona, C and Siniscalchi, A and Mercuri, N. B and {G. Bernardi}}, - month = apr, - year = {1998}, - keywords = {cortex, epilepsy, neuroprotection, patch-clamp, voltage-activated currents}, - pages = {931--938}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XEPX9VYZ\\Zona et al. - 1998 - Riluzole interacts with voltage-activated sodium a.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H34UM8PN\\S0306452297006040.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EC3WBB3L\\S0306452297006040.html:text/html}, -} - -@article{brodie_sodium_2017, - title = {Sodium {Channel} {Blockers} in the {Treatment} of {Epilepsy}}, - volume = {31}, - issn = {1179-1934}, - url = {https://doi.org/10.1007/s40263-017-0441-0}, - doi = {10.1007/s40263-017-0441-0}, - abstract = {Sodium channel blockers have been the mainstay of the pharmacological management of focal and generalised tonic–clonic seizures for more than 70 years. The focus of this paper will be on phenytoin, carbamazepine, lamotrigine, oxcarbazepine, rufinamide, lacosamide and eslicarbazepine acetate. All these antiepileptic drugs have similar efficacy and share similar dose-dependent, adverse effect profiles, although phenytoin, carbamazepine and oxcarbazepine are more likely to cause idiosyncratic reactions than the others. With the exception of lamotrigine, rufinamide and lacosamide, all are enzyme inducers and most are minor teratogens; although data on teratogenicity are sparse with lacosamide and eslicarbazepine acetate. There is increasing evidence that these drugs differ mechanistically, with the newer agents, lacosamide and eslicarbazepine acetate, having their major pharmacological effect on the slow inactivation state of the sodium channel, which may be associated with better tolerability at higher dosage, although hard evidence in support of this observation is currently not available. Rufinamide is licensed only for Lennox-Gastaut syndrome in children aged 4 years and above. There is a move away from using enzyme inducers, particularly phenytoin and carbamazepine, in everyday clinical practice. There seems little doubt, however, that some sodium channel blockers will have an enduring place in the management of epilepsy well into the 21st century.}, - language = {en}, - number = {7}, - urldate = {2021-05-19}, - journal = {CNS Drugs}, - author = {Brodie, Martin J.}, - month = jul, - year = {2017}, - pages = {527--534}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\PML7LIPE\\Brodie - 2017 - Sodium Channel Blockers in the Treatment of Epilep.pdf:application/pdf}, -} - -@article{theile_inhibition_2011, - title = {Inhibition of {Navβ4} {Peptide}-{Mediated} {Resurgent} {Sodium} {Currents} in {Nav1}.7 {Channels} by {Carbamazepine}, {Riluzole}, and {Anandamide}}, - volume = {80}, - copyright = {Copyright © 2011 The American Society for Pharmacology and Experimental Therapeutics}, - issn = {0026-895X, 1521-0111}, - url = {https://molpharm.aspetjournals.org/content/80/4/724}, - doi = {10.1124/mol.111.072751}, - abstract = {Paroxysmal extreme pain disorder (PEPD) and inherited erythromelalgia (IEM) are inherited pain syndromes arising from different sets of gain-of-function mutations in the sensory neuronal sodium channel isoform Nav1.7. Mutations associated with PEPD, but not IEM, result in destabilized inactivation of Nav1.7 and enhanced resurgent sodium currents. Resurgent currents arise after relief of ultra-fast open-channel block mediated by an endogenous blocking particle and are thought to influence neuronal excitability. As such, enhancement of resurgent currents may constitute a pathological mechanism contributing to sensory neuron hyperexcitability and pain hypersensitivity associated with PEPD. Furthermore, pain associated with PEPD, but not IEM, is alleviated by the sodium channel inhibitor carbamazepine. We speculated that selective attenuation of PEPD-enhanced resurgent currents might contribute to this therapeutic effect. Here we examined whether carbamazepine and two other sodium channel inhibitors, riluzole and anandamide, exhibit differential inhibition of resurgent currents. To gain further insight into the potential mechanism(s) of resurgent currents, we examined whether these inhibitors produced correlative changes in other properties of sodium channel inactivation. Using stably transfected human embryonic kidney 293 cells expressing wild-type Nav1.7 and the PEPD mutants T1464I and M1627K, we examined the effects of the three drugs on Navβ4 peptide-mediated resurgent currents. We observed a correlation between resurgent current inhibition and a drug-mediated increase in the rate of inactivation and inhibition of persistent sodium currents. Furthermore, although carbamazepine did not selectively target resurgent currents, anandamide strongly inhibited resurgent currents with minimal effects on the peak transient current amplitude, demonstrating that resurgent currents can be selectively targeted.}, - language = {en}, - number = {4}, - urldate = {2021-05-19}, - journal = {Molecular Pharmacology}, - author = {Theile, Jonathan W. and Cummins, Theodore R.}, - month = oct, - year = {2011}, - pages = {724--734}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RNAEDV4Q\\Theile and Cummins - 2011 - Inhibition of Navβ4 Peptide-Mediated Resurgent Sod.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8KGSK8R9\\Theile and Cummins - 2011 - Inhibition of Navβ4 Peptide-Mediated Resurgent Sod.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AIIPSDJT\\724.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\67NLFB9U\\724.html:text/html}, -} - -@article{diao_diphenytoin_2013, - title = {Diphenytoin, {Riluzole} and {Lidocaine}: three sodium channel blockers, with different mechanisms of action, decrease hippocampal epileptiform activity}, - volume = {73}, - issn = {0028-3908}, - shorttitle = {Diphenytoin, {Riluzole} and {Lidocaine}}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3766392/}, - doi = {10.1016/j.neuropharm.2013.04.057}, - abstract = {Epilepsy is a condition affecting 1–2\% of the population, characterized by the presence of spontaneous, recurrent seizures. The most common type of acquired epilepsy is temporal lobe epilepsy (TLE). Up to 30\% of patients with TLE are refractory to currently available compounds, and there is an urgent need to identify novel targets for therapy. Here, we utilized the in-vitro CA3 burst preparation to examine alterations in network excitability, characterized by changes in interburst interval and bursting thresholds. Specifically, we show that bath application of three different sodium channel blockers—diphenytoin, riluzole, and lidocaine—slow spontaneous CA3 bursts. This in turn, decreased the epileptiform activity. These compounds work at different sites on voltage-gated sodium channels, but produce a similar network phenotype of decreased excitability. In the case of diphenytoin and riluzole, the change in network activity (i.e., increased interburst intervals) was persistent following drug washout. Lidocaine application, however, only increased the CA3 interburst interval when it was in the bath solution. Thus, its action was not permanent and resulted in returning CA3 bursting to baseline levels. These data demonstrate that the CA3 burst preparation provides a relatively easy and quick platform for identifying compounds that can decrease network excitability, providing the initial screen for further and more complex in-vivo, freely-behaving animal studies.}, - urldate = {2021-05-19}, - journal = {Neuropharmacology}, - author = {Diao, Lihong and Hellier, Jennifer L. and Uskert-Newsom, Jessica and Williams, Philip A. and Staley, Kevin J. and Yee, Audrey S.}, - month = oct, - year = {2013}, - pages = {48--55}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\IBLRMVFZ\\Diao et al. - 2013 - Diphenytoin, Riluzole and Lidocaine three sodium .pdf:application/pdf}, -} - -@article{lukacs_non-blocking_2018, - title = {Non-blocking modulation contributes to sodium channel inhibition by a covalently attached photoreactive riluzole analog}, - volume = {8}, - copyright = {2018 The Author(s)}, - issn = {2045-2322}, - url = {https://www.nature.com/articles/s41598-018-26444-y}, - doi = {10.1038/s41598-018-26444-y}, - abstract = {Sodium channel inhibitor drugs decrease pathological hyperactivity in various diseases including pain syndromes, myotonia, arrhythmias, nerve injuries and epilepsies. Inhibiting pathological but not physiological activity, however, is a major challenge in drug development. Sodium channel inhibitors exert their effects by a dual action: they obstruct ion flow (“block”), and they alter the energetics of channel opening and closing (“modulation”). Ideal drugs would be modulators without blocking effect, because modulation is inherently activity-dependent, therefore selective for pathological hyperactivity. Can block and modulation be separated? It has been difficult to tell, because the effect of modulation is obscured by conformation-dependent association/dissociation of the drug. To eliminate dynamic association/dissociation, we used a photoreactive riluzole analog which could be covalently bound to the channel; and found, unexpectedly, that drug-bound channels could still conduct ions, although with modulated gating. The finding that non-blocking modulation is possible, may open a novel avenue for drug development because non-blocking modulators could be more specific in treating hyperactivity-linked diseases.}, - language = {en}, - number = {1}, - urldate = {2021-05-19}, - journal = {Scientific Reports}, - author = {Lukacs, Peter and Földi, Mátyás C. and Valánszki, Luca and Casanova, Emilio and Biri-Kovács, Beáta and Nyitray, László and Málnási-Csizmadia, András and Mike, Arpad}, - month = may, - year = {2018}, - pages = {8110}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WDK8KNIX\\Lukacs et al. - 2018 - Non-blocking modulation contributes to sodium chan.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FNJX2GAJ\\Lukacs et al. - 2018 - Non-blocking modulation contributes to sodium chan.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\W6F62AAK\\s41598-018-26444-y.html:text/html}, -} - -@article{xie_blockade_2011, - title = {Blockade of {Persistent} {Sodium} {Currents} {Contributes} to the {Riluzole}-{Induced} {Inhibition} of {Spontaneous} {Activity} and {Oscillations} in {Injured} {DRG} {Neurons}}, - volume = {6}, - issn = {1932-6203}, - url = {https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0018681}, - doi = {10.1371/journal.pone.0018681}, - abstract = {In addition to a fast activating and immediately inactivating inward sodium current, many types of excitable cells possess a noninactivating or slowly inactivating component: the persistent sodium current (INaP). The INaP is found in normal primary sensory neurons where it is mediated by tetrodotoxin-sensitive sodium channels. The dorsal root ganglion (DRG) is the gateway for ectopic impulses that originate in pathological pain signals from the periphery. However, the role of INaP in DRG neurons remains unclear, particularly in neuropathic pain states. Using in vivo recordings from single medium- and large-diameter fibers isolated from the compressed DRG in Sprague-Dawley rats, we show that local application of riluzole, which blocks the INaP, also inhibits the spontaneous activity of A-type DRG neurons in a dose-dependent manner. Significantly, riluzole also abolished subthreshold membrane potential oscillations (SMPOs), although DRG neurons still responded to intracellular current injection with a single full-sized spike. In addition, the INaP was enhanced in medium- and large-sized neurons of the compressed DRG, while bath-applied riluzole significantly inhibited the INaP without affecting the transient sodium current (INaT). Taken together, these results demonstrate for the first time that the INaP blocker riluzole selectively inhibits INaP and thereby blocks SMPOs and the ectopic spontaneous activity of injured A-type DRG neurons. This suggests that the INaP of DRG neurons is a potential target for treating neuropathic pain at the peripheral level.}, - language = {en}, - number = {4}, - urldate = {2021-05-19}, - journal = {PLOS ONE}, - author = {Xie, Rou-Gang and Zheng, Da-Wei and Xing, Jun-Ling and Zhang, Xu-Jie and Song, Ying and Xie, Ya-Bin and Kuang, Fang and Dong, Hui and You, Si-Wei and Xu, Hui and Hu, San-Jue}, - month = apr, - year = {2011}, - keywords = {Neurons, Neuropathic pain, Action potentials, Membrane potential, Allodynia, Ganglia, Nerve fibers, Sodium channels}, - pages = {e18681}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\G5J74HJR\\Xie et al. - 2011 - Blockade of Persistent Sodium Currents Contributes.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\I7CXMK5Y\\article.html:text/html}, -} - -@article{spadoni_lamotrigine_2002, - title = {Lamotrigine derivatives and riluzole inhibit {INa},{P} in cortical neurons}, - volume = {13}, - issn = {0959-4965}, - url = {https://journals.lww.com/neuroreport/Fulltext/2002/07020/Lamotrigine_derivatives_and_riluzole_inhibit_INa,P.19.aspx}, - abstract = {The persistent, slowly inactivating fraction of the sodium current is involved in key functions in the CNS such as dendritic integration of synaptic inputs and cellular excitability. We have studied whether established anti-epileptic drugs and neuroprotective agents target the persistent sodium current. Two lamotrigine derivatives (sipatrigine and 202W92) and riluzole inhibited the persistent sodium current at low, therapeutic concentrations. In contrast, lamotrigine and the classical antiepileptic agents phenytoin and valproic acid blocked the fast-inactivating sodium channel but failed to affect the persistent fraction. The ability to influence either mode of channel activaty may represent a defining feature of each drug subclass, changing profoundly their clinical indications. Given the damaging role of a sustained influx of sodium in both pharmaco-resistant seizures or excitotoxic insults, we suggest the utilization of drugs that suppress the persistent conductance.}, - language = {en-US}, - number = {9}, - urldate = {2021-05-19}, - journal = {NeuroReport}, - author = {Spadoni, Francesca and Hainsworth, Atticus Henry and Mercuri, Nicola Biagio and Caputi, Luigi and Martella, Giuseppina and Lavaroni, Franco and Bernardi, Giorgio and Stefani, Alessandro}, - month = jul, - year = {2002}, - pages = {1167--1170}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4BRGNDA8\\Lamotrigine_derivatives_and_riluzole_inhibit_INa,P.19.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ZHP264G3\\Lamotrigine_derivatives_and_riluzole_inhibit_INa,P.19.html:text/html}, -} - -@article{stefani_differential_1997, - title = {Differential {Inhibition} by {Riluzole}, {Lamotrigine}, and {Phenytoin} of {Sodium} and {Calcium} {Currents} in {Cortical} {Neurons}: {Implications} for {Neuroprotective} {Strategies}}, - volume = {147}, - issn = {0014-4886}, - shorttitle = {Differential {Inhibition} by {Riluzole}, {Lamotrigine}, and {Phenytoin} of {Sodium} and {Calcium} {Currents} in {Cortical} {Neurons}}, - url = {https://www.sciencedirect.com/science/article/pii/S0014488697965547}, - doi = {10.1006/exnr.1997.6554}, - abstract = {Among the several classes of drugs currently studied as neuroprotective agents, glutamate release blockers have been indicated as being rather effective. In particular, lamotrigine and riluzole have shown promise in the treatment of either acutely developing cellular damages (stroke, posttraumatic lesions) or slowly progressing neurodegenerative diseases as amyotrophic lateral sclerosis. These drugs are supposed to interfere with the release of endogenous glutamatein situ,yet the mechanisms underlying this effect are not fully defined. One possibility is that lamotrigine and riluzole act by inhibiting voltage-dependent inward conductances active in the soma and/or in the axon terminal region. Therefore, we have investigated the effects of lamotrigine and riluzole on the voltage-gated sodium and calcium currents of acutely isolated neurons from the adult rat neocortex. In addition, since phenytoin is a well-known blocker of the sodium channel, we have compared lamotrigine and riluzole responses with the peak current inhibition produced by phenytoin in the same cells. Lamotrigine produced a large reduction of the high-voltage-activated calcium currents and a smaller, use-dependent inhibition of the sodium conductance. Riluzole inhibited significantly the sodium current at surprisingly low concentrations (nanomolar range) and by up to 80\% at saturating doses (1–10 μM). Furthermore, riluzole inhibited both high- and low-voltage-activated calcium currents in neocortical neurons isolated from adult and young animals. By contrast, phenytoin caused only a slight reduction of high-voltage-activated calcium currents even at supratherapeutic doses (by {\textless}12\% at 10 μM). Taken together, the different pharmacological profiles of the tested agents might indicate that glutamate release blockers do not represent a homogenous class of drugs. Conversely, our findings could support their selective utilization in different disease status.}, - language = {en}, - number = {1}, - urldate = {2021-05-19}, - journal = {Experimental Neurology}, - author = {Stefani, A. and Spadoni, F. and Bernardi, G.}, - month = sep, - year = {1997}, - pages = {115--122}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7ZYT3ZKL\\Stefani et al. - 1997 - Differential Inhibition by Riluzole, Lamotrigine, .pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7BPTYF8N\\Stefani et al. - 1997 - Differential Inhibition by Riluzole, Lamotrigine, .pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\QNH3CJ5Q\\S0014488697965547.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\47EBIML7\\S0014488697965547.html:text/html}, -} - -@article{urbani_riluzole_2000, - title = {Riluzole inhibits the persistent sodium current in mammalian {CNS} neurons}, - volume = {12}, - copyright = {© Federation of European Neuroscience Societies}, - issn = {1460-9568}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1460-9568.2000.00242.x}, - doi = {https://doi.org/10.1046/j.1460-9568.2000.00242.x}, - abstract = {The effects of 0.1–100 μm riluzole, a neuroprotective agent with anticonvulsant properties, were studied on neurons from rat brain cortex. Patch-clamp whole-cell recordings in voltage-clamp mode were performed on thin slices to examine the effects of the drug on a noninactivating (persistent) Na+ current (INa,p). INa,p was selected because it enhances neuronal excitability near firing threshold, which makes it a potential target for anticonvulsant drugs. When added to the external solution, riluzole dose-dependently inhibited INa,p up to a complete blocking of the current (EC50 2 μm), showing a significant effect at therapeutic drug concentrations. A comparative dose-effect study was carried out in the same cells for the other main known action of riluzole, the inhibitory effect on the fast transient sodium current. This effect was confirmed in our experiments, but we found that it was achieved at levels much higher than putative therapeutic concentrations. Only the effect on INa,p, and not that on fast sodium current, can account for the reduction in neuronal excitability observed in cortical neurons following riluzole treatment at therapeutic concentrations, and this might represent a novel mechanism accounting for the anticonvulsant and neuroprotective properties of riluzole.}, - language = {en}, - number = {10}, - urldate = {2021-05-19}, - journal = {European Journal of Neuroscience}, - author = {Urbani, Andrea and Belluzzi, Ottorino}, - year = {2000}, - keywords = {patch-clamp, amyotrophic lateral sclerosis, cortical neurons, Na+-current, slice preparation}, - pages = {3567--3574}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9KI63EDH\\Urbani and Belluzzi - 2000 - Riluzole inhibits the persistent sodium current in.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5CMWNZVW\\j.1460-9568.2000.00242.html:text/html}, -} - -@article{xu_neuroprotective_2001, - title = {Neuroprotective {Agent} {Riluzole} {Dramatically} {Slows} {Inactivation} of {Kv1}.4 {Potassium} {Channels} by a {Voltage}-{Dependent} {Oxidative} {Mechanism}}, - volume = {299}, - copyright = {The American Society for Pharmacology and Experimental Therapeutics}, - issn = {0022-3565, 1521-0103}, - url = {https://jpet.aspetjournals.org/content/299/1/227}, - abstract = {The modulation of Kv1.4 K+ channels by the neuroprotective agent riluzole was studied in bovine adrenal zona fasciculata cells by using whole-cell patch clamp. At concentrations ranging from 1 to 100 μM, riluzole reversibly inhibited Kv1.4 channels (IC50 = 70 μM) and irreversibly slowed Kv1.4 inactivation. Riluzole (100 μM) increased the inactivation time constant (τi) from a control value of 28.9 ± 3.9 to 623 ± 47.6 ms (n = 13). The slowing of bKv1.4 inactivation was not affected by substituting poorly hydrolyzable nucleotides for ATP in the pipette solution, or by the addition of cAMP. Riluzole-induced slowing of bKv1.4 inactivation was nearly eliminated by the presence of the antioxidant reduced glutathione (3 mM) or dithiothreitol (3–5 mM) in the recording pipette, or when cells were superfused with riluzole at a holding potential of −40 mV rather than −80 mV. These results are consistent with a model in which riluzole inhibits bKv1.4 currents and slows inactivation by separate mechanisms. Slowing of inactivation is independent of protein kinases, but probably involves oxidation of a cysteine in the N-terminal inactivation domain. Failure of riluzole to slow inactivation when applied to a depolarized cell suggests that this cysteine is protected in an inactivated Kv1.4 channel. The neuroprotective action of riluzole involves inhibition of glutamate release from presynaptic terminals within the central nervous system. Kv1.4 K+ channels are distributed throughout the brain in axons and nerve terminals, including those from which glutamate is released. The pronounced slowing of Kv1.4 inactivation by riluzole in these neurons could be an important mechanism underlying the inhibition of glutamate release and the therapeutic actions of this drug.}, - language = {en}, - number = {1}, - urldate = {2021-05-19}, - journal = {Journal of Pharmacology and Experimental Therapeutics}, - author = {Xu, Lin and Enyeart, Judith A. and Enyeart, John J.}, - month = oct, - year = {2001}, - pages = {227--237}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\66RL6LTD\\227.html:text/html}, -} - -@article{song_differential_1997, - title = {Differential {Action} of {Riluzole} on {Tetrodotoxin}-{Sensitive} and {Tetrodotoxin}-{Resistant} {Sodium} {Channels}}, - volume = {282}, - copyright = {The American Society for Pharmacology and Experimental Therapeutics}, - issn = {0022-3565, 1521-0103}, - url = {https://jpet.aspetjournals.org/content/282/2/707}, - abstract = {The effects of riluzole, a neuroprotective drug, on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) sodium channels in rat dorsal root ganglion neurons were studied using the whole-cell patch clamp technique. At the resting potential, riluzole preferentially blocked TTX-S sodium channels, whereas at more negative potentials, it blocked both types of sodium channels almost equally. The apparent dissociation constants for riluzole to block TTX-S and TTX-R sodium channels in their resting state were 90 and 143 μM, respectively. Riluzole shifted the voltage dependence of activation of TTX-R sodium channels in the depolarizing direction more than that of TTX-S sodium channels. The voltage dependence of the fast inactivation of both types of sodium channels was shifted in the hyperpolarizing direction in a dose-dependent manner, and the apparent dissociation constants for riluzole to block the inactivated channels were estimated to be 2 and 3 μM for the TTX-S and TTX-R sodium channels, respectively, indicating a much higher affinity for the inactivated channels than for the resting channels. Riluzole was equally effective in blocking both types of sodium channels in their slow inactivated state. Since more TTX-S channels are inactivated than TTX-R channels at the resting potential, riluzole blocks TTX-S sodium channels more potently than TTX-R sodium channels. It was concluded that one of the mechanisms by which riluzole exerts its neuroprotective action is to preferentially block the inactivated sodium channel of damaged or depolarized neurons under ischemic conditions, thereby suppressing excess stimulation of the glutamatergic receptors and massive influx of Ca++.}, - language = {en}, - number = {2}, - urldate = {2021-05-19}, - journal = {Journal of Pharmacology and Experimental Therapeutics}, - author = {Song, Jin-Ho and Huang, Chao-Sheng and Nagata, Keiichi and Yeh, Jay Z. and Narahashi, Toshio}, - month = aug, - year = {1997}, - pages = {707--714}, - file = {Differential Action of Riluzole on Tetrodotoxin-Sensitive and Tetrodotoxin-Resistant Sodium Channels | Journal of Pharmacology and Experimental Therapeutics:C\:\\Users\\nilsk\\Zotero\\storage\\R6JEQXXG\\707.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\57LLK943\\707.html:text/html}, -} - -@article{benoit_riluzole_1991, - title = {Riluzole specifically blocks inactivated {Na} channels in myelinated nerve fibre}, - volume = {419}, - issn = {1432-2013}, - url = {https://doi.org/10.1007/BF00370302}, - doi = {10.1007/BF00370302}, - abstract = {The effects of 0.15–250 μM riluzole, a novel psychotropic agent with anticonvulsant properties, were studied on voltage-clamped nodes of Ranvier of isolated nerve fibres of the frog. When added to the external solution, the drug rapidly and reversibly inhibited both K and Na currents with an apparent dissociation constant of 0.09 mM. The riluzole-induced decrease of these currents was not “use-dependent”. At concentrations up to 100μM, the drug had no noticeable effect on the time course of Na current inactivation nor on the shape and the position along voltage axis of the Na conductance/voltage relationship. On the other hand, it induced substantial shifts towards negative voltages of the steady-state Na inactivation/voltage curve. From these results, according to the modulated-receptor model, an apparent dissociation constant of 0.29 μM could be calculated for riluzole-induced blockage of inactivated Na channels. The recovery from Na current inactivation was also affected by the drug. It is concluded that riluzole is a highly specific blocker of inactivated Na channels, which is more than 300 times more effective on these channels than on K or resting Na channels.}, - language = {en}, - number = {6}, - urldate = {2021-05-19}, - journal = {Pflügers Archiv}, - author = {Benoit, Evelyne and Escande, Denis}, - month = dec, - year = {1991}, - pages = {603--609}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\V9HS43E9\\Benoit and Escande - 1991 - Riluzole specifically blocks inactivated Na channe.pdf:application/pdf}, -} - -@article{aledo-serrano_sodium_2021, - title = {Sodium channel blockers for the treatment of epilepsy in {CDKL5} deficiency disorder: {Findings} from a multicenter cohort}, - volume = {118}, - issn = {1525-5050}, - shorttitle = {Sodium channel blockers for the treatment of epilepsy in {CDKL5} deficiency disorder}, - url = {https://www.sciencedirect.com/science/article/pii/S1525505021001803}, - doi = {10.1016/j.yebeh.2021.107946}, - abstract = {Objective -This study was aimed to analyze the effectiveness of sodium channel blockers (SCBs) in CDKL5 deficiency disorder (CDD)-related epilepsy. -Methods -A retrospective, observational study was performed, including patients with CDD diagnosis evaluated between 2016 and 2019 at three tertiary Epilepsy Centers. Demographic, electroclinical and genetic features, as well as ASM treatments and their outcomes were analyzed, with special focus on SCBs. -Results -Twenty-one patients evaluated at three tertiary Epilepsy Centers were included, of which 19 presented with epilepsy (90.5\%); all had pathogenic mutations of CDKL5. Six patients (31.6\%) were classified as SCB responders (more than 50\% reduction), four being currently seizure free (mean seizure-free period of 8 years). Most frequent SCB drugs were oxcarbazepine (OXC), carbamazepine (CBZ), and lacosamide (LCM). None of them presented relevant adverse events. In contrast, three patients showed seizure aggravation in the non-responder group. When comparing both groups, responders had statistically significant younger age at SCB treatment and epilepsy onset, higher proportion of focal epileptiform activity and less frequent history of West syndrome. -Conclusions -The results of this study indicate that treatment with SCBs might be effective and safe in a subset of patients with CDD-related epilepsy.}, - language = {en}, - urldate = {2021-05-20}, - journal = {Epilepsy \& Behavior}, - author = {Aledo-Serrano, Ángel and Gómez-Iglesias, Patricia and Toledano, Rafael and Garcia-Peñas, Juan Jose and Garcia-Morales, Irene and Anciones, Carla and Soto-Insuga, Victor and Benke, Timothy A. and del Pino, Isabel and Gil-Nagel, Antonio}, - month = may, - year = {2021}, - keywords = {Antiseizure medication, Carbamazepine, CDD, Developmental and epileptic encephalopathies, Genetic epilepsy}, - pages = {107946}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\R7ETP9N5\\S1525505021001803.html:text/html}, -} - -@article{adney_functional_2020, - title = {Functional and pharmacological evaluation of a novel {SCN2A} variant linked to early‐onset epilepsy}, - volume = {7}, - issn = {2328-9503}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7480906/}, - doi = {10.1002/acn3.51105}, - abstract = {Objective -We identified a novel de novo SCN2A variant (M1879T) associated with infantile‐onset epilepsy that responded dramatically to sodium channel blocker antiepileptic drugs. We analyzed the functional and pharmacological consequences of this variant to establish pathogenicity, and to correlate genotype with phenotype and clinical drug response. - -Methods -The clinical and genetic features of an infant boy with epilepsy are presented. We investigated the effect of the variant using heterologously expressed recombinant human NaV1.2 channels. We performed whole‐cell patch clamp recording to determine the functional consequences and response to carbamazepine. - -Results -The M1879T variant caused disturbances in channel inactivation including substantially depolarized voltage dependence of inactivation, slower time course of inactivation, and enhanced resurgent current that collectively represent a gain‐of‐function. Carbamazepine partially normalized the voltage dependence of inactivation and produced use‐dependent block of the variant channel at high pulsing frequencies. Carbamazepine also suppresses resurgent current conducted by M1879T channels, but this effect was explained primarily by reducing the peak transient current. Molecular modeling suggests that the M1879T variant disrupts contacts with nearby residues in the C‐terminal domain of the channel. - -Interpretation -Our study demonstrates the value of conducting functional analyses of SCN2A variants of unknown significance to establish pathogenicity and genotype–phenotype correlations. We also show concordance of in vitro pharmacology using heterologous cells with the drug response observed clinically in a case of SCN2A‐associated epilepsy.}, - number = {9}, - urldate = {2021-05-20}, - journal = {Annals of Clinical and Translational Neurology}, - author = {Adney, Scott K. and Millichap, John J. and DeKeyser, Jean‐Marc and Abramova, Tatiana and Thompson, Christopher H. and George, Alfred L.}, - month = aug, - year = {2020}, - pages = {1488--1501}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YMNWKHEY\\Adney et al. - 2020 - Functional and pharmacological evaluation of a nov.pdf:application/pdf}, -} - -@article{welzel_drugdrug_2021, - title = {Drug–drug and drug–food interactions in an infant with early-onset {SCN2A} epilepsy treated with carbamazepine, phenytoin and a ketogenic diet}, - volume = {87}, - copyright = {© 2020 The British Pharmacological Society}, - issn = {1365-2125}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/bcp.14503}, - doi = {https://doi.org/10.1111/bcp.14503}, - abstract = {Sodium channel 2 subunit α (SCN2A) mutations cause difficult-to-treat early-onset epilepsy. Effective treatment includes high-dose phenytoin or carbamazepine ± ketogenic diet (KD). We describe an infant with early-onset SCN2A-epilepsy with subtherapeutic carbamazepine concentration during transition from phenytoin treatment to avoid long-term neurotoxicity. The transition from high-dose phenytoin (20 mg kg−1 d−1, concentration: ≥20 mg/L) with KD, to carbamazepine (50–75 mg kg−1 d−1, concentration: 9–12 mg/L) lasted 85 days, which we suspected was due to significant drug–drug and/or drug–food interactions. Model-based analysis of carbamazepine pharmacokinetics quantified significant time- and dose-dependent phenytoin-mediated CYP3A4 induction and carbamazepine concentration-dependent auto-induction (apparent clearance increased up to 2.5/3-fold). Lower carbamazepine concentrations under KD were modelled as decreased relative bioavailability (44\%), potentially related to decreased fraction absorbed (unexpected for this lipophilic drug), increased intestinal/hepatic metabolism and/or decreased protein-binding with KD. This suggests importance of carbamazepine-concentration monitoring during KD-introduction/removal and necessity of high carbamazepine doses to achieve therapeutic concentrations, especially in infants treated with high-dose phenytoin.}, - language = {en}, - number = {3}, - urldate = {2021-05-20}, - journal = {British Journal of Clinical Pharmacology}, - author = {Welzel, Tatjana and Ziesenitz, Victoria C. and Weber, Peter and Datta, Alexandre N. and Anker, Johannes N. van den and Gotta, Verena}, - year = {2021}, - keywords = {carbamazepine, drug–drug interaction, food–drug interaction, ketogenic diet, pharmacokinetic changes, phenytoin, SCN2A epilepsy, sodium channel blocker}, - pages = {1568--1573}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7SUT23VU\\Welzel et al. - 2021 - Drug–drug and drug–food interactions in an infant .pdf:application/pdf}, -} - -@article{pechmann_novo_2019, - title = {De novo variant in {SCN4A} causes neonatal sodium channel myotonia with general muscle stiffness and respiratory failure}, - volume = {29}, - issn = {1873-2364}, - doi = {10.1016/j.nmd.2019.09.001}, - abstract = {Variants of the skeletal muscle sodium channel gene SCN4A are associated with different neuromuscular disorders including sodium channel myotonia. Here, we report an infant with a de novo variant in SCN4A presenting with neonatal onset of severe muscle stiffness with involvement of facial and eyelid muscles, and life-threatening events with respiratory failure due to severe apnoea and thorax rigidity. The boy dramatically improved in both respiratory and motor function under carbamazepine therapy.}, - language = {eng}, - number = {11}, - journal = {Neuromuscular disorders: NMD}, - author = {Pechmann, Astrid and Eckenweiler, Matthias and Schorling, David and Stavropoulou, Dimitra and Lochmüller, Hanns and Kirschner, Janbernd}, - month = nov, - year = {2019}, - keywords = {Male, Humans, Infant, Infant, Newborn, Elasticity, Genetic Variation, Muscle stiffness, Muscular Diseases, Myotonia, Myotonia Congenita, NAV1.4 Voltage-Gated Sodium Channel, Phenotype, Respiratory failure, Respiratory Insufficiency, SCN4A}, - pages = {907--909}, -} - -@article{fedorova_lidocaine_2019, - title = {Lidocaine and carbamazepine inhibit while phenytoin and lamotrigine paradoxically enhance the insect neuromuscular transmission}, - volume = {19}, - issn = {1439-1104}, - url = {https://doi.org/10.1007/s10158-019-0224-z}, - doi = {10.1007/s10158-019-0224-z}, - abstract = {Primary mechanism of action of local anesthetics and various anticonvulsants is the voltage-gated sodium channel block. Many of these small molecules also have other targets in nervous system of vertebrates. However, little is known about their action on invertebrate nervous system. Nevertheless, insect-based models are suggested for high-throughput screening of antiepileptic drugs. In the present work, we characterized action of lidocaine, carbamazepine, lamotrigine, and phenytoin on the neuromuscular transition of Calliphora vicina fly larvae using conventional voltage-clamp approach. Carbamazepine and lidocaine caused inhibition of synaptic transmission, which has presynaptic origin. This action is in agreement with inhibition of voltage-gated sodium channels that reduces depolarization of nerve terminals and, thus, calcium entry. Surprisingly, phenytoin and lamotrigine produced a prominent increase in the evoked postsynaptic currents without any effect on frequency or amplitude of spontaneous miniature currents. Potassium channel blocker 4-aminopyridine affects synaptic transmission in similar way. Elevation of synaptic quantal content via increase in calcium concentration or via application of 1 mM 4-aminopyridine eliminates the enhancement effect or even turns it to modest inhibition. We propose that lamotrigine and phenytoin act as inhibitors of insect potassium channels that cause the membrane depolarization and thus facilitates calcium entry into the nerve terminal.}, - language = {en}, - number = {1}, - urldate = {2021-05-20}, - journal = {Invertebrate Neuroscience}, - author = {Fedorova, Irina M. and Tikhonov, Denis B.}, - month = feb, - year = {2019}, - pages = {4}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RMECNUVC\\Fedorova and Tikhonov - 2019 - Lidocaine and carbamazepine inhibit while phenytoi.pdf:application/pdf}, -} - -@article{nazish_possible_2018, - title = {The possible effect of {SCN1A} and {SCN2A} genetic variants on carbamazepine response among {Khyber} {Pakhtunkhwa} epileptic patients, {Pakistan}}, - volume = {14}, - issn = {1176-6336}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6254658/}, - doi = {10.2147/TCRM.S180827}, - abstract = {Purpose -SCN1A (3184 A{\textgreater}G) and SCN2A (56G{\textgreater}A) gene encodes α subunit of the neuronal voltage-gated sodium channel, which is a target for carbamazepine (CBZ). Recent studies have demonstrated that polymorphism of SCN1A (3184 A{\textgreater}G) and SCN2A (56G{\textgreater}A) was associated with use of CBZ. However, it has not been determined whether the polymorphism affects CBZ or other antiepileptic drug responsiveness. The aim of the study was to establish whether the SCN1A (3184 A{\textgreater}G) and SCN2A (56G{\textgreater}A) polymorphisms of the SCN1A and SCN2A genes affect responsiveness to CBZ. - -Methods -SCN1A (3184 A{\textgreater}G) and SCN2A (56G{\textgreater}A) gene polymorphisms were genotyped in 93 Khyber Pakhtunkhwa epileptic patients treated with CBZ. The association between CBZ responsiveness and the polymorphism was estimated by adjusting for clinical factors affecting the outcome of therapy. The number of seizure episodes was documented at baseline, and the therapy of each of the 93 patients was followed up. The plasma level of CBZ was determined using reverse-phase high-performance liquid chromatography. SCN1A and SCN2A genes were genotyped using RFLP. Data were analyzed using Graph Pad Prism 6. - -Results -Mean age of the patients was 18.6±9.3 at the 3rd month and 18.7±9.5 at the 6th month. The baseline dose of CBZ was 468±19.8 mg/d and titrated at the rate of 48±1.4 and 4.0±0.2 mg/d. The difference in plasma level of CBZ was significant (P=0.004) between 3rd and 6th month among different genotypes of SCN1A gene in nonresponder and responder patients. At the 3rd month of the therapy, the poor responders were more likely (P=0.003 and P=0.01) to have variants (3184AG and 3184GG) of SCN1A gene. Similarly, poor responsders were more likely (P=0.0007 and P=0.001) to have variant genotypes (56GA, 56AA) of SCN2A gene at the 3rd month of the therapy. - -Conclusion -This study demonstrated a significant association between the SCN1A (3184 AG and GG) and SCN2A (56GA and AA) genotype with CBZ-nonresponsive epilepsy.}, - urldate = {2021-05-20}, - journal = {Therapeutics and Clinical Risk Management}, - author = {Nazish, Haleema Rehana and Ali, Niaz and Ullah, Shakir}, - month = nov, - year = {2018}, - pages = {2305--2313}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YQJUEUYR\\Nazish et al. - 2018 - The possible effect of SCN1A and SCN2A genetic var.pdf:application/pdf}, -} - -@article{sharawat_response_2019, - title = {Response to {Carbamazepine} in {KCNQ2} {Related} {Early} {Infantile} {Epileptic} {Encephalopathy}}, - volume = {86}, - issn = {0973-7693}, - url = {https://doi.org/10.1007/s12098-018-2796-8}, - doi = {10.1007/s12098-018-2796-8}, - language = {en}, - number = {3}, - urldate = {2021-05-20}, - journal = {The Indian Journal of Pediatrics}, - author = {Sharawat, Indar Kumar and Kasinathan, Ananthanarayanan and Sahu, Jitendra Kumar and Sankhyan, Naveen}, - month = mar, - year = {2019}, - pages = {301--302}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XKHGKL3I\\Sharawat et al. - 2019 - Response to Carbamazepine in KCNQ2 Related Early I.pdf:application/pdf}, -} - -@article{sands_rapid_2016, - title = {Rapid and safe response to low-dose carbamazepine in neonatal epilepsy}, - volume = {57}, - issn = {1528-1167}, - doi = {10.1111/epi.13596}, - abstract = {OBJECTIVE: To evaluate treatment responses in benign familial neonatal epilepsy (BFNE). -METHODS: We recruited patients with BFNE through a multicenter international collaboration and reviewed electroclinical and genetic details, and treatment response. All patients were tested at minimum for mutations/deletions in the KCNQ2, KCNQ3, and SCN2A genes. -RESULTS: Nineteen patients were included in this study. A family history of neonatal seizures was positive in 16 patients, and one additional patient had a family history of infantile seizures. Mutations or deletions of KCNQ2 were found in 14, and of KCNQ3 in 2, of the 19 patients. In all patients, seizures began at 2-5 days of life and occurred multiple times per day. Four patients developed status epilepticus. Seizures were focal, alternating between hemispheres, and characterized by asymmetric tonic posturing associated with apnea and desaturation, followed by unilateral or bilateral asynchronous clonic jerking. Twelve of 19 patients were treated with multiple medications prior to seizure cessation. Seventeen of (88\%) 19 patients were seizure-free within hours of receiving oral carbamazepine (CBZ) or oxcarbazepine (OXC). Earlier initiation of CBZ was associated with shorter hospitalization (p {\textless} 0.01). No side effects of CBZ were reported. All patients had normal development and remain seizure-free at a mean follow-up period of 7.8 years (6 months-16 years). -SIGNIFICANCE: This study provides evidence that CBZ is safe and rapidly effective in neonates with BFNE, even in status epilepticus. We propose that CBZ should be the drug of choice in benign familial neonatal seizures.}, - language = {eng}, - number = {12}, - journal = {Epilepsia}, - author = {Sands, Tristan T. and Balestri, Martina and Bellini, Giulia and Mulkey, Sarah B. and Danhaive, Olivier and Bakken, Eliza Hayes and Taglialatela, Maurizio and Oldham, Michael S. and Vigevano, Federico and Holmes, Gregory L. and Cilio, Maria Roberta}, - month = dec, - year = {2016}, - keywords = {Electroencephalography, Male, Humans, Female, Magnetic Resonance Imaging, Child, Preschool, Infant, Carbamazepine, Anticonvulsants, Benign familial neonatal epilepsy, Epilepsy, Benign Neonatal, Family Health, Follow-Up Studies, Gestational Age, KCNQ2, KCNQ3, Mutation, NAV1.2 Voltage-Gated Sodium Channel, Neonatal seizures, Oxcarbazepine, Potassium Channels}, - pages = {2019--2030}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\DE9DHN9V\\Sands et al. - 2016 - Rapid and safe response to low-dose carbamazepine .pdf:application/pdf}, -} - -@article{weckhuysen_extending_2013, - title = {Extending the {KCNQ2} encephalopathy spectrum: clinical and neuroimaging findings in 17 patients}, - volume = {81}, - issn = {1526-632X}, - shorttitle = {Extending the {KCNQ2} encephalopathy spectrum}, - doi = {10.1212/01.wnl.0000435296.72400.a1}, - abstract = {OBJECTIVES: To determine the frequency of KCNQ2 mutations in patients with neonatal epileptic encephalopathy (NEE), and to expand the phenotypic spectrum of KCNQ2 epileptic encephalopathy. -METHODS: Eighty-four patients with unexplained NEE were screened for KCNQ2 mutations using classic Sanger sequencing. Clinical data of 6 additional patients with KCNQ2 mutations detected by gene panel were collected. Detailed phenotyping was performed with particular attention to seizure frequency, cognitive outcome, and video-EEG. -RESULTS: In the cohort, we identified 9 different heterozygous de novo KCNQ2 missense mutations in 11 of 84 patients (13\%). Two of 6 missense mutations detected by gene panel were recurrent and present in patients of the cohort. Seizures at onset typically consisted of tonic posturing often associated with focal clonic jerking, and were accompanied by apnea with desaturation. One patient diagnosed by gene panel had seizure onset at the age of 5 months. Based on seizure frequency at onset and cognitive outcome, we delineated 3 clinical subgroups, expanding the spectrum of KCNQ2 encephalopathy to patients with moderate intellectual disability and/or infrequent seizures at onset. Recurrent mutations lead to relatively homogenous phenotypes. One patient responded favorably to retigabine; 5 patients had a good response to carbamazepine. In 6 patients, seizures with bradycardia were recorded. One patient died of probable sudden unexpected death in epilepsy. -CONCLUSION: KCNQ2 mutations cause approximately 13\% of unexplained NEE. Patients present with a wide spectrum of severity and, although rare, infantile epilepsy onset is possible.}, - language = {eng}, - number = {19}, - journal = {Neurology}, - author = {Weckhuysen, Sarah and Ivanovic, Vanja and Hendrickx, Rik and Van Coster, Rudy and Hjalgrim, Helle and Møller, Rikke S. and Grønborg, Sabine and Schoonjans, An-Sofie and Ceulemans, Berten and Heavin, Sinead B. and Eltze, Christin and Horvath, Rita and Casara, Gianluca and Pisano, Tiziana and Giordano, Lucio and Rostasy, Kevin and Haberlandt, Edda and Albrecht, Beate and Bevot, Andrea and Benkel, Ira and Syrbe, Steffan and Sheidley, Beth and Guerrini, Renzo and Poduri, Annapurna and Lemke, Johannes R. and Mandelstam, Simone and Scheffer, Ingrid and Angriman, Marco and Striano, Pasquale and Marini, Carla and Suls, Arvid and De Jonghe, Peter and {KCNQ2 Study Group}}, - month = nov, - year = {2013}, - keywords = {Electroencephalography, Male, Humans, Female, Infant, Genetic Predisposition to Disease, Mutation, Cohort Studies, DNA Mutational Analysis, KCNQ2 Potassium Channel, Spasms, Infantile, Video Recording}, - pages = {1697--1703}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\WC59IFXF\\Weckhuysen et al. - 2013 - Extending the KCNQ2 encephalopathy spectrum clini.pdf:application/pdf}, -} - -@article{pisano_early_2015, - title = {Early and effective treatment of {KCNQ2} encephalopathy}, - volume = {56}, - issn = {1528-1167}, - doi = {10.1111/epi.12984}, - abstract = {OBJECTIVES: To describe the antiepileptic drug (AED) treatment of patients with early infantile epileptic encephalopathy due to KCNQ2 mutations during the neonatal phase and the first year of life. -METHODS: We identified 15 patients and reviewed the electroclinical, neuroimaging, and AED treatment data. -RESULTS: Seizure onset was between 1 and 4 days of age with daily tonic asymmetric, focal and clonic seizures in nine patients and status epilepticus in the remaining six. Electroencephalography (EEG) showed multifocal epileptiform abnormalities in nine patients and a burst-suppression pattern in six. All patients were trialed with adequate daily doses of several AEDs before they reached seizure freedom. Six patients (40\%) achieved seizure control within 2 weeks of carbamazepine (CBZ) administration and five (33\%) were seizure-free with phenytoin (PHT). The last four patients (27\%) were successfully treated with topiramate (TPM) (two patients), levetiracetam (LEV) (one), and a combination of LEV with TPM (one). Most patients reached seizure freedom within the first year of life and remained seizure-free thereafter. Twelve patients had moderate-to-severe developmental delay at follow-up. However, the two patients whose seizures ceased within a few days of onset showed only mild cognitive impairment. -SIGNIFICANCE: Our findings suggest that drugs acting on sodium channels including CBZ and PHT should be considered as first-line treatment in patients with KCNQ2 encephalopathy. Voltage-gated sodium and potassium channels co-localize at the neuronal membrane. Therefore, the efficacy of drugs acting as sodium-channel blockers could be linked to their modulating effect on both channels. The type of KCNQ2 mutation might influence AED response as well as developmental outcome. Early recognition of KCNQ2 encephalopathy followed by the most appropriate and effective treatment may be important for reducing the neurodevelopmental impairment associated with this disorder.}, - language = {eng}, - number = {5}, - journal = {Epilepsia}, - author = {Pisano, Tiziana and Numis, Adam L. and Heavin, Sinéad B. and Weckhuysen, Sarah and Angriman, Marco and Suls, Arvid and Podesta, Barbara and Thibert, Ronald L. and Shapiro, Kevin A. and Guerrini, Renzo and Scheffer, Ingrid E. and Marini, Carla and Cilio, Maria Roberta}, - month = may, - year = {2015}, - keywords = {Electroencephalography, Male, Humans, Epilepsy, Female, Child, Child, Preschool, Infant, Neuroimaging, Anticonvulsants, Mutation, KCNQ2 Potassium Channel, Antiepileptic drug treatment, Cognition Disorders, KCNQ2 encephalopathy, Movement Disorders, Pharmacogenetics, Retrospective Studies}, - pages = {685--691}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\9P2RY7MC\\Pisano et al. - 2015 - Early and effective treatment of KCNQ2 encephalopa.pdf:application/pdf}, -} - -@article{evans_carbamazepine-induced_2018, - title = {Carbamazepine-induced suppression of repetitive firing in {CA1} pyramidal neurons is greater in the dorsal hippocampus than the ventral hippocampus}, - volume = {145}, - issn = {0920-1211}, - url = {https://www.sciencedirect.com/science/article/pii/S0920121118301207}, - doi = {10.1016/j.eplepsyres.2018.05.014}, - abstract = {Medial temporal lobe epilepsy (mTLE)–the most common form of focal epilepsy–is defined by recurrent partial seizures originating within the medial temporal lobe. Such seizures are commonly associated with the anterior hippocampus (as opposed to the posterior hippocampus), and refractory to the currently available anti-epileptic drugs (AED) for about one third of patients. Unfortunately, the mechanisms driving seizure generation and AED efficacy along the longitudinal hippocampal axis remain poorly understood. Recently, several groups investigating differences in excitability along the rodent longitudinal hippocampal axis have demonstrated that CA1 pyramidal neurons from the rodent ventral hippocampus (the rodent homolog of the human anterior hippocampus) are intrinsically more excitable than their dorsal counterparts (the rodent homolog of the human posterior hippocampus). This phenotypic difference is accompanied by significant differences in gene expression along the longitudinal hippocampal axis, which include gene products–such as voltage-gated sodium channel β-subunits–known to influence AED efficacy. Given this phenotypic heterogeneity, and the differential expression of gene products known to influence anti-epileptic drug efficacy, we sought to investigate the efficacy of the classical use-dependent sodium channel blocker, carbamazepine, in CA1 pyramidal neurons across the longitudinal hippocampal axis. Accordingly, we performed whole-cell current-clamp recordings on CA1 pyramidal neurons from acute hippocampal slices prepared from the dorsal and ventral hippocampus, and found that acute exposure to 100 μM carbamazepine induced a significantly greater suppression of repetitive firing for dorsal neurons relative to ventral neurons by inducing profound spike frequency adaptation (SFA). Moreover, we observed a small, but significant depolarization of resting membrane potential (RMP) for dorsal neurons (but not ventral neurons), following exposure to carbamazepine. Together, these observations demonstrate that carbamazepine’s effect is concentrated in the dorsal hippocampus, which could provide meaningful insight into the side effect profile of carbamazepine (and related anti-epileptic drugs) in non-epileptic tissue, and inform future work investigating the mechanisms of carbamazepine resistance in epileptic tissue.}, - language = {en}, - urldate = {2021-05-20}, - journal = {Epilepsy Research}, - author = {Evans, Madeline Collette and Dougherty, Kelly Ann}, - month = sep, - year = {2018}, - keywords = {Carbamazepine, Anti-Epileptic drug, CA1 pyramidal neuron, Dorsal hippocampus, Intrinsic excitability}, - pages = {63--72}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\RX579VRB\\S0920121118301207.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8SWRXRDC\\S0920121118301207.html:text/html}, -} - -@article{petty_antiepileptic_2016, - title = {The antiepileptic medications carbamazepine and phenytoin inhibit native sodium currents in murine osteoblasts}, - volume = {57}, - copyright = {Wiley Periodicals, Inc. © 2016 International League Against Epilepsy}, - issn = {1528-1167}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/epi.13474}, - doi = {https://doi.org/10.1111/epi.13474}, - abstract = {Objective Fracture risk is a serious comorbidity in epilepsy and may relate to the use of antiepileptic drugs (AEDs). Many AEDs inhibit ion channel function, and the expression of these channels in osteoblasts raises the question of whether altered bone signaling increases bone fragility. We aimed to confirm the expression of voltage-gated sodium (NaV) channels in mouse osteoblasts, and to investigate the action of carbamazepine and phenytoin on NaV channels. Methods Immunocytochemistry was performed on primary calvarial osteoblasts extracted from neonatal C57BL/6J mice and additional RNA sequencing (RNASeq) was included to confirm expression of NaV. Whole-cell patch-clamp recordings were made to identify the native currents expressed and to assess the actions of carbamazepine (50 μm) or phenytoin (50 μm). Results NaV expression was demonstrated with immunocytochemistry, RNA sequencing, and functionally, with demonstration of robust tetrodotoxin-sensitive and voltage-activated inward currents. Application of carbamazepine or phenytoin resulted in significant inhibition of current amplitude for carbamazepine (31.6 ± 5.9\%, n = 9; p {\textless} 0.001), and for phenytoin (35.5 ± 6.9\%, n = 7; p {\textless} 0.001). Significance Mouse osteoblasts express NaV, and native NaV currents are blocked by carbamazepine and phenytoin, supporting our hypothesis that AEDs can directly influence osteoblast function and potentially affect bone strength.}, - language = {en}, - number = {9}, - urldate = {2021-05-20}, - journal = {Epilepsia}, - author = {Petty, Sandra J. and Milligan, Carol J. and Todaro, Marian and Richards, Kay L. and Kularathna, Pamuditha K. and Pagel, Charles N. and French, Chris R. and Hill-Yardin, Elisa L. and O'Brien, Terence J. and Wark, John D. and Mackie, Eleanor J. and Petrou, Steven}, - year = {2016}, - keywords = {Electrophysiology, Epilepsy, Bone health, Osteoblast, Voltage-gated sodium channel}, - pages = {1398--1405}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8GG8UL4V\\Petty et al. - 2016 - The antiepileptic medications carbamazepine and ph.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4CXFMC3F\\epi.html:text/html}, -} - -@article{namazi_scn1a_2015, - title = {{SCN1A} and {SCN1B} gene polymorphisms and their association with plasma concentrations of carbamazepine and carbamazepine 10, 11 epoxide in {Iranian} epileptic patients}, - volume = {18}, - issn = {2008-3866}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4744361/}, - abstract = {Objective (s): -From a genetic point of view, epilepsy is a polygenic multifactorial syndrome. The SCN1A and B genes belong to a family of genes that provide instructions for making sodium channels. Understanding the relevance of SCN1A and SCN1B gene polymorphisms to plasma concentration of carbamazepine (CBZ) and ’its active metabolite carbamazepine 10, 11 epoxide (CBZE), may shed more light on inter-individual variations in response to CBZ. - -Materials and Methods: -In this cross-sectional study, genotype distribution and allele frequency of six non-synonymous exonic single nucleotide polymorphisms (SNPs) of the SCN1A and B genes were selected and determined using PCR-RFLP in 70 epileptic patients treated with CBZ for at least 6 months. The patients had no hepatic or renal diseases and received no medications known to have a major interaction with CBZ. Serum concentrations of CBZ and CBZE were measured using High-Performance Liquid Chromatography (HPLC). - -Results: -The AA, AG and GG alleles of SCN1A were found in 23, 37 and 10 patients, respectively. There were no statistically significant differences in the mean (± standard deviation) of plasma concentrations of CBZ (P=0.8) and CBZE (P=0.1) among these 3 groups. Likewise, there was no statistically significant relationship between SCN1A polymorphisms and CBZ concentration/dose ratio (P=0.7). A significant association was found between CBZ plasma level and CBZ concentration/dose with CBZ daily dose. All patients had the same genotype of SCN1B gene(CC). and no statistical analysis was performed. - -Conclusion: -No significant association between SCN1A gene polymorphisms and plasma levels of CBZ and CBZE were found[u1].}, - number = {12}, - urldate = {2021-05-20}, - journal = {Iranian Journal of Basic Medical Sciences}, - author = {Namazi, Soha and Azarpira, Negar and Javidnia, Katayoon and Emami, Mehrdad and Rahjoo, Rahimeh and Berahmand, Razieh and Borhani-Haghighi, Afshin}, - month = dec, - year = {2015}, - pages = {1215--1220}, -} - -@article{shi_efficacy_2016, - title = {Efficacy of antiepileptic drugs for the treatment of {Dravet} syndrome with different genotypes}, - volume = {38}, - issn = {1872-7131}, - doi = {10.1016/j.braindev.2015.06.008}, - abstract = {OBJECTIVE: Evaluation of the efficacy of antiepileptic drugs (AEDs) used in the treatment of Dravet syndrome (DS) with different genotypes. -METHODS: Patients with DS were recruited from different tertiary hospitals. Using a direct sequencing method and Multiplex Ligation-Dependent Probe Amplification (MLPA), genetic abnormalities were assessed within the exons and flanking introns of SCN1A gene, which encodes the α1 subunit of neuronal sodium channels. Patients were divided into SCN1A-positive and SCN1A-negative groups according to the results of genetic tests. Medical records, including detailed treatment information, were surveyed to compare the effect of different AEDs on clonic or tonic-clonic seizures (GTCS). Efficacy variable was responder rate with regard to seizure reduction. -RESULTS: One hundred and sixty of 276 (57.97\%) patients had mutation in SCN1A gene (only 128 of them had provided detailed medical records). Among the 116 patients without SCN1A mutations, 87 had provided detailed medical records. Both older AEDs (valproate, phenobarbital, bromide, carbamazepine, clonazepam, and clobazam) and newer AEDs such as zonisamide were used in these patients. Valproate was the most frequently used AED (86.72\% in the SCN1A-positive group, 78.16\% in the SCN1A-negative group), with 52.25\% and 41.18\% responder rates in SCN1A-positive and SCN1A-negative patients, respectively (P=0.15). Bromide was used in 40.63\% of the SCN1A-positive patients and 20.69\% of the SCN1A-negative patients, and its responder rates were 71.15\% and 94.44\% in SCN1A-positive and SCN1A-negative patients, respectively (P=0.05). Efficacy rates of clonazepam, clobazam, phenobarbital, and zonisamide ranged from 30\% to 50\%, and these rates were not correlated with different genotypes (P{\textgreater}0.05). Carbamazepine had either no effect or aggravated seizures in all SCN1A-positive patients. -SIGNIFICANCE: Bromide is most effective and is a well-tolerated drug among DS patients, especially among SCN1A-negative patients. Carbamazepine should be avoided in patients with SCN1A mutations.}, - language = {eng}, - number = {1}, - journal = {Brain \& Development}, - author = {Shi, Xiu-Yu and Tomonoh, Yuko and Wang, Wen-Ze and Ishii, Atsushi and Higurashi, Norimichi and Kurahashi, Hirokazu and Kaneko, Sunao and Hirose, Shinichi and {Epilepsy Genetic Study Group, Japan}}, - month = jan, - year = {2016}, - keywords = {Seizures, Male, Humans, Female, Adult, Young Adult, Adolescent, Child, Child, Preschool, Infant, Treatment Outcome, Carbamazepine, Anticonvulsants, Mutation, Retrospective Studies, Antiepileptic drug therapy, Bromides, Dravet syndrome, Efficacy, Epilepsies, Myoclonic, Genetic tests, Genotype, Genotyping Techniques, NAV1.1 Voltage-Gated Sodium Channel}, - pages = {40--46}, -} - -@article{sitges_effects_2016, - title = {Effects of {Levetiracetam}, {Carbamazepine}, {Phenytoin}, {Valproate}, {Lamotrigine}, {Oxcarbazepine}, {Topiramate}, {Vinpocetine} and {Sertraline} on {Presynaptic} {Hippocampal} {Na}(+) and {Ca}(2+) {Channels} {Permeability}}, - volume = {41}, - issn = {1573-6903}, - doi = {10.1007/s11064-015-1749-0}, - abstract = {Ion channels are targets of various antiepileptic drugs. In cerebral presynaptic nerve endings Na(+) and Ca(2+) channels are particularly abundant, as they control neurotransmitter release, including the release of glutamate (Glu), the most concentrated excitatory amino acid neurotransmitter in the brain. Several pre-synaptic channels are implicated in the mechanism of action of the pro-convulsive agent, 4-aminopyridine (4-AP). In the present study the effects of levetiracetam and other established and newer (vinpocetine) anti-epileptic drugs, as well as of the anti-depressant, sertraline on the increase in Ca(2+) induced by 4-AP in hippocampal isolated nerve endings were investigated. Also the effects of some of the anti-seizure drugs on the selective increase in Ca(2+) induced by high K(+), or on the selective increase in Na(+) induced by veratridine were tested. Sertraline and vinpocetine effectively inhibited the rise in Ca(2+) induced by 4-AP, which was dependent on the out-in Na(+) gradient and tetrodotoxin sensitive. Carbamazepine, phenytoin, lamotrigine and oxcarbazepine inhibited the rise in Ca(2+) induced by 4-AP too, but at higher concentrations than sertraline and vinpocetine, whereas levetiracetam, valproic acid and topiramate did not. The three latter antiepileptic drugs also failed in modifying other responses mediated by the activation of brain presynaptic Na(+) or Ca(2+) channels, including Glu release. This indicates that levetiracetam, valproic acid and topiramate mechanisms of action are unrelated with a decrease in presynaptic Na(+) or Ca(2+) channels permeability. It is concluded that depolarized cerebral isolated nerve endings represent a useful tool to unmask potential antiepileptic drugs targeting presynaptic Na(+) and/or Ca(2+) channels in the brain; such as vinpocetine or the anti-depressant sertraline, which high effectiveness to control seizures in the animal in vivo has been demonstrated.}, - language = {eng}, - number = {4}, - journal = {Neurochemical Research}, - author = {Sitges, María and Chiu, Luz María and Reed, Ronald C.}, - month = apr, - year = {2016}, - keywords = {Animals, Glutamic Acid, Male, Rats, Wistar, Calcium, Calcium channels, In Vitro Techniques, Hippocampus, Sodium channels, Anticonvulsants, 4-aminopirydine, Anti-epileptic drugs, Calcium Channels, Glu release, Hippocampus nerve endings, Presynaptic Terminals, Sodium Channels}, - pages = {758--769}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ZZXKY9AF\\Sitges et al. - 2016 - Effects of Levetiracetam, Carbamazepine, Phenytoin.pdf:application/pdf}, -} - -@article{kuo_essential_2006, - title = {Essential role of the persistent sodium current in spike initiation during slowly rising inputs in mouse spinal neurones}, - volume = {574}, - copyright = {© 2006 The Journal of Physiology © 2006 The Physiological Society}, - issn = {1469-7793}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.2006.107094}, - doi = {https://doi.org/10.1113/jphysiol.2006.107094}, - abstract = {Spinal motoneurons, like many neurons, respond with repetitive spiking to sustained inputs. The afterhyperpolarization (AHP) that follows each spike, however, decays relatively slowly in motoneurons. The slow depolarization during this decay should allow sodium (Na+) channel inactivation to keep up with its activation and thus should prevent initiation of the next spike. We hypothesized that the persistent component of the total Na+ current provides the mechanism that generates a rate of rise sufficiently rapid to generate a spike. In large cultured spinal neurons, presumed to be primarily motoneurons, inhibition of persistent sodium current (NaP) by the drug riluzole at low concentrations resulted in a loss of repetitive firing. However, cells remained fully capable of producing spikes to transient inputs. These effects of riluzole were not due to insufficient depolarization, enhancement of the AHP, or sustained Na+ channel inactivation. To further test this hypothesis, computer simulations were performed with a kinetic Na+ channel model that provided greater independent control of NaP relative to transient Na+ current (NaT) than that provided by riluzole administration. The model was tuned to generate substantial NaP and exhibited good repetitive firing to slowly rising inputs. When NaP was sharply reduced without significantly altering NaT, the model reproduced the effects of riluzole administration, inducing failure of repetitive firing but allowing single spikes in response to sharp transients. These results strongly support the essential role of NaP in spike initiation to slow inputs in spinal neurons. NaP may play a fundamental role in determining how a neuron responds to sustained inputs.}, - language = {en}, - number = {3}, - urldate = {2021-05-24}, - journal = {The Journal of Physiology}, - author = {Kuo, J. J. and Lee, R. H. and Zhang, L. and Heckman, C. J.}, - year = {2006}, - pages = {819--834}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TKU8RK6Y\\Kuo et al. - 2006 - Essential role of the persistent sodium current in.pdf:application/pdf;PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ZTGECFYC\\Kuo et al. - 2006 - Essential role of the persistent sodium current in.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\W52NFTE7\\jphysiol.2006.html:text/html}, -} - -@article{cho_contribution_2015, - title = {Contribution of persistent sodium currents to the excitability of tonic firing substantia gelatinosa neurons of the rat}, - volume = {591}, - issn = {0304-3940}, - url = {https://www.sciencedirect.com/science/article/pii/S0304394015001536}, - doi = {10.1016/j.neulet.2015.02.039}, - abstract = {The roles of persistent Na+ currents (INaP) in intrinsic membrane properties were examined in rat substantia gelatinosa (SG) neurons of the trigeminal subnucleus caudalis using a conventional whole-cell patch clamp technique. In a voltage-clamp mode, riluzole inhibited the slow voltage ramp-induced INaP but had little effect on the peak amplitude of transient Na+ currents in SG neurons. In a current-clamp mode, most SG neurons exhibited spontaneous action potentials and tonic firing pattern. Riluzole reduced both spontaneous and elicited action potentials in a concentration-dependent manner. The present results suggest that the riluzole-sensitive INaP plays an important role in the excitability of SG neurons and are thus, likely to contribute to the modulation of nociceptive transmission from the orofacial tissues.}, - language = {en}, - urldate = {2021-05-24}, - journal = {Neuroscience Letters}, - author = {Cho, Jin-Hwa and Choi, In-Sun and Lee, Seok-Ho and Lee, Maan-Gee and Jang, Il-Sung}, - month = mar, - year = {2015}, - keywords = {Patch clamp, Substantia gelatinosa, Trigeminal subnucleus caudalis, Voltage-gated Na channels}, - pages = {192--196}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JR6DSF36\\Cho et al. - 2015 - Contribution of persistent sodium currents to the .pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\INBP36DP\\Cho et al. - 2015 - Contribution of persistent sodium currents to the .pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\F2EYL6N4\\S0304394015001536.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XKJ7QSBM\\S0304394015001536.html:text/html}, -} - -@article{centonze_electrophysiology_1998, - title = {Electrophysiology of the neuroprotective agent riluzole on striatal spiny neurons}, - volume = {37}, - issn = {0028-3908}, - url = {https://www.sciencedirect.com/science/article/pii/S0028390898000811}, - doi = {10.1016/S0028-3908(98)00081-1}, - abstract = {Striatal spiny neurons are selectively vulnerable in Huntington’s disease (HD). No effective treatment is available to limit neuronal death in this pathological condition. In an experimental model of HD, a beneficial effect has recently been reported by the neuroprotective agent riluzole. We performed intracellular recordings in order to characterize the electrophysiological effects of this compound on striatal spiny neurons. Riluzole (0.1–100 μM) affected neither the resting membrane potential nor the input resistance/membrane conductance of the recorded cells. Bath application of this pharmacological agent produced a dose-dependent reduction of the number of spikes evoked by long-lasting depolarizing pulses. The EC50 value for this effect was 0.5 μM. Low doses of riluzole selectively reduced the firing frequency in the last part of the depolarizing pulse suggesting a use-dependent action at low concentrations of this compound. Riluzole produced a dose-dependent reduction of the amplitude of the corticostriatal glutamatergic excitatory post-synaptic potentials (EPSPs) with an extrapolated EC50 value of 6 μM. This effect was reversible and maximal at a concentration of 100 μM. Paired-pulse facilitation (PPF) was not affected by riluzole suggesting that the reduction of excitatory transmission was not only caused by a decrease of presynaptic release. Accordingly, riluzole also reduced the amplitude of membrane depolarization induced by exogenous glutamate. The modulatory action of riluzole on the activity of striatal spiny neurons might support the use of this drug in experimental models of excitotoxicity and in the neurodegenerative disorders involving the striatum.}, - language = {en}, - number = {8}, - urldate = {2021-05-24}, - journal = {Neuropharmacology}, - author = {Centonze, Diego and Calabresi, Paolo and Pisani, Antonio and Marinelli, Silvia and Marfia, Girolama Alessandra and Bernardi, Giorgio}, - month = aug, - year = {1998}, - keywords = {Striatum, Excitatory amino acids, Huntington disease, Intracellular recordings, Synaptic transmission}, - pages = {1063--1070}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\LEADVGRC\\Centonze et al. - 1998 - Electrophysiology of the neuroprotective agent ril.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FS3DXB4X\\S0028390898000811.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B572P3U7\\S0028390898000811.html:text/html}, -} - -@article{ptak_sodium_2005, - title = {Sodium {Currents} in {Medullary} {Neurons} {Isolated} from the {Pre}-{Bötzinger} {Complex} {Region}}, - volume = {25}, - copyright = {Copyright © 2005 Society for Neuroscience 0270-6474/05/255159-12.00/0}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/25/21/5159}, - doi = {10.1523/JNEUROSCI.4238-04.2005}, - abstract = {The pre-Bötzinger complex (preBötC) in the ventrolateral medulla contains interneurons important for respiratory rhythm generation. Voltage-dependent sodium channels mediate transient current (INaT), underlying action potentials, and persistent current (INaP), contributing to repetitive firing, pacemaker properties, and the amplification of synaptic inputs. Voltage-clamp studies of the biophysical properties of these sodium currents were conducted on acutely dissociated preBötC region neurons. Reverse transcription-PCR demonstrated the presence of mRNA for Nav1.1, Nav1.2, and Nav1.6 α-subunits in individual neurons. A TTX-sensitive INaP was evoked in all tested neurons by ramp depolarization from -80 to 0 mV. Including a constant in the Boltzmann equation for inactivation by estimating the steady-state fraction of Na+ channels available for inactivation allowed prediction of a window current that did not decay to 0 at voltages positive to -20 mV and closely matched the measured INaP. Riluzole (3 μm), a putative INaP antagonist, reduced both INaP and INaT and produced a hyperpolarizing shift in the voltage dependence of steady-state inactivation. The latter decreased the predicted window current by an amount equivalent to the decrease in INaP. Riluzole also decreased the inactivation time constant at potentials in which the peak window/persistent currents are generated. Together, these findings imply that INaP and INaT arise from the same channels and that a simple modification of the Hodgkin-Huxley model can satisfactorily account for both currents. In the rostral ventral respiratory group (immediately caudal to preBötC), INaP was also detected, but peak conductance, current density, and input resistance were smaller than in preBötC region cells.}, - language = {en}, - number = {21}, - urldate = {2021-05-24}, - journal = {Journal of Neuroscience}, - author = {Ptak, Krzysztof and Zummo, Greer G. and Alheid, George F. and Tkatch, Tatiana and Surmeier, D. James and McCrimmon, Donald R.}, - month = may, - year = {2005}, - keywords = {respiration, sodium channels, central pattern generator, pacemaker, persistent current, pre-Bötzinger, riluzole}, - pages = {5159--5170}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FFXLRP6Q\\Ptak et al. - 2005 - Sodium Currents in Medullary Neurons Isolated from.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MUYT2U2Y\\5159.html:text/html}, -} - -@article{willow_voltage_1985, - title = {Voltage clamp analysis of the inhibitory actions of diphenylhydantoin and carbamazepine on voltage-sensitive sodium channels in neuroblastoma cells.}, - volume = {27}, - issn = {0026-895X, 1521-0111}, - url = {https://molpharm.aspetjournals.org/content/27/5/549}, - abstract = {The actions of diphenylhydantoin (DPH) and carbamazepine (CBZ) on sodium channels in mouse neuroblastoma cells (clone N18) were analyzed using the patch voltage clamp procedure in the whole cell configuration. DPH and CBZ reduced sodium currents without effect on the voltage dependence of sodium channel activation. Half-maximal inhibition was observed with approximately 30 microM of each drug. Depolarization increased and hyperpolarization reversed channel block by these two drugs in the voltage range from -90 to -45 mV. Repetitive stimulation at 2 Hz or greater enhanced inhibition of sodium channels. The half-time for recovery from voltage-dependent inhibition was greater for DPH (1.36 sec) than for CBZ (0.38 sec). A combination of prolonged depolarizing pulses of 15 mV with superimposed brief maximal depolarizations designed to mimic the electrical activity in an epileptic focus gave additive effects of voltage-dependent and frequency-dependent inhibition. The results support the previous proposal that DPH and CBZ are sodium channel-selective anticonvulsants and provide a potential basis for specific inhibition of neurons in epileptic foci. The mechanism of DPH and CBZ action is considered in terms of an allosteric or modulated receptor model of drug binding and action.}, - language = {en}, - number = {5}, - urldate = {2021-05-25}, - journal = {Molecular Pharmacology}, - author = {Willow, M. and Gonoi, T. and Catterall, W. A.}, - month = may, - year = {1985}, - pages = {549--558}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UTGINYR3\\Willow et al. - 1985 - Voltage clamp analysis of the inhibitory actions o.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5UCDX2R2\\549.html:text/html}, -} - -@article{huang_effects_1997, - title = {Effects of the {Neuroprotective} {Agent} {Riluzole} on the {High} {Voltage}-{Activated} {Calcium} {Channels} of {Rat} {Dorsal} {Root} {Ganglion} {Neurons}}, - volume = {282}, - copyright = {The American Society for Pharmacology and Experimental Therapeutics}, - issn = {0022-3565, 1521-0103}, - url = {https://jpet.aspetjournals.org/content/282/3/1280}, - abstract = {The effects of riluzole, a neuroprotective drug, on high voltage-activated (HVA) calcium channels of rat dorsal root ganglion neurons were studied using the whole-cell patch-clamp technique. Riluzole inhibited HVA calcium channel currents in a dose-dependent, time-dependent and reversible manner. The apparent dissociation constants for riluzole inhibition of the transient and sustained components of the current were 42.6 and 39.5 μM, respectively. Riluzole accelerated the activation kinetics of calcium channels without affecting the voltage dependence of activation. It accelerated the fast component of deactivation kinetics without affecting the slow component. It also accelerated fast and slow inactivation kinetics of the HVA channels. However, only one of the two components in the steady-state inactivation curve for the HVA channels was shifted in the hyperpolarizing direction by riluzole, which indicates differential block of the multiple-type HVA channels. By use of the specific blockers nimodipine, ω-conotoxin GVIA and ω-agatoxin IVA, the HVA calcium channels were found to comprise L-type (10\%), N-type (63\%), P/Q-type (23\%) and R-type (9\%). Riluzole blocked N- and P/Q-type channels, but not L-type channel, with the order of efficacy of P/Q- {\textgreater} N- ≫ L-type channels. Riluzole inhibition of N- and P/Q-type calcium channels may result in reduced calcium influx at presynaptic terminals, which thereby decreases excessive excitatory neurotransmitter release, especially glutamate, a mechanism known to cause neuronal death in ischemic conditions.}, - language = {en}, - number = {3}, - urldate = {2021-05-25}, - journal = {Journal of Pharmacology and Experimental Therapeutics}, - author = {Huang, Chao-Sheng and Song, Jin-Ho and Nagata, Keiichi and Yeh, Jay Z. and Narahashi, Toshio}, - month = sep, - year = {1997}, - pages = {1280--1290}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\L3BFG6LP\\1280.html:text/html}, -} - -@article{vreugdenhil_modulation_1999, - title = {Modulation of {Sodium} {Currents} in {Rat} {CA1} {Neurons} by {Carbamazepine} and {Valproate} {After} {Kindling} {Epileptogenesis}}, - volume = {40}, - issn = {1528-1167}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1528-1157.1999.tb02034.x}, - doi = {https://doi.org/10.1111/j.1528-1157.1999.tb02034.x}, - abstract = {Summary: Purpose: To determine the modulation of sodium currents in hippocampal CA1 neurons by carbamazepine (CBZ) and valproate (VPA), before and after kindling epileptogenesis. Methods: Voltage-dependent sodium current was measured in isolated hippocampal CA1 neurons, by using the whole-cell voltage-clamp technique. CBZ (15–100 μM) or VPA (0.5-5 mM) was applied by bath perfusion. Cells from fully kindled rats were compared with controls, 1 day and 5 weeks after the tenth generalized seizure. Results: CBZ did not affect sodium current activation but selectively shifted the voltage dependence of steady-state inactivation to more hyperpolarized potentials. One day after the last kindled generalized seizure, the shift induced by 15 μM CBZ was 2.1 ± 0.5 mV (mean ± SEM; n = 20) compared with 4.3 ± 0.3 mV (n = 16; p {\textgreater} 0.001) in matched controls. The EC50 of the concentration-effect relation was 57 ± 6 μM compared with 34 ± 2 μM (p {\textgreater} 0.01) in controls. Five weeks after kindling, these values had recovered to a level not different from control. VPA induces at a relatively high concentration a similar but smaller shift in voltage dependence of inactivation than does CBZ. After kindling, the shift induced by 2 mM VPA (2.8 ± 0.6 mV; n = 19) was not different from controls (3.0 ± 0.5 mV; n = 22). The EC50 for VPA was 2.6 ± 0.3 mM compared with 2.5 ± 0.4 mM in controls. Conclusions: Both CBZ and VPA selectively modulate the voltage dependence of sodium current steady-state inactivation and as a consequence reduce cellular excitability. The effect of CBZ was reduced immediately after kindling epileptogenesis, apparently by a reduced affinity of its receptor. In contrast, the shift induced by VPA was not different at any stage after kindling epileptogenesis. The change in CBZ sensitivity after kindling is related to epileptic activity rather than to the epileptic state, because it almost completely recovers in a period without seizures.}, - language = {en}, - number = {11}, - urldate = {2021-05-25}, - journal = {Epilepsia}, - author = {Vreugdenhil, Martin and Wadman, Wytse J.}, - year = {1999}, - keywords = {Epilepsy, Hippocampus, Antiepileptic drug, Inactivation, Sensitivity}, - pages = {1512--1522}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\QWTRHF9K\\Vreugdenhil and Wadman - 1999 - Modulation of Sodium Currents in Rat CA1 Neurons b.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\APUNKZVB\\Vreugdenhil and Wadman - 1999 - Modulation of Sodium Currents in Rat CA1 Neurons b.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ADQQEURJ\\j.1528-1157.1999.tb02034.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ZZJH75AB\\j.1528-1157.1999.tb02034.html:text/html}, -} - -@article{dash_two_2018, - title = {Two {Decades}-{Long} {Journey} from {Riluzole} to {Edaravone}: {Revisiting} the {Clinical} {Pharmacokinetics} of the {Only} {Two} {Amyotrophic} {Lateral} {Sclerosis} {Therapeutics}}, - volume = {57}, - issn = {1179-1926}, - shorttitle = {Two {Decades}-{Long} {Journey} from {Riluzole} to {Edaravone}}, - url = {https://doi.org/10.1007/s40262-018-0655-4}, - doi = {10.1007/s40262-018-0655-4}, - abstract = {The recent approval of edaravone has provided an intravenous option to treat amyotrophic lateral sclerosis (ALS) in addition to the existing oral agent, riluzole. The present work was primarily undertaken to provide a comprehensive clinical pharmacokinetic summary of the two approved ALS therapeutics. The key objectives of the review were to (i) tabulate the clinical pharmacokinetics of riluzole and edaravone with emphasis on absorption, distribution, metabolism and excretion (ADME) properties; (ii) provide a comparative scenario of the pharmacokinetics of the two drugs wherever possible; and (iii) provide perspectives and introspection on the gathered clinical pharmacokinetic data of the two drugs with appropriate conjectures to quench scientific curiosity. Based on this review, the following key highlights were deduced: (i) as a result of both presystemic metabolism and polymorphic hepatic cytochrome P450 (CYP) metabolism, the oral drug riluzole exhibited more inter-subject variability than that of intravenous edaravone; (ii) using various parameters for comparison, including the published intravenous data for riluzole, it was apparent that edaravone was achieving the desired systemic concentrations to possibly drive the local brain concentrations for its efficacy in ALS patients with lesser variability than riluzole; (iii) using scientific conjectures, it was deduced that the availability of intravenous riluzole may not be beneficial in therapy due to its fast systemic clearance; (iv) on the contrary, however, there appeared to be an opportunity for the development of an oral dosage form of edaravone, which may potentially benefit the therapy option for ALS patients by avoiding hospitalization costs; and (v) because of the existence of pharmaco-resistance for the brain entry in ALS patients, it appeared prudent to consider combination strategies of edaravone and/or riluzole with suitable P-glycoprotein efflux-blocking drugs to gain more favorable outcomes in ALS patients.}, - language = {en}, - number = {11}, - urldate = {2021-05-25}, - journal = {Clinical Pharmacokinetics}, - author = {Dash, Ranjeet Prasad and Babu, R. Jayachandra and Srinivas, Nuggehally R.}, - month = nov, - year = {2018}, - pages = {1385--1398}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6VP294T5\\Dash et al. - 2018 - Two Decades-Long Journey from Riluzole to Edaravon.pdf:application/pdf}, -} - -@article{groeneveld_riluzole_2003, - title = {Riluzole serum concentrations in patients with {ALS}: {Associations} with side effects and symptoms}, - volume = {61}, - copyright = {© 2003}, - issn = {0028-3878, 1526-632X}, - shorttitle = {Riluzole serum concentrations in patients with {ALS}}, - url = {https://n.neurology.org/content/61/8/1141}, - doi = {10.1212/01.WNL.0000090459.76784.49}, - abstract = {Riluzole exerts a dose-dependent effect on survival of patients with ALS and, although serum levels show a high interindividual variability, is usually prescribed in a fixed dose. In this study, riluzole serum levels and area under the curve per kilogram of body weight (AUC/kg) of 169 patients with ALS showed a high interindividual variability. Patients with high serum levels and AUC/kg more often had diarrhea but less often had fasciculations and muscle stiffness. It may therefore be advantageous to raise the riluzole dose in patients with low riluzole serum concentrations without the risk of serious side effects.}, - language = {en}, - number = {8}, - urldate = {2021-05-25}, - journal = {Neurology}, - author = {Groeneveld, G. J. and Kan, H. J. M. Van and Kalmijn, S. and Veldink, J. H. and Guchelaar, H.-J. and Wokke, J. H. J. and Berg, L. H. Van den}, - month = oct, - year = {2003}, - pages = {1141--1143}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\IDR4WVUC\\Groeneveld et al. - 2003 - Riluzole serum concentrations in patients with ALS.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FHZ52JBZ\\1141.html:text/html}, -} - -@article{groeneveld_inter-_2001, - title = {Inter- and intraindividual variability of riluzole serum concentrations in patients with {ALS}}, - volume = {191}, - issn = {0022-510X}, - url = {https://www.sciencedirect.com/science/article/pii/S0022510X0100613X}, - doi = {10.1016/S0022-510X(01)00613-X}, - abstract = {All patients with amyotrophic lateral sclerosis (ALS) are treated with the same dose of riluzole: 50 mg twice daily. Reasonably large interindividual differences in clearance of the drug have been reported. The relatively small group of patients with high blood concentrations of riluzole has probably primarily influenced the efficacy and the incidence of side-effects in the previously conducted clinical trials with riluzole. Individual dosing of the drug may, in the case of large interindividual differences in serum concentrations of the drug, be necessary in the future. Exact data concerning the plasma and serum concentrations of riluzole in patients with ALS, after standardized intake of the drug, diet and blood sampling are unknown so far. In this study, inter- and intraindividual variability of serum and plasma levels of riluzole in 21 patients with “probable” or “definite” ALS were determined. The interindividual variability of peak serum levels (coefficient of variation=74\%) was significantly larger than intraindividual variability (p{\textless}0.001). Serum levels were not correlated with age or smoking status. The determination of a correlation between riluzole serum concentrations and survival of patients with ALS will be the aim of further studies.}, - language = {en}, - number = {1}, - urldate = {2021-05-25}, - journal = {Journal of the Neurological Sciences}, - author = {Groeneveld, G. J and van Kan, H. J. M and Sastre Toraño, J and Veldink, J. H and Guchelaar, H. -J and Wokke, J. H. J and van den Berg, L. H}, - month = oct, - year = {2001}, - keywords = {Polymorphism, Amyotrophic lateral sclerosis, CYP1A2, Drug metabolism, Riluzole, Treatment}, - pages = {121--125}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WHHEQMRT\\Groeneveld et al. - 2001 - Inter- and intraindividual variability of riluzole.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\YHXCRJ4C\\S0022510X0100613X.html:text/html}, -} - -@article{colovic_liquid_2004, - title = {Liquid chromatographic assay for riluzole in mouse plasma and central nervous system tissues}, - volume = {803}, - issn = {1570-0232}, - url = {https://www.sciencedirect.com/science/article/pii/S1570023204000261}, - doi = {10.1016/j.jchromb.2004.01.004}, - abstract = {An isocratic, reversed-phase high-performance liquid chromatographic procedure (HPLC) was developed for determination of the neuroprotective agent riluzole in mice plasma, brain and spinal cord. The procedure is based on isolation of the compound and the internal standard from plasma and central nervous system tissues using a Bakerbond spe™ C8 cartridge, with satisfactory recovery and specificity. Separation was on a C18 column, coupled with an UV detector at 263 nm. The assay was linear over a wide range, with a lower limit of quantification of 100ngml−1 or g−1 using 0.1ml of plasma and about 100mg of brain tissue. The precision and accuracy were within the acceptable limits for an HPLC assay. The method is currently used to support pharmacological studies of the activity of riluzole when given in combination with other potential neuroprotective agents in an animal model of familiar amyotrophic lateral sclerosis (SOD1-G93A transgenic mice).}, - language = {en}, - number = {2}, - urldate = {2021-05-25}, - journal = {Journal of Chromatography B}, - author = {Colovic, Milena and Zennaro, Eleonora and Caccia, Silvio}, - month = apr, - year = {2004}, - keywords = {Riluzole}, - pages = {305--309}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SN7J9LYV\\Colovic et al. - 2004 - Liquid chromatographic assay for riluzole in mouse.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EHKNQ2EB\\S1570023204000261.html:text/html}, -} - -@article{milane_minocycline_2007, - title = {Minocycline and riluzole brain disposition: interactions with p-glycoprotein at the blood–brain barrier}, - volume = {103}, - issn = {1471-4159}, - shorttitle = {Minocycline and riluzole brain disposition}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1471-4159.2007.04772.x}, - doi = {https://doi.org/10.1111/j.1471-4159.2007.04772.x}, - abstract = {Amyotrophic lateral sclerosis is a neurodegenerative fatal disease. The only drug recognized to increase the survival time is riluzole(RLZ). In animal models, minocycline (MNC) delayed the onset of the disease and increased the survival time (in combination with RLZ). The objective of our work was to study the interactions between RLZ, MNC and the efflux pump p-glycoprotein (p-gp) at the blood–brain barrier. We investigated these two drugs as: (i) p-gp substrates by comparing their brain uptake in CF1 mdr1a (−/−) and mdr1a (+/+) mice, (ii) p-gp modulators by studying their effect on the cerebral uptake of digoxin. mdr1a (−/−) mice showed higher brain uptake of MNC and RLZ than mdr1a (+/+) (in a 1.6- and 1.4-fold, respectively); and in mdr1a (+/+) mice pre-treated with repeated doses of MNC, brain uptake of digoxin was increased. When both drugs were administrated to mdr1a (+/+) mice, MNC increased the brain uptake of RLZ in a 2.1-fold. In conclusion, MNC and RLZ are both p-gp substrates. MNC is also a p-gp inhibitor and increases the brain diffusion of RLZ. In vitro experiments with the GPNT cell line confirmed these results. These interactions should be taken into account in the design of future clinical trials.}, - language = {en}, - number = {1}, - urldate = {2021-05-25}, - journal = {Journal of Neurochemistry}, - author = {Milane, Aline and Fernandez, Christine and Vautier, Sarah and Bensimon, Gilbert and Meininger, Vincent and Farinotti, Robert}, - year = {2007}, - keywords = {amyotrophic lateral sclerosis, riluzole, blood–brain barrier, GPNT cell line, minocycline, p-glycoprotein}, - pages = {164--173}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YRPKE5AX\\Milane et al. - 2007 - Minocycline and riluzole brain disposition intera.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MEXQFMK8\\j.1471-4159.2007.04772.html:text/html}, -} - -@article{jr_riluzole_2008, - title = {Riluzole in psychiatry: a systematic review of the literature}, - volume = {4}, - issn = {1742-5255}, - shorttitle = {Riluzole in psychiatry}, - url = {https://doi.org/10.1517/17425255.4.9.1223}, - doi = {10.1517/17425255.4.9.1223}, - abstract = {Background: The glutamate system seems to be an important contributor to the pathophysiology of mood and anxiety disorders. Thus, glutamatergic modulators are reasonable candidate drugs to test in patients with mood and anxiety disorders. Riluzole, a neuroprotective agent with anticonvulsant properties approved for the treatment of amyotrophic lateral sclerosis (ALS) is one such agent. Objective: To assess the potential risks and benefits of riluzole treatment in psychiatric patients. Methods: A PubMed search was performed using the keywords ‘riluzole’, ‘inhibitor of glutamate release’ and ‘glutamatergic modulator’ to identify all clinical studies and case reports involving riluzole in psychiatric patients. Results/conclusion: Riluzole's side effect profile is favorable and preliminary results regarding riluzole for the treatment of severe mood, anxiety and impulsive disorders are encouraging.}, - number = {9}, - urldate = {2021-05-25}, - journal = {Expert Opinion on Drug Metabolism \& Toxicology}, - author = {Jr, Carlos A. Zarate and Manji, Husseini K.}, - month = sep, - year = {2008}, - keywords = {glutamate, plasticity, depression, antidepressant, riluzole, anxiety disorder, bipolar disorder, mania, psychiatry, treatment}, - pages = {1223--1234}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6BWJ5K7W\\Jr and Manji - 2008 - Riluzole in psychiatry a systematic review of the.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\94FGS6M5\\17425255.4.9.html:text/html}, -} - -@article{pacheco-rojas_riluzole_2021, - title = {Riluzole inhibits {Kv4}.2 channels acting on the closed and closed inactivated states}, - volume = {899}, - issn = {0014-2999}, - url = {https://www.sciencedirect.com/science/article/pii/S0014299921001795}, - doi = {10.1016/j.ejphar.2021.174026}, - abstract = {Riluzole is an anticonvulsant drug also used to treat the amyotrophic lateral sclerosis and major depressive disorder. This compound has antiglutamatergic activity and is an important multichannel blocker. However, little is known about its actions on the Kv4.2 channels, the molecular correlate of the A-type K+ current (IA) and the fast transient outward current (Itof). Here, we investigated the effects of riluzole on Kv4.2 channels transiently expressed in HEK-293 cells. Riluzole inhibited Kv4.2 channels with an IC50 of 190 ± 14 μM and the effect was voltage- and frequency-independent. The activation rate of the current (at +50 mV) was not affected by the drug, nor the voltage dependence of channel activation, but the inactivation rate was accelerated by 100 and 300 μM riluzole. When Kv4.2 channels were maintained at the closed state, riluzole incubation induced a tonic current inhibition. In addition, riluzole significantly shifted the voltage dependence of inactivation to hyperpolarized potentials without affecting the recovery from inactivation. In the presence of the drug, the closed-state inactivation was significantly accelerated, and the percentage of inactivated channels was increased. Altogether, our findings indicate that riluzole inhibits Kv4.2 channels mainly affecting the closed and closed-inactivated states.}, - language = {en}, - urldate = {2021-05-25}, - journal = {European Journal of Pharmacology}, - author = {Pacheco-Rojas, David O. and Delgado-Ramírez, Mayra and Villatoro-Gómez, Kathya and Moreno-Galindo, Eloy G. and Rodríguez-Menchaca, Aldo A. and Sánchez-Chapula, José A. and Ferrer, Tania}, - month = may, - year = {2021}, - keywords = {Riluzole, Closed state inactivation, Inhibition, Kv4.2}, - pages = {174026}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ENRRABDI\\S0014299921001795.html:text/html}, -} - -@article{milane_brain_2009, - title = {Brain and {Plasma} {Riluzole} {Pharmacokinetics}: {Effect} of {Minocycline} {Combination}}, - volume = {12}, - copyright = {Copyright (c)}, - issn = {1482-1826}, - shorttitle = {Brain and {Plasma} {Riluzole} {Pharmacokinetics}}, - url = {https://journals.library.ualberta.ca/jpps/index.php/JPPS/article/view/4596}, - doi = {10.18433/J36C78}, - language = {en}, - number = {2}, - urldate = {2021-05-25}, - journal = {Journal of Pharmacy \& Pharmaceutical Sciences}, - author = {Milane, Aline and Tortolano, Lionel and Fernandez, Christine and Bensimon, Gilbert and Meininger, Vincent and Farinotti, Robert}, - month = aug, - year = {2009}, - pages = {209--217}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P8D979EL\\Milane et al. - 2009 - Brain and Plasma Riluzole Pharmacokinetics Effect.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\KURWE7NC\\4596.html:text/html}, -} - -@article{czitrom_one-factor-at--time_1999, - title = {One-{Factor}-at-a-{Time} versus {Designed} {Experiments}}, - volume = {53}, - issn = {0003-1305}, - url = {https://www.jstor.org/stable/2685731}, - doi = {10.2307/2685731}, - abstract = {Many engineers and scientists perform one-factor-at-a-time (OFAT) experiments. They will continue to do so until they understand the advantages of designed experiments over OFAT experiments, and until they learn to recognize OFAT experiments so they can avoid them. A very effective way to illustrate the advantages of designed experiments, and to show ways in which OFAT experiments present themselves in real life, is to introduce real examples of OFAT experiments and then demonstrate why a designed experiment would have been better. Three engineering examples of OFAT experiments are presented, as well as designed experiments that would have been better. The three examples have been successfully used in an industrial workshop and can also be used in academic courses.}, - number = {2}, - urldate = {2021-06-02}, - journal = {The American Statistician}, - author = {Czitrom, Veronica}, - year = {1999}, - pages = {126--131}, - file = {Submitted Version:C\:\\Users\\nilsk\\Zotero\\storage\\GW8BJJXX\\Czitrom - 1999 - One-Factor-at-a-Time versus Designed Experiments.pdf:application/pdf}, -} - -@article{saltelli_how_2010, - title = {How to avoid a perfunctory sensitivity analysis}, - volume = {25}, - issn = {1364-8152}, - url = {https://www.sciencedirect.com/science/article/pii/S1364815210001180}, - doi = {10.1016/j.envsoft.2010.04.012}, - abstract = {Mathematical modelers from different disciplines and regulatory agencies worldwide agree on the importance of a careful sensitivity analysis (SA) of model-based inference. The most popular SA practice seen in the literature is that of ’one-factor-at-a-time’ (OAT). This consists of analyzing the effect of varying one model input factor at a time while keeping all other fixed. While the shortcomings of OAT are known from the statistical literature, its widespread use among modelers raises concern on the quality of the associated sensitivity analyses. The present paper introduces a novel geometric proof of the inefficiency of OAT, with the purpose of providing the modeling community with a convincing and possibly definitive argument against OAT. Alternatives to OAT are indicated which are based on statistical theory, drawing from experimental design, regression analysis and sensitivity analysis proper.}, - language = {en}, - number = {12}, - urldate = {2021-06-02}, - journal = {Environmental Modelling \& Software}, - author = {Saltelli, Andrea and Annoni, Paola}, - month = dec, - year = {2010}, - keywords = {Mathematical modeling, One-at-a-time, Robustness, Sensitivity analysis, Uncertainty analysis}, - pages = {1508--1517}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SWBUI32R\\Saltelli and Annoni - 2010 - How to avoid a perfunctory sensitivity analysis.pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P9EGLCTE\\Saltelli and Annoni - 2010 - How to avoid a perfunctory sensitivity analysis.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JLYYH3WR\\S1364815210001180.html:text/html}, -} - -@article{saltelli_why_2019, - title = {Why so many published sensitivity analyses are false: {A} systematic review of sensitivity analysis practices}, - volume = {114}, - issn = {1364-8152}, - shorttitle = {Why so many published sensitivity analyses are false}, - url = {https://www.sciencedirect.com/science/article/pii/S1364815218302822}, - doi = {10.1016/j.envsoft.2019.01.012}, - abstract = {Sensitivity analysis provides information on the relative importance of model input parameters and assumptions. It is distinct from uncertainty analysis, which addresses the question ‘How uncertain is the prediction?’ Uncertainty analysis needs to map what a model does when selected input assumptions and parameters are left free to vary over their range of existence, and this is equally true of a sensitivity analysis. Despite this, many uncertainty and sensitivity analyses still explore the input space moving along one-dimensional corridors leaving space of the input factors mostly unexplored. Our extensive systematic literature review shows that many highly cited papers (42\% in the present analysis) fail the elementary requirement to properly explore the space of the input factors. The results, while discipline-dependent, point to a worrying lack of standards and recognized good practices. We end by exploring possible reasons for this problem, and suggest some guidelines for proper use of the methods.}, - language = {en}, - urldate = {2021-06-02}, - journal = {Environmental Modelling \& Software}, - author = {Saltelli, Andrea and Aleksankina, Ksenia and Becker, William and Fennell, Pamela and Ferretti, Federico and Holst, Niels and Li, Sushan and Wu, Qiongli}, - month = apr, - year = {2019}, - pages = {29--39}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KSIZPHDG\\Saltelli et al. - 2019 - Why so many published sensitivity analyses are fal.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5ZQJVX2C\\S1364815218302822.html:text/html}, -} - -@article{niespodziany_discovery_2019, - title = {Discovery of a small molecule modulator of the {Kv1}.1/{Kvβ1} channel complex that reduces neuronal excitability and in vitro epileptiform activity}, - volume = {25}, - copyright = {© 2018 John Wiley \& Sons Ltd}, - issn = {1755-5949}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/cns.13060}, - doi = {https://doi.org/10.1111/cns.13060}, - abstract = {Aims Kv1.1 (KCNA1) channels contribute to the control of neuronal excitability and have been associated with epilepsy. Kv1.1 channels can associate with the cytoplasmic Kvβ1 subunit resulting in rapid inactivating A-type currents. We hypothesized that removal of channel inactivation, by modulating Kv1.1/Kvβ1 interaction with a small molecule, would lead to decreased neuronal excitability and anticonvulsant activity. Methods We applied high-throughput screening to identify ligands able to modulate the Kv1.1-T1 domain/Kvβ1 protein complex. We then selected a compound that was characterized on recombinant Kv1.1/Kvβ1 channels by electrophysiology and further evaluated on sustained neuronal firing and on in vitro epileptiform activity using a high K+-low Ca2+ model in hippocampal slices. Results We identified a novel compound able to modulate the interaction of the Kv1.1/Kvβ1 complex and that produced a functional inhibition of Kv1.1/Kvβ1 channel inactivation. We demonstrated that this compound reduced the sustained repetitive firing in hippocampal neurons and was able to abolish the development of in vitro epileptiform activity. Conclusions This study describes a rational drug discovery approach for the identification of novel ligands that inhibit Kv1.1 channel inactivation and provides pharmacological evidence that such a mechanism translates into physiological effects by reducing in vitro epileptiform activity.}, - language = {en}, - number = {4}, - urldate = {2021-06-07}, - journal = {CNS Neuroscience \& Therapeutics}, - author = {Niespodziany, Isabelle and Mullier, Brice and André, Véronique Marie and Ghisdal, Philippe and Jnoff, Eric and Moreno-Delgado, David and Swinnen, Dominique and Sands, Zara and Wood, Martyn and Wolff, Christian}, - year = {2019}, - keywords = {electrophysiology, epilepsy, potassium channels}, - pages = {442--451}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\VTTUC4BK\\Niespodziany et al. - 2019 - Discovery of a small molecule modulator of the Kv1.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Z92IBWEY\\cns.html:text/html}, -} - -@article{roeper_nip_1998, - title = {{NIP} domain prevents {N}-type inactivation in voltage-gated potassium channels}, - volume = {391}, - copyright = {1998 Macmillan Magazines Ltd.}, - issn = {1476-4687}, - url = {https://www.nature.com/articles/34916}, - doi = {10.1038/34916}, - abstract = {Shaker-related voltage-gated K+ (Kv) channels1,2 are assembled from ion-conducting Kvα subunits, which are integral membrane proteins, and auxiliary Kvβ subunits. This leads to the formation of highly diverse heteromultimeric Kv channels that mediate outward currents with a wide range of time courses for inactivation. Two principal inactivation mechanisms have been recognized1: C-type inactivation correlated with carboxy-terminal Kvα-subunit structures3, and N-type inactivation conferred by ‘ball’ domains in the amino termini of certain Kvα4,5 and Kvβ6 subunits. Assembly of heteromultimers with one or more Kvα4,7- and/or Kvβ6 ball domains appears to be an essential principle of the generation of A-type Kv channel diversity. Here we show that, unexpectedly, the presence of Kvα- or Kvβ-ball domains does not dominate the gating phenotype in heteromultimers containing Kv1.6α subunits. These heteromultimers mediate non-inactivating currents because of the dominant-negative activity of a new type of N-type inactivation-prevention (NIP) domain present in the Kv1.6 amino terminus. Mutations in the NIP domain lead to loss of function, and its transfer to another Kvα subunit leads to gain of function. Our discovery of the NIP domain, which neutralizes the activity of Kvα- and Kvβ-inactivation gates, establishes a new determinant for the gating behaviour of heteromultimeric Kv channels.}, - language = {en}, - number = {6665}, - urldate = {2021-06-07}, - journal = {Nature}, - author = {Roeper, Jochen and Sewing, Sabine and Zhang, Ying and Sommer, Tobias and Wanner, Siegmund G. and Pongs, Olaf}, - month = jan, - year = {1998}, - pages = {390--393}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BPJPQVJA\\Roeper et al. - 1998 - NIP domain prevents N-type inactivation in voltage.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8V4C3VA2\\34916.html:text/html}, -} - -@article{rettig_inactivation_1994, - title = {Inactivation properties of voltage-gated {K} + channels altered by presence of β-subunit}, - volume = {369}, - copyright = {1994 Nature Publishing Group}, - issn = {1476-4687}, - url = {https://www.nature.com/articles/369289a0}, - doi = {10.1038/369289a0}, - abstract = {Structural and functional diversity of voltage-gated Kv1-type potassium channels in rat brain is enhanced by the association of two different types of subunits, the membrane-bound, pore-forming α-subunits and a peripheral β-subunit. We have cloned a β-subunit (Kvβ1) that is specifically expressed in the rat nervous system. Association of Kvβ1 with α-subunits confers rapid A-type inactivation on non-inactivating Kv1 channels (delayed rectifiers) in expression systems in vitro. This effect is mediated by an inactivating ball domain in the Kvβ1 amino terminus.}, - language = {en}, - number = {6478}, - urldate = {2021-06-07}, - journal = {Nature}, - author = {Rettig, Jens and Heinemann, Stefan H. and Wunder, Frank and Lorra, Christoph and Parcej, David N. and Oliver Dolly, J. and Pongs, Olaf}, - month = may, - year = {1994}, - pages = {289--294}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RCEYBSD2\\Rettig et al. - 1994 - Inactivation properties of voltage-gated K + chann.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9X7D2PY4\\Rettig et al. - 1994 - Inactivation properties of voltage-gated K + chann.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WYSLLXAL\\369289a0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WCK725TD\\369289a0.html:text/html}, -} - -@article{wang__1999, - title = {α {Subunit} compositions of {Kv1}.1-containing {K}+ channel subtypes fractionated from rat brain using dendrotoxins}, - volume = {263}, - issn = {1432-1033}, - url = {https://febs.onlinelibrary.wiley.com/doi/abs/10.1046/j.1432-1327.1999.00493.x}, - doi = {https://doi.org/10.1046/j.1432-1327.1999.00493.x}, - abstract = {K+ channels from the Kv1 subfamily contain four α-subunits and the combinations (from Kv1.1–1.6) determine susceptibility to dendrotoxin (DTX) homologues. The subunit composition of certain subtypes in rat brain was investigated using DTXk which only interacts with Kv1.1-containing channels and αDTX (and its closely related homologue DTXi) that binds preferentially to Kv1.2-possessing homo- or hetero-oligomers. Covalent attachment of [125I]DTXk bound to channels in synaptic membranes unveiled subunits of Mr = 78 000 and 96 000. Immunoprecipitation of these solubilized and dissociated cross-linked proteins with IgG specific for each of the α-subunits identified Kv1.1, 1.2 and 1.4; this led to assemblies of Kv1.1/1.2 and 1.1/1.4 being established. Kv1.2-enriched channels, purified from rat brain by chromatography on immobilized DTXi, contained Kv1.1, 1.2 and 1.6 confirming one of the above-noted pairs and indicating an additional Kv1.1-containing oligomer (Kv1.1/1.2/1.6); the notable lack of Kv1.4 excludes a Kv1.1/1.2/1.4 combination. On the other hand, channels with Kv1.1 as a constituent, isolated using DTXk, possessed Kv1.4 in addition to those found in the DTXi-purified oligomers; this provides convergent support for the occurrence of the three combinations established above but adds a possible fourth (Kv1.1/1.4/1.6), though this was not confirmed. Moreover, sequential purification on DTXi and DTXk resins yielded channels containing only Kv1.1/1.2 but with an apparent predominance of Kv1.1, reaffirming the latter multimer.}, - language = {en}, - number = {1}, - urldate = {2021-06-07}, - journal = {European Journal of Biochemistry}, - author = {Wang, Fan C. and Parcej, David N. and Dolly, J. Oliver}, - year = {1999}, - keywords = {K+ channels, dendrotoxins., hetero-oligomers, voltage-gated, α and β subunits}, - pages = {230--237}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UZDUM8RP\\Wang et al. - 1999 - α Subunit compositions of Kv1.1-containing K+ chan.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\99X9K88C\\j.1432-1327.1999.00493.html:text/html}, -} - -@article{stuhmer_molecular_1989, - title = {Molecular basis of functional diversity of voltage-gated potassium channels in mammalian brain.}, - volume = {8}, - issn = {0261-4189}, - url = {https://www.embopress.org/doi/abs/10.1002/j.1460-2075.1989.tb08483.x}, - doi = {10.1002/j.1460-2075.1989.tb08483.x}, - abstract = {Cloning and sequencing of cDNAs isolated from a rat cortex cDNA library reveals that a gene family encodes several highly homologous K+ channel forming (RCK) proteins. Functional characterization of the channels expressed in Xenopus laevis oocytes following microinjection of in vitro transcribed RCK-specific RNAs shows that each of the RCK proteins forms K+ channels that differ greatly in both their functional and pharmacological properties. This suggests that the molecular basis for the diversity of voltage-gated K+ channels in mammalian brain is based, at least partly, on the expression of several RCK proteins by a family of genes and their assembly to homooligomeric K+ channels with different functional properties.}, - number = {11}, - urldate = {2021-06-07}, - journal = {The EMBO Journal}, - author = {Stühmer, W. and Ruppersberg, J.p. and Schröter, K.h. and Sakmann, B. and Stocker, M. and Giese, K.p. and Perschke, A. and Baumann, A. and Pongs, O.}, - month = nov, - year = {1989}, - pages = {3235--3244}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\T4DRXSVK\\Stühmer et al. - 1989 - Molecular basis of functional diversity of voltage.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\T22LZI5H\\j.1460-2075.1989.tb08483.html:text/html}, -} - -@article{mishra_scn2a_2017, - title = {Scn2a deletion improves survival and brain–heart dynamics in the {Kcna1}-null mouse model of sudden unexpected death in epilepsy ({SUDEP})}, - volume = {26}, - issn = {0964-6906}, - url = {https://doi.org/10.1093/hmg/ddx104}, - doi = {10.1093/hmg/ddx104}, - abstract = {People with epilepsy have greatly increased probability of premature mortality due to sudden unexpected death in epilepsy (SUDEP). Identifying which patients are most at risk of SUDEP is hindered by a complex genetic etiology, incomplete understanding of the underlying pathophysiology and lack of prognostic biomarkers. Here we evaluated heterozygous Scn2a gene deletion (Scn2a+/−) as a protective genetic modifier in the Kcna1 knockout mouse (Kcna1–/–) model of SUDEP, while searching for biomarkers of SUDEP risk embedded in electroencephalography (EEG) and electrocardiography (ECG) recordings. The human epilepsy gene Kcna1 encodes voltage-gated Kv1.1 potassium channels that act to dampen neuronal excitability whereas Scn2a encodes voltage-gated Nav1.2 sodium channels important for action potential initiation and conduction. SUDEP-prone Kcna1–/– mice with partial genetic ablation of Nav1.2 channels (i.e. Scn2a+/–; Kcna1–/–) exhibited a two-fold increase in survival. Classical analysis of EEG and ECG recordings separately showed significantly decreased seizure durations in Scn2a+/–; Kcna1–/– mice compared with Kcna1–/– mice, without substantial modification of cardiac abnormalities. Novel analysis of the EEG and ECG together revealed a significant reduction in EEG–ECG association in Kcna1–/– mice compared with wild types, which was partially restored in Scn2a+/–; Kcna1–/– mice. The degree of EEG–ECG association was also proportional to the survival rate of mice across genotypes. These results show that Scn2a gene deletion acts as protective genetic modifier of SUDEP and suggest measures of brain–heart association as potential indices of SUDEP susceptibility.}, - number = {11}, - urldate = {2021-06-07}, - journal = {Human Molecular Genetics}, - author = {Mishra, Vikas and Karumuri, Bharat K. and Gautier, Nicole M. and Liu, Rui and Hutson, Timothy N. and Vanhoof-Villalba, Stephanie L. and Vlachos, Ioannis and Iasemidis, Leonidas and Glasscock, Edward}, - month = jun, - year = {2017}, - pages = {2091--2103}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KRVFMLWC\\Mishra et al. - 2017 - Scn2a deletion improves survival and brain–heart d.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AW6UNLU2\\3072109.html:text/html}, -} - -@article{nieus_ltp_2006, - title = {{LTP} {Regulates} {Burst} {Initiation} and {Frequency} at {Mossy} {Fiber}–{Granule} {Cell} {Synapses} of {Rat} {Cerebellum}: {Experimental} {Observations} and {Theoretical} {Predictions}}, - volume = {95}, - issn = {0022-3077}, - shorttitle = {{LTP} {Regulates} {Burst} {Initiation} and {Frequency} at {Mossy} {Fiber}–{Granule} {Cell} {Synapses} of {Rat} {Cerebellum}}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00696.2005}, - doi = {10.1152/jn.00696.2005}, - abstract = {Long-term potentiation (LTP) is a synaptic change supposed to provide the cellular basis for learning and memory in brain neuronal circuits. Although specific LTP expression mechanisms could be critical to determine the dynamics of repetitive neurotransmission, this important issue remained largely unexplored. In this paper, we have performed whole cell patch-clamp recordings of mossy fiber–granule cell LTP in acute rat cerebellar slices and studied its computational implications with a mathematical model. During LTP, stimulation with short impulse trains at 100 Hz revealed earlier initiation of granule cell spike bursts and a smaller nonsignificant spike frequency increase. In voltage-clamp recordings, short AMPA excitatory postsynaptic current (EPSC) trains showed short-term facilitation and depression and a sustained component probably generated by spillover. During LTP, facilitation disappeared, depression accelerated, and the sustained current increased. The N-methyl-d-aspartate (NMDA) current also increased. In agreement with a presynaptic expression caused by increased release probability, similar changes were observed by raising extracellular [Ca2+]. A mathematical model of mossy fiber–granule cell neurotransmission showed that increasing release probability efficiently modulated the first-spike delay. Glutamate spillover, by causing tonic NMDA and AMPA receptor activation, accelerated excitatory postsynaptic potential (EPSP) temporal summation and maintained a sustained spike discharge. The effect of increasing neurotransmitter release could not be replicated by increasing receptor conductance, which, like postsynaptic manipulations enhancing intrinsic excitability, proved very effective in raising granule cell output frequency. Independent regulation of spike burst initiation and frequency during LTP may provide mechanisms for temporal recoding and gain control of afferent signals at the input stage of cerebellar cortex.}, - number = {2}, - urldate = {2021-06-07}, - journal = {Journal of Neurophysiology}, - author = {Nieus, Thierry and Sola, Elisabetta and Mapelli, Jonathan and Saftenku, Elena and Rossi, Paola and D'Angelo, Egidio}, - month = feb, - year = {2006}, - pages = {686--699}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\83BTACU3\\Nieus et al. - 2006 - LTP Regulates Burst Initiation and Frequency at Mo.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\REF62GTY\\jn.00696.html:text/html}, -} - -@article{dangelo_theta-frequency_2001, - title = {Theta-{Frequency} {Bursting} and {Resonance} in {Cerebellar} {Granule} {Cells}: {Experimental} {Evidence} and {Modeling} of a {Slow} {K}+-{Dependent} {Mechanism}}, - volume = {21}, - issn = {0270-6474}, - shorttitle = {Theta-{Frequency} {Bursting} and {Resonance} in {Cerebellar} {Granule} {Cells}}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6762330/}, - doi = {10.1523/JNEUROSCI.21-03-00759.2001}, - abstract = {Neurons process information in a highly nonlinear manner, generating oscillations, bursting, and resonance, enhancing responsiveness at preferential frequencies. It has been proposed that slow repolarizing currents could be responsible for both oscillation/burst termination and for high-pass filtering that causes resonance (). However, different mechanisms, including electrotonic effects (), the expression of resurgent currents (), and network feedback, may also be important. In this study we report theta-frequency (3–12 Hz) bursting and resonance in rat cerebellar granule cells and show that these neurons express a previously unidentified slow repolarizing K+ current (IK-slow). Our experimental and modeling results indicate that IK-slow was necessary for both bursting and resonance. A persistent (and potentially a resurgent) Na+ current exerted complex amplifying actions on bursting and resonance, whereas electrotonic effects were excluded by the compact structure of the granule cell. Theta-frequency bursting and resonance in granule cells may play an important role in determining synchronization, rhythmicity, and learning in the cerebellum.}, - number = {3}, - urldate = {2021-06-07}, - journal = {The Journal of Neuroscience}, - author = {D'Angelo, Egidio and Nieus, Thierry and Maffei, Arianna and Armano, Simona and Rossi, Paola and Taglietti, Vanni and Fontana, Andrea and Naldi, Giovanni}, - month = feb, - year = {2001}, - pages = {759--770}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9C7QQJ6X\\D'Angelo et al. - 2001 - Theta-Frequency Bursting and Resonance in Cerebell.pdf:application/pdf}, -} - -@article{solinas_realistic_2010, - title = {A {Realistic} {Large}-{Scale} {Model} of the {Cerebellum} {Granular} {Layer} {Predicts} {Circuit} {Spatio}-{Temporal} {Filtering} {Properties}}, - volume = {4}, - issn = {1662-5102}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2876868/}, - doi = {10.3389/fncel.2010.00012}, - abstract = {The way the cerebellar granular layer transforms incoming mossy fiber signals into new spike patterns to be related to Purkinje cells is not yet clear. Here, a realistic computational model of the granular layer was developed and used to address four main functional hypotheses: center-surround organization, time-windowing, high-pass filtering in responses to spike bursts and coherent oscillations in response to diffuse random activity. The model network was activated using patterns inspired by those recorded in vivo. Burst stimulation of a small mossy fiber bundle resulted in granule cell bursts delimited in time (time windowing) and space (center-surround) by network inhibition. This burst–burst transmission showed marked frequency-dependence configuring a high-pass filter with cut-off frequency around 100 Hz. The contrast between center and surround properties was regulated by the excitatory–inhibitory balance. The stronger excitation made the center more responsive to 10–50 Hz input frequencies and enhanced the granule cell output (with spikes occurring earlier and with higher frequency and number) compared to the surround. Finally, over a certain level of mossy fiber background activity, the circuit generated coherent oscillations in the theta-frequency band. All these processes were fine-tuned by NMDA and GABA-A receptor activation and neurotransmitter vesicle cycling in the cerebellar glomeruli. This model shows that available knowledge on cellular mechanisms is sufficient to unify the main functional hypotheses on the cerebellum granular layer and suggests that this network can behave as an adaptable spatio-temporal filter coordinated by theta-frequency oscillations.}, - urldate = {2021-06-07}, - journal = {Frontiers in Cellular Neuroscience}, - author = {Solinas, Sergio and Nieus, Thierry and D'Angelo, Egidio}, - month = may, - year = {2010}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YCSWLTPQ\\Solinas et al. - 2010 - A Realistic Large-Scale Model of the Cerebellum Gr.pdf:application/pdf}, -} - -@article{campolongo_screening_2011, - title = {From screening to quantitative sensitivity analysis. {A} unified approach}, - volume = {182}, - issn = {0010-4655}, - url = {https://www.sciencedirect.com/science/article/pii/S0010465510005321}, - doi = {10.1016/j.cpc.2010.12.039}, - abstract = {The present work is a sequel to a recent one published on this journal where the superiority of ‘radial design’ to compute the ‘total sensitivity index’ was ascertained. Both concepts belong to sensitivity analysis of model output. A radial design is the one whereby starting from a random point in the hyperspace of the input factors one step in turn is taken for each factor. The procedure is iterated a number of times with a different starting random point as to collect a sample of elementary shifts for each factor. The total sensitivity index is a powerful sensitivity measure which can be estimated based on such a sample. Given the similarity between the total sensitivity index and a screening test known as method of the elementary effects (or method of Morris), we test the radial design on this method. Both methods are best practices: the total sensitivity index in the class of the quantitative measures and the elementary effects in that of the screening methods. We find that the radial design is indeed superior even for the computation of the elementary effects method. This opens the door to a sensitivity analysis strategy whereby the analyst can start with a small number of points (screening-wise) and then – depending on the results – possibly increase the numeral of points up to compute a fully quantitative measure. Also of interest to practitioners is that a radial design is nothing else than an iterated ‘One factor At a Time’ (OAT) approach. OAT is a radial design of size one. While OAT is not a good practice, modelers in all domains keep using it for sensitivity analysis for reasons discussed elsewhere (Saltelli and Annoni, 2010) [23]. With the present approach modelers are offered a straightforward and economic upgrade of their OAT which maintain OAT's appeal of having just one factor moved at each step.}, - language = {en}, - number = {4}, - urldate = {2021-06-07}, - journal = {Computer Physics Communications}, - author = {Campolongo, Francesca and Saltelli, Andrea and Cariboni, Jessica}, - month = apr, - year = {2011}, - keywords = {Sensitivity analysis, Elementary effect method, Radial design, Variance based measures}, - pages = {978--988}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YEEU3NRL\\Campolongo et al. - 2011 - From screening to quantitative sensitivity analysi.pdf:application/pdf}, -} - -@article{campolongo_effective_2007, - series = {Modelling, computer-assisted simulations, and mapping of dangerous phenomena for hazard assessment}, - title = {An effective screening design for sensitivity analysis of large models}, - volume = {22}, - issn = {1364-8152}, - url = {https://www.sciencedirect.com/science/article/pii/S1364815206002805}, - doi = {10.1016/j.envsoft.2006.10.004}, - abstract = {In 1991 Morris proposed an effective screening sensitivity measure to identify the few important factors in models with many factors. The method is based on computing for each input a number of incremental ratios, namely elementary effects, which are then averaged to assess the overall importance of the input. Despite its value, the method is still rarely used and instead local analyses varying one factor at a time around a baseline point are usually employed. In this piece of work we propose a revised version of the elementary effects method, improved in terms of both the definition of the measure and the sampling strategy. In the present form the method shares many of the positive qualities of the variance-based techniques, having the advantage of a lower computational cost, as demonstrated by the analytical examples. The method is employed to assess the sensitivity of a chemical reaction model for dimethylsulphide (DMS), a gas involved in climate change. Results of the sensitivity analysis open up the ground for model reconsideration: some model components may need a more thorough modelling effort while some others may need to be simplified.}, - language = {en}, - number = {10}, - urldate = {2021-06-07}, - journal = {Environmental Modelling \& Software}, - author = {Campolongo, Francesca and Cariboni, Jessica and Saltelli, Andrea}, - month = oct, - year = {2007}, - keywords = {Sensitivity analysis, Dimethylsulphide (DMS), Effective sampling strategy, Model-free methods, Screening problem}, - pages = {1509--1518}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XU7ZHUJ5\\Campolongo et al. - 2007 - An effective screening design for sensitivity anal.pdf:application/pdf}, -} - -@article{kleijnen_state---art_2005, - title = {State-of-the-{Art} {Review}: {A} {User}’s {Guide} to the {Brave} {New} {World} of {Designing} {Simulation} {Experiments}}, - volume = {17}, - issn = {1091-9856}, - shorttitle = {State-of-the-{Art} {Review}}, - url = {https://pubsonline.informs.org/doi/10.1287/ijoc.1050.0136}, - doi = {10.1287/ijoc.1050.0136}, - abstract = {Many simulation practitioners can get more from their analyses by using the statistical theory on design of experiments (DOE) developed specifically for exploring computer models. We discuss a toolkit of designs for simulators with limited DOE expertise who want to select a design and an appropriate analysis for their experiments. Furthermore, we provide a research agenda listing problems in the design of simulation experiments—as opposed to real-world experiments—that require more investigation. We consider three types of practical problems: (1) developing a basic understanding of a particular simulation model or system, (2) finding robust decisions or policies as opposed to so-called optimal solutions, and (3) comparing the merits of various decisions or policies. Our discussion emphasizes aspects that are typical for simulation, such as having many more factors than in real-world experiments, and the sequential nature of the data collection. Because the same problem type may be addressed through different design types, we discuss quality attributes of designs, such as the ease of design construction, the flexibility for analysis, and efficiency considerations. Moreover, the selection of the design type depends on the metamodel (response surface) that the analysts tentatively assume; for example, complicated metamodels require more simulation runs. We present several procedures to validate the metamodel estimated from a specific design, and we summarize a case study illustrating several of our major themes. We conclude with a discussion of areas that merit more work to achieve the potential benefits—either via new research or incorporation into standard simulation or statistical packages.}, - number = {3}, - urldate = {2021-06-07}, - journal = {INFORMS Journal on Computing}, - author = {Kleijnen, Jack P. C. and Sanchez, Susan M. and Lucas, Thomas W. and Cioppa, Thomas M.}, - month = aug, - year = {2005}, - pages = {263--289}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\NNFMLGBS\\ijoc.1050.html:text/html}, -} - -@book{law_simulation_2014, - title = {Simulation {Modeling} and {Analysis}}, - url = {https://www.mheducation.com/highered/product/simulation-modeling-analysis-law/M9780073401324.html}, - abstract = {Simulation Modeling and Analysis, 5th Edition by Averill Law (9780073401324) Preview the textbook, purchase or get a FREE instructor-only desk copy.}, - language = {en}, - urldate = {2021-06-07}, - author = {Law, Averill}, - month = jan, - year = {2014}, -} - -@article{orhan_retigabineezogabine_2012, - title = {Retigabine/{Ezogabine}, a {KCNQ}/{KV7} channel opener: pharmacological and clinical data}, - volume = {13}, - issn = {1465-6566}, - shorttitle = {Retigabine/{Ezogabine}, a {KCNQ}/{KV7} channel opener}, - url = {https://doi.org/10.1517/14656566.2012.706278}, - doi = {10.1517/14656566.2012.706278}, - abstract = {Introduction: Epilepsy is a serious and common chronic neurological disease with an urgent need for novel treatment options, because 30\% of all epilepsy patients do not respond to currently available drugs. Retigabine/Ezogabine (RTG) is a third-generation antiepileptic drug (AED) with a novel mechanism of action. It enhances the activity of voltage-gated KV7 potassium channels. Areas covered: The mechanism of action of RTG is reported in this paper, along with its pharmacodynamics and pharmacokinetics, based on a literature search from 1995 to 2011. Assessment of clinical efficacy and safety was performed using the published data of one Phase II and two Phase III clinical trials (RESTORE 1 and 2). Expert opinion: RTG is an efficacious AED with a unique mechanism of action. It offers a new treatment option which could be particularly interesting for patients who are resistant to currently available AEDs. However, future investigations will show if such a "rational drug therapy" will be truly advantageous. RTG seems to have a low interaction profile, but its interactions with lamotrigine in particular should be further explored. Side effects are common and mainly related to the central nervous system, but also affect peripheral organs, such as the bladder, due its relaxing effect on smooth muscle. Slow titration could be an option to reduce such side effects.}, - number = {12}, - urldate = {2021-06-10}, - journal = {Expert Opinion on Pharmacotherapy}, - author = {Orhan, Gökce and Wuttke, Thomas V. and Nies, Anne T. and Schwab, Matthias and Lerche, Holger}, - month = aug, - year = {2012}, - keywords = {epilepsy, potassium channel, antiepileptic drug, pharmacotherapy, retigabine/ezogabine}, - pages = {1807--1816}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WVD6W3XD\\14656566.2012.html:text/html}, -} - -@article{graves_nongenetic_2010, - title = {Nongenetic factors influence severity of episodic ataxia type 1 in monozygotic twins}, - volume = {75}, - copyright = {© 2010}, - issn = {0028-3878, 1526-632X}, - url = {https://n.neurology.org/content/75/4/367}, - doi = {10.1212/WNL.0b013e3181ea9ee3}, - abstract = {Objective: Episodic ataxia type 1 (EA1) is a monogenic channelopathy caused by mutations of the potassium channel gene KCNA1. Affected individuals carrying the same mutation can exhibit considerable variability in the severity of ataxia, neuromyotonia, and other associated features. We investigated the phenotypic heterogeneity of EA1 in 2 sets of identical twins to determine the contribution of environmental factors to disease severity. One of the mutations was also found in a distantly related family, providing evidence of the influence of genetic background on the EA1 phenotype. -Methods: We evaluated 3 families with an EA1 phenotype, 2 of which included monozygotic twins. We sequenced the KCNA1 gene and studied the biophysical consequences of the mutations in HEK cells. -Results: We identified a new KCNA1 mutation in each pair of twins. Both pairs reported striking differences in the clinical severity of symptoms. The F414S mutation identified in one set of twins also occurred in a distantly related family in which seizures complicated the EA1 phenotype. The other twins had an R307C mutation, the first EA1 mutation to affect an arginine residue in the voltage-sensor domain. Both mutants when expressed exerted a dominant-negative effect on wild-type channels. -Conclusion: These results broaden the range of KCNA1 mutations and reveal an unexpectedly large contribution of nongenetic factors to phenotypic variability in EA1. The occurrence of epilepsy in 1 of 2 families with the F414S mutation suggests an interplay of KCNA1 with other genetic factors.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Neurology}, - author = {Graves, T. D. and Rajakulendran, S. and Zuberi, S. M. and Morris, H. R. and Schorge, S. and Hanna, M. G. and Kullmann, D. M.}, - month = jul, - year = {2010}, - pages = {367--372}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XEQ37HGF\\Graves et al. - 2010 - Nongenetic factors influence severity of episodic .pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6B3SEDXW\\Graves et al. - 2010 - Nongenetic factors influence severity of episodic .pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6V54KTWJ\\Graves et al. - 2010 - Nongenetic factors influence severity of episodic .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GH6Q8FJ6\\367.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\C325GBHQ\\367.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\KYSSLTKM\\367.html:text/html}, -} - -@article{zhao_common_2020, - title = {A {Common} {Kinetic} {Property} of {Mutations} {Linked} to {Episodic} {Ataxia} {Type} 1 {Studied} in the {Shaker} {Kv} {Channel}}, - volume = {21}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - url = {https://www.mdpi.com/1422-0067/21/20/7602}, - doi = {10.3390/ijms21207602}, - abstract = {(1) Background: Episodic ataxia type 1 is caused by mutations in the KCNA1 gene encoding for the voltage-gated potassium channel Kv1.1. There have been many mutations in Kv1.1 linked to episodic ataxia reported and typically investigated by themselves or in small groups. The aim of this article is to determine whether we can define a functional parameter common to all Kv1.1 mutants that have been linked to episodic ataxia. (2) Methods: We introduced the disease mutations linked to episodic ataxia in the drosophila analog of Kv1.1, the Shaker Kv channel, and expressed the channels in Xenopus oocytes. Using the cut-open oocyte technique, we characterized the gating and ionic currents. (3) Results: We found that the episodic ataxia mutations variably altered the different gating mechanisms described for Kv channels. The common characteristic was a conductance voltage relationship and inactivation shifted to less polarized potentials. (4) Conclusions: We suggest that a combination of a prolonged action potential and slowed and incomplete inactivation leads to development of ataxia when Kv channels cannot follow or adapt to high firing rates.}, - language = {en}, - number = {20}, - urldate = {2021-06-10}, - journal = {International Journal of Molecular Sciences}, - author = {Zhao, Juan and Petitjean, Dimitri and Haddad, Georges A. and Batulan, Zarah and Blunck, Rikard}, - month = jan, - year = {2020}, - keywords = {electrophysiology, episodic ataxia, gating, voltage-gated potassium channel}, - pages = {7602}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\A2Q2B2UZ\\Zhao et al. - 2020 - A Common Kinetic Property of Mutations Linked to E.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7DVZLKI7\\Zhao et al. - 2020 - A Common Kinetic Property of Mutations Linked to E.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2EXHPJBW\\7602.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\V8EV5IKK\\7602.html:text/html}, -} - -@article{chi_manipulation_2007, - title = {Manipulation of the {Potassium} {Channel} {Kv1}.1 and {Its} {Effect} on {Neuronal} {Excitability} in {Rat} {Sensory} {Neurons}}, - volume = {98}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00437.2007}, - doi = {10.1152/jn.00437.2007}, - abstract = {Potassium channels play a critical role in regulating many aspects of action potential (AP) firing. To establish the contribution of the voltage-dependent potassium channel Kv1.1 in regulating excitability, we used the selective blocker dendrotoxin-K (DTX-K) and small interfering RNA (siRNA) targeted to Kv1.1 to determine their effects on AP firing in small-diameter capsaicin-sensitive sensory neurons. A 5-min exposure to 10 nM DTX-K suppressed the total potassium current (IK) measured at +40 mV by about 33\%. DTX-K produced a twofold increase in the number of APs evoked by a ramp of depolarizing current. Associated with increased firing was a decrease in firing threshold and rheobase. DTX-K did not alter the resting membrane potential or the AP duration. A 48-h treatment with siRNA targeted to Kv1.1 reduced the expression of this channel protein by about 60\% as measured in Western blots. After treatment with siRNA, IK was no longer sensitive to DTX-K, indicating a loss of functional protein. Similarly, after siRNA treatment exposure to DTX-K had no effect on the number of evoked APs, firing threshold, or rheobase. However, after siRNA treatment, the firing threshold had values similar to those obtained after acute exposure to DTX-K, suggesting that the loss of Kv1.1 plays a critical role in setting this parameter of excitability. These results demonstrate that Kv1.1 plays an important role in limiting AP firing and that siRNA may be a useful approach to establish the role of specific ion channels in the absence of selective antagonists.}, - number = {5}, - urldate = {2021-06-10}, - journal = {Journal of Neurophysiology}, - author = {Chi, Xian Xuan and Nicol, G. D.}, - month = nov, - year = {2007}, - pages = {2683--2692}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4K5J2PLY\\Chi and Nicol - 2007 - Manipulation of the Potassium Channel Kv1.1 and It.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\K6U2R6HN\\jn.00437.html:text/html}, -} - -@article{van_dyke_hereditary_1975, - title = {Hereditary myokymia and periodic ataxia}, - volume = {25}, - issn = {0022-510X}, - url = {https://www.sciencedirect.com/science/article/pii/0022510X75901914}, - doi = {10.1016/0022-510X(75)90191-4}, - abstract = {A kindred in which at least 11 individuals in 3 consecutive generations have continuous muscle movement, i.e., myokymia, and periodic ataxia, has been studied. Three patients, a 24-year-old woman, her 4-year-old son and her 27-year-old sister, have been studied in detail. The disorder is inherited as an autosomal-dominant trait and presents in early childhood with attacks of ataxia of 1–2 min in duration, with associated jerking movements of the head, arms and legs. Attacks are provoked by abrupt postural change, emotional stimulus, and caloric-vestibular stimulation. At the age of 12 years approximately, facial and extremity myokymia appears. Physical findings include large calves, normal muscle strength and widespread myokymia of face, hands, arms and legs with a hand posture resembling carpopedal spasm. EMG studies at rest showed continuous spontaneous activity of otherwise normal motor units. Nerve conduction velocities were normal. Gastrocnemius biopsy in 2 patients showed fiber type grouping and small angular fibers, and was consistent with denervation. Histographic analysis of the biopsies demonstrated enlargement of both fiber types, particularly of Type I fibers. These findings are consistent with chronic denervation and an abnormality of motor neuron population or firing. The myokymia described here is of interest not only because of its genetic association with a movement disorder, but also because the muscle findings support a peripheral basis for the muscle movements.}, - language = {en}, - number = {1}, - urldate = {2021-06-10}, - journal = {Journal of the Neurological Sciences}, - author = {Van Dyke, D. H. and Griggs, R. C. and Murphy, M. J. and Goldstein, M. N.}, - month = may, - year = {1975}, - pages = {109--118}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GZD6WJU6\\Van Dyke et al. - 1975 - Hereditary myokymia and periodic ataxia.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XQD53H6D\\0022510X75901914.html:text/html}, -} - -@article{brunt_familial_1990, - title = {Familial {Paroxysmal} {Kinesigenic} {Ataxia} and {Continuous} {Myokymia}}, - volume = {113}, - issn = {0006-8950}, - url = {https://doi.org/10.1093/brain/113.5.1361}, - doi = {10.1093/brain/113.5.1361}, - abstract = {A large family with paroxysmal ataxia and continuous myokymic discharges is described. The disorder is of autosomal dominant inheritance. During attacks coordination of movements and balance are disturbed; often a postural tremor of the head and the hands and fine twitching in some of the facial and hand muscles are present. The attacks usually last a few minutes and may occur several times per day. They first appear in childhood and tend to abate after early adulthood. The attacks are frequently precipitated by kinesigenic stimuli similar to those in paroxysmal kinesigenic choreoathetosis. Their occurrence can be reduced or prevented by carbonic anhydrase inhibitors. Between attacks a slight postural tremor and ataxia was found in a few of the elderly affected members. Fine rippling myokymia was obvious in a few and could be detected on close inspection in about half of the adults. Electromyography (EMG) showed myokymic discharges in all affected members. The characteristics and reactivity of this myokymic activity suggest multiple impulse generation in the peripheral nerves.}, - number = {5}, - urldate = {2021-06-10}, - journal = {Brain}, - author = {Brunt, Ewout R. P. and van Weerden, Tiemen W.}, - month = oct, - year = {1990}, - pages = {1361--1382}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\558YAH37\\BRUNT and VAN WEERDEN - 1990 - FAMILIAL PAROXYSMAL KINESIGENIC ATAXIA AND CONTINU.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2PIA368R\\267626.html:text/html}, -} - -@article{graves_episodic_2014, - title = {Episodic ataxia type 1: clinical characterization, quality of life and genotype–phenotype correlation}, - volume = {137}, - issn = {0006-8950}, - shorttitle = {Episodic ataxia type 1}, - url = {https://doi.org/10.1093/brain/awu012}, - doi = {10.1093/brain/awu012}, - abstract = {Episodic ataxia type 1 is considered a rare neuronal ion channel disorder characterized by brief attacks of unsteadiness and dizziness with persistent myokymia. To characterize the natural history, develop outcome measures for future clinical trials, and correlate genotype with phenotype, we undertook an international, prospective, cross-sectional study. Thirty-nine individuals (51\% male) were enrolled: median age 37 years (range 15–65 years). We identified 10 different pathogenic point mutations in KCNA1 that accounted for the genetic basis of 85\% of the cohort. Participants with KCNA1 mutations were more likely to have a positive family history. Analysis of the total cohort showed that the first episode of ataxia occurred before age 20 in all but one patient, with an average age of onset of 7.9 years. Physical exertion, emotional stress and environmental temperature were the most common triggers for attacks. Attack frequency ranged from daily to monthly, even with the same KCNA1 genotype. Average attack duration was in the order of minutes. Ten participants (26\%) developed permanent cerebellar signs, which were related to disease duration. The average Scale for the Assessment and Rating of Ataxia score (SARA, a standardized measure of cerebellar dysfunction on clinical examination, scores range from 0–40) was an average of 3.15 for all participants (range 0–14), but was only 2 in those with isolated episodic ataxia compared with 7.7 in those with progressive cerebellar ataxia in addition to episodic ataxia. Thirty-seven participants completed the SF-36, a quality of life survey; all eight domain norm-based average scores (mean = 50) were below normal with mental health being the lowest (41.3) in those with mutation positive episodic ataxia type 1. Scores on SF-36 correlated negatively with attack frequency. Of the 39 participants in the study, 33 harboured mutations in KCNA1 whereas the remaining six had no mutation identified. Episodic ataxia type 1 phenocopies have not been described previously and we report their clinical features, which appear to be different to those with a KCNA1 mutation. This large prospective study of both genetically confirmed episodic ataxia type 1 and episodic ataxia type 1 phenocopies provides detailed baseline characteristics of these disorders and their impact on participants. We found that attacks had a significant effect on quality of life. Unlike previous studies, we found that a significant number of individuals with genetically confirmed episodic ataxia type 1 (21\%) had accumulated persistent cerebellar symptoms and signs. These data will enable the development of outcome measures for clinical trials of treatment.}, - number = {4}, - urldate = {2021-06-10}, - journal = {Brain}, - author = {Graves, Tracey D. and Cha, Yoon-Hee and Hahn, Angelika F. and Barohn, Richard and Salajegheh, Mohammed K. and Griggs, Robert C. and Bundy, Brian N. and Jen, Joanna C. and Baloh, Robert W. and Hanna, Michael G. and {on behalf of the CINCH Investigators}}, - month = apr, - year = {2014}, - pages = {1009--1018}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GW4CYP4I\\Graves et al. - 2014 - Episodic ataxia type 1 clinical characterization,.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\962LHS6A\\Graves et al. - 2014 - Episodic ataxia type 1 clinical characterization,.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\G5KRDWAE\\367720.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FAHUQPK8\\367720.html:text/html}, -} - -@article{jen_primary_2007, - title = {Primary episodic ataxias: diagnosis, pathogenesis and treatment}, - volume = {130}, - issn = {0006-8950}, - shorttitle = {Primary episodic ataxias}, - url = {https://doi.org/10.1093/brain/awm126}, - doi = {10.1093/brain/awm126}, - abstract = {Primary episodic ataxias are autosomal dominant channelopathies that manifest as attacks of imbalance and incoordination. Mutations in two genes, KCNA1 and CACNA1A, cause the best characterized and account for the majority of identified cases of episodic ataxia. We summarize current knowledge of clinical and genetic diagnosis, genotype–phenotype correlations, pathophysiology and treatment of episodic ataxia syndromes. We focus on unresolved issues including phenotypic and genetic heterogeneity, lessons from animal models and technological advancement, rationale and feasibility of various treatment strategies, and shared mechanisms underlying episodic ataxia and other far more prevalent paroxysmal conditions such as epilepsy and migraine.}, - number = {10}, - urldate = {2021-06-10}, - journal = {Brain}, - author = {Jen, J.C. and Graves, T.D. and Hess, E.J. and Hanna, M.G. and Griggs, R.C. and Baloh, R.W. and {the CINCH investigators}}, - month = oct, - year = {2007}, - pages = {2484--2493}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7VS52FIB\\Jen et al. - 2007 - Primary episodic ataxias diagnosis, pathogenesis .pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\STLLRYY4\\Jen et al. - 2007 - Primary episodic ataxias diagnosis, pathogenesis .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WWTFDAFS\\372064.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\G7MY4DE3\\372064.html:text/html}, -} - -@article{herson_mouse_2003, - title = {A mouse model of episodic ataxia type-1}, - volume = {6}, - copyright = {2003 Nature Publishing Group}, - issn = {1546-1726}, - url = {https://www.nature.com/articles/nn1025}, - doi = {10.1038/nn1025}, - abstract = {Episodic ataxia type-1 (EA1) is a dominant human neurological disorder characterized by stress-induced attacks of ataxia. EA1 is caused by mutations in the voltage-gated potassium channel Kv1.1, and affected individuals are heterozygous. Here we introduced the V408A EA1 mutation into mice using homologous recombination. In contrast to Kv1.1 null mice, homozygous V408A/V408A mice died after embryonic day 3 (E3). V408A/+ mice showed stress-induced loss of motor coordination that was ameliorated by acetazolamide, a carbonic anhydrase inhibitor that minimizes EA1 symptoms in human patients. We made electrophysiological recordings from cerebellar Purkinje cells in both V408A/+ mice and their wild-type littermates. V408A/+ mice showed a greater frequency and amplitude of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) than did wild type; however, the amplitude or frequency of miniature IPSCs and the basket cell firing frequency did not differ between groups. The stress-induced motor dysfunction in V408A mice is similar to that of family members harboring the EA1 allele, and our findings suggest that these behavioral changes are linked to changes in GABA release.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Nature Neuroscience}, - author = {Herson, Paco S. and Virk, Michael and Rustay, Nathan R. and Bond, Chris T. and Crabbe, John C. and Adelman, John P. and Maylie, James}, - month = apr, - year = {2003}, - pages = {378--383}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JRPIS56T\\Herson et al. - 2003 - A mouse model of episodic ataxia type-1.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\S4FX96QP\\nn1025.html:text/html}, -} - -@article{rajakulendran_episodic_2007, - title = {Episodic ataxia type 1: {A} neuronal potassium channelopathy}, - volume = {4}, - issn = {1878-7479}, - shorttitle = {Episodic ataxia type 1}, - url = {https://doi.org/10.1016/j.nurt.2007.01.010}, - doi = {10.1016/j.nurt.2007.01.010}, - abstract = {Episodic ataxia type 1 is a paroxysmal neurological disorder characterized by short-lived attacks of recurrent midline cerebellar dysfunction and continuous motor activity. Mutations in KCN1A, the gene encoding Kv1.1, a voltage-gated neuronal potassium channel, are associated with the disorder. Although rare, the syndrome highlights the fundamental features of genetic ion-channel diseases and serves as a useful model for understanding more common paroxysmal disorders, such as epilepsy and migraine. This review examines our current understanding of episodic ataxia type 1, focusing on its clinical and genetic features, pathophysiology, and treatment.}, - language = {en}, - number = {2}, - urldate = {2021-06-10}, - journal = {Neurotherapeutics}, - author = {Rajakulendran, Sanjeev and Schorge, Stephanie and Kullmann, Dimitri M. and Hanna, Michael G.}, - month = apr, - year = {2007}, - pages = {258--266}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TCNZXIXP\\Rajakulendran et al. - 2007 - Episodic ataxia type 1 A neuronal potassium chann.pdf:application/pdf}, -} - -@article{zuberi_novel_1999, - title = {A novel mutation in the human voltage-gated potassium channel gene ({Kv1}.1) associates with episodic ataxia type 1 and sometimes with partial epilepsy}, - volume = {122}, - issn = {0006-8950}, - url = {https://doi.org/10.1093/brain/122.5.817}, - doi = {10.1093/brain/122.5.817}, - abstract = {Episodic ataxia type 1 (EA1) is a rare autosomal dominant disorder characterized by brief episodes of ataxia associated with continuous interattack myokymia. Point mutations in the human voltage-gated potassium channel (Kv1.1) gene on chromosome 12p13 have recently been shown to associate with EA1. A Scottish family with EA1 harbouring a novel mutation in this gene is reported. Of the five affected individuals over three generations, two had partial epilepsy in addition to EA1. The detailed clinical, electrophysiological and molecular genetic findings are presented. The heterozygous point mutation is located at nucleotide position 677 and results in a radical amino acid substitution at a highly conserved position in the second transmembrane domain of the potassium channel. Functional studies indicated that mutant subunits exhibited a dominant negative effect on potassium channel function and would be predicted to impair neuronal repolarization. Potassium channels determine the excitability of neurons and blocking drugs are proconvulsant. A critical review of previously reported EA1 families shows an over-representation of epilepsy in family members with EA1 compared with unaffected members. These observations indicate that this mutation is pathogenic and suggest that the epilepsy in EA1 may be caused by the dysfunctional potassium channel. It is possible that such dysfunction may be relevant to other epilepsies in man.}, - number = {5}, - urldate = {2021-06-10}, - journal = {Brain}, - author = {Zuberi, S. M. and Eunson, L. H. and Spauschus, A. and De Silva, R. and Tolmie, J. and Wood, N. W. and McWilliam, R. C. and Stephenson, J. P. B. and Kullmann, D. M. and Hanna, M. G.}, - month = may, - year = {1999}, - pages = {817--825}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SEX9BDH8\\Zuberi et al. - 1999 - A novel mutation in the human voltage-gated potass.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Q6HMRVKV\\296621.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Y5C7TN83\\296621.html:text/html}, -} - -@article{veh_immunohistochemical_1995, - title = {Immunohistochemical {Localization} of {Five} {Members} of the {KV1} {Channel} {Subunits}: {Contrasting} {Subcellular} {Locations} and {Neuron}-specific {Co}-localizations in {Rat} {Brain}}, - volume = {7}, - issn = {1460-9568}, - shorttitle = {Immunohistochemical {Localization} of {Five} {Members} of the {KV1} {Channel} {Subunits}}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.1995.tb00641.x}, - doi = {10.1111/j.1460-9568.1995.tb00641.x}, - abstract = {A large variety of potassium channels is involved in regulating integration and transmission of electrical signals in the nervous system. Different types of neurons, therefore, require specific patterns of potassium channel subunit expression and specific regulation of subunit coassembly into heteromultimeric channels, as well as subunit-specific sorting and segregation. This was investigated by studying in detail the expression of six different α-subunits of voltage-gated potassium channels in the rat hippocampus, cerebellum, olfactory bulb and spinal cord, combining in situ hybridization and immunocytochemistry. Specific polyclonal antibodies were prepared for five α-subunits (KV1.1, KV1.2, KV1.3, KV1.4, KV1.6) of the Shaker-related subfamily of rat Kv channels, which encode delayed-rectifier type and rapidly inactivating A-type potassium channels. Their distribution was compared to that of an A-type potassium channel (KV3.4), belonging to the Shaw-related subfamily of rat Kv channels. Our results show that these Kv channel α-subunits are differentially expressed in rat brain neurons. We did not observe in various neurons a stereotypical distribution of Kv channel α-subunits to dendritic and axonal compartments, but a complex differential subcellular subunit distribution. The different Kv channel subunits are targeted either to presynaptic or to postsynaptic domains, depending on neuronal cell type. Thus, distinct combinations of Kv1 α-subunits are co-localized in different neurons. The implications of these findings are that both differential expression and assembly as well as subcellular targeting of Kv channel α-subunits may contribute to Kv channel diversity and thereby to presynaptic and postsynaptic membrane excitability.}, - language = {en}, - number = {11}, - urldate = {2021-06-10}, - journal = {European Journal of Neuroscience}, - author = {Veh, Rüdiger W. and Lichtinghagen, Ralf and Sewing, Sabine and Wunder, Frank and Grumbach, Isabella M. and Pongs, Olaf}, - year = {1995}, - keywords = {potassium channels, hybridization, in situ, rat brain}, - pages = {2189--2205}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FBDVD9YW\\Veh et al. - 1995 - Immunohistochemical Localization of Five Members o.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2DYEMJUC\\Veh et al. - 1995 - Immunohistochemical Localization of Five Members o.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\TCXWZH3V\\j.1460-9568.1995.tb00641.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\CQNWEC4V\\j.1460-9568.1995.tb00641.html:text/html}, -} - -@article{browne_episodic_1994, - title = {Episodic ataxia/myokymia syndrome is associated with point mutations in the human potassium channel gene, {KCNA1}}, - volume = {8}, - copyright = {1994 Nature Publishing Group}, - issn = {1546-1718}, - url = {https://www.nature.com/articles/ng1094-136}, - doi = {10.1038/ng1094-136}, - abstract = {Episodic ataxia (EA) is a rare, familial disorder producing attacks of generalized ataxia, with normal or near-normal neurological function between attacks. One type of EA is characterized by brief episodes of ataxia with myokymia (rippling of muscles) evident between attacks. Linkage studies in four such families suggested localization of an EA/ myokymia gene near the voltage gated K+ channel gene, KCNA1 (Kv1.1), on chromosome 12p. Mutation analysis of the KCNA1 coding region in these families identified four different missense point mutations present in the heterozygous state, indicating that EA/myokymia can result from mutations in this gene.}, - language = {en}, - number = {2}, - urldate = {2021-06-10}, - journal = {Nature Genetics}, - author = {Browne, David L. and Gancher, Stephen T. and Nutt, John G. and Brunt, Ewout R. P. and Smith, Eric A. and Kramer, Patricia and Litt, Michael}, - month = oct, - year = {1994}, - pages = {136--140}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WKWMG5CL\\Browne et al. - 1994 - Episodic ataxiamyokymia syndrome is associated wi.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UZJSGF2J\\Browne et al. - 1994 - Episodic ataxiamyokymia syndrome is associated wi.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H7HS6X9W\\ng1094-136.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JUTGMKPM\\ng1094-136.html:text/html}, -} - -@article{glasscock_kv11_2019, - title = {Kv1.1 channel subunits in the control of neurocardiac function}, - volume = {13}, - issn = {1933-6950}, - url = {https://doi.org/10.1080/19336950.2019.1635864}, - doi = {10.1080/19336950.2019.1635864}, - abstract = {Voltage-gated Kv1.1 potassium channel α-subunits are broadly expressed in the nervous system where they act as critical regulators of neuronal excitability. Mutations in the KCNA1 gene, which encodes Kv1.1, are associated with the neurological diseases episodic ataxia and epilepsy. Studies in mouse models have shown that Kv1.1 is important for neural control of the heart and that Kcna1 deletion leads to cardiac dysfunction that appears to be brain-driven. Traditionally, KCNA1 was not believed to be expressed in the heart. However, recent studies have revealed that Kv1.1 subunits are not only present in cardiomyocytes, but that they also make an important heart-intrinsic functional contribution to outward K+ currents and action potential repolarization. This review recounts the winding history of discovery of KCNA1 gene expression and neurocardiac function from fruit flies to mammals and from brain to heart and looks at some of the salient questions that remain to be answered regarding emerging cardiac roles of Kv1.1.}, - number = {1}, - urldate = {2021-06-10}, - journal = {Channels}, - author = {Glasscock, Edward}, - month = jan, - year = {2019}, - keywords = {epilepsy, action potential, Kv1.1, SUDEP, heart, Kcna1}, - pages = {299--307}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9HL7ES5Y\\Glasscock - 2019 - Kv1.1 channel subunits in the control of neurocard.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\QZIHSRYT\\19336950.2019.html:text/html}, -} - -@incollection{jen_chapter_2018, - series = {The {Cerebellum}: {Disorders} and {Treatment}}, - title = {Chapter 13 - {Episodic} ataxias}, - volume = {155}, - url = {https://www.sciencedirect.com/science/article/pii/B9780444641892000135}, - abstract = {Primary episodic ataxias (EAs) are a group of dominantly inherited disorders characterized by transient recurrent incoordination and truncal instability, often triggered by physical exertion and emotional stress, variably associated with progressive baseline ataxia. There are now eight designated subtypes based largely on genetic loci. Mutations have been identified in multiple individuals and families with EA1, EA2, and EA6, mostly with onset before adulthood. EA1 and EA2 are prototypical neurologic channelopathies. EA1 is caused by heterozygous mutations in KCNA1, which encodes the α1 subunit of a neuronal voltage-gated potassium channel, Kv1.1. EA2, the most common and best characterized, is caused by heterozygous mutations in CACNA1A, which encodes the α1A subunit of a neuronal voltage-gated calcium channel, Cav2.1. EA6 is caused by heterozygous mutations in SLC1A3, which encodes a subunit of a glial excitatory amino acid transporter, EAAT1. The other EA subtypes were defined in single families awaiting gene identification and further confirmation. This chapter focuses on the best-characterized EA syndromes, the clinical assessment and genetic diagnosis of EA, and the management of EA, as well as newly recognized allelic disorders that have greatly expanded the clinical spectrum of EA2. Illustrative cases are discussed, with a focus on sporadic patients with congenital features without episodic ataxia who present diagnostic and therapeutic challenges.}, - language = {en}, - urldate = {2021-06-10}, - booktitle = {Handbook of {Clinical} {Neurology}}, - publisher = {Elsevier}, - author = {Jen, Joanna C. and Wan, Jijun}, - editor = {Manto, Mario and Huisman, Thierry A. G. M.}, - month = jan, - year = {2018}, - keywords = {calcium channel, channelopathies, potassium channel, episodic ataxias, glial excitatory amino acid transporter}, - pages = {205--215}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\W2B4UCRT\\B9780444641892000135.html:text/html}, -} - -@article{orsucci_therapy_2019, - title = {Therapy of episodic ataxias: case report and review of the literature}, - volume = {8}, - issn = {17404398}, - shorttitle = {Therapy of episodic ataxias}, - url = {https://drugsincontext.com/therapy-of-episodic-ataxias:-case-report-and-review-of-the-literature}, - doi = {10.7573/dic.212576}, - urldate = {2021-06-10}, - journal = {Drugs in Context}, - author = {Orsucci, Daniele and Raglione, Laura Maria and Mazzoni, Monica and Vista, Marco}, - month = mar, - year = {2019}, - pages = {1--6}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\QFB8QH5X\\Orsucci et al. - 2019 - Therapy of episodic ataxias case report and revie.pdf:application/pdf}, -} - -@incollection{zittel_episodic_2021, - address = {Cham}, - title = {Episodic {Ataxias}}, - isbn = {978-3-030-53721-0}, - url = {https://doi.org/10.1007/978-3-030-53721-0_11}, - abstract = {Episodic ataxias (EA) are rare autosomal dominant channelopathies characterized by recurrent episodes of ataxia, vertigo and incoordination. So far, eight subtypes have been described with identified gene mutations in five of them (EA1, EA2, EA5, EA6 and EA8). Clinical clues, for example precipitating triggers, duration of attacks, associated interictal signs and treatment response, can aid the distinction of the different subtypes of EA. The current chapter will give an overview of clinical symptoms, genetic background and treatment for the different subtypes of EA. It will also briefly discuss the clinico-genetic characteristics of further disorders that may present with recurring bouts of paroxysmal ataxia and may, therefore, fall within the episodic ataxia spectrum.}, - language = {en}, - urldate = {2021-06-10}, - booktitle = {Paroxysmal {Movement} {Disorders}: {A} {Practical}, {Concise} {Guide}}, - publisher = {Springer International Publishing}, - author = {Zittel, Simone and Ganos, Christos}, - editor = {Sethi, Kapil D. and Erro, Roberto and Bhatia, Kailash P.}, - year = {2021}, - keywords = {4-Aminopyridine, Acetazolamide, CACNA1A mutation, Channelopathy, Episodic ataxias, Genetics, KCNA1 mutation, Trigger}, - pages = {133--140}, -} - -@article{ferrick-kiddie_mutations_2017, - title = {Mutations underlying {Episodic} {Ataxia} type-1 antagonize {Kv1}.1 {RNA} editing}, - volume = {7}, - copyright = {2017 The Author(s)}, - issn = {2045-2322}, - url = {https://www.nature.com/articles/srep41095}, - doi = {10.1038/srep41095}, - abstract = {Adenosine-to-inosine RNA editing in transcripts encoding the voltage-gated potassium channel Kv1.1 converts an isoleucine to valine codon for amino acid 400, speeding channel recovery from inactivation. Numerous Kv1.1 mutations have been associated with the human disorder Episodic Ataxia Type-1 (EA1), characterized by stress-induced ataxia, myokymia, and increased prevalence of seizures. Three EA1 mutations, V404I, I407M, and V408A, are located within the RNA duplex structure required for RNA editing. Each mutation decreased RNA editing both in vitro and using an in vivo mouse model bearing the V408A allele. Editing of transcripts encoding mutant channels affects numerous biophysical properties including channel opening, closing, and inactivation. Thus EA1 symptoms could be influenced not only by the direct effects of the mutations on channel properties, but also by their influence on RNA editing. These studies provide the first evidence that mutations associated with human genetic disorders can affect cis-regulatory elements to alter RNA editing.}, - language = {en}, - number = {1}, - urldate = {2021-06-10}, - journal = {Scientific Reports}, - author = {Ferrick-Kiddie, Elizabeth A. and Rosenthal, Joshua J. C. and Ayers, Gregory D. and Emeson, Ronald B.}, - month = feb, - year = {2017}, - pages = {41095}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7EZLVKXD\\Ferrick-Kiddie et al. - 2017 - Mutations underlying Episodic Ataxia type-1 antago.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JGXBGBFW\\srep41095.html:text/html}, -} - -@article{yuan_two_2020, - title = {Two novel {KCNA1} variants identified in two unrelated {Chinese} families affected by episodic ataxia type 1 and neurodevelopmental disorders}, - volume = {8}, - copyright = {© 2020 The Authors. Molecular Genetics \& Genomic Medicine published by Wiley Periodicals LLC.}, - issn = {2324-9269}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mgg3.1434}, - doi = {10.1002/mgg3.1434}, - abstract = {Background Pathogenic KCNA1 variants have been linked to episodic ataxia type 1 (EA1), a rare neurological syndrome characterized by continuous myokymia and attacks of generalized ataxia that can be triggered by fever, abrupt movements, emotional stress, and fatigue. Currently, over 40 KCNA1 variants have been identified in individuals with EA1. Methods A male patient displayed partial seizures in addition to EA1 symptoms, often triggered by fever. A sibling presented with typical EA1 symptoms, seizures, and learning difficulties. In addition, the older brother displayed cognitive impairment, developmental delay, and slurred speech, which were absent in his younger sister. Whole-exome sequencing was performed for the patients. Results A novel de novo missense variant in KCNA1 (p.Ala261Thr) was identified in the male patient, which is located in a base of the 3rd transmembrane domain (S3). The other novel KCNA1 variant (p.Gly376Ser) was identified in the sibling and was inherited from an unaffected father with low-level mosaicism. The variant was located in the S5–S6 extracellular linker of the voltage sensor domain of the Kv channel. Next, we systematically reviewed the available clinical phenotypes of individuals with EA1 and observed that individuals with KCNA1 variants at the C-terminus were more likely to suffer from seizures and neurodevelopmental disorders than those with variants at the N-terminus. Conclusion Our study expands the mutation spectrum of KCNA1 and improves our understanding of the genotype–phenotype correlations of KCNA1. Definitive genetic diagnosis is beneficial for the genetic counseling and clinical management of individuals with EA1.}, - language = {en}, - number = {10}, - urldate = {2021-06-10}, - journal = {Molecular Genetics \& Genomic Medicine}, - author = {Yuan, Haiming and Yuan, Huihua and Wang, Qingming and Ye, Wanhua and Yao, Ruixia and Xu, Wanfang and Liu, Yanhui}, - year = {2020}, - keywords = {seizures, episodic ataxia type 1, KCNA1, low-level mosaicism, neurodevelopmental disorder}, - pages = {e1434}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6I8ANRUM\\Yuan et al. - 2020 - Two novel KCNA1 variants identified in two unrelat.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\UWMYWBL2\\mgg3.html:text/html}, -} - -@article{paulhus_clinical_2020, - title = {Clinical {Spectrum} of {KCNA1} {Mutations}: {New} {Insights} into {Episodic} {Ataxia} and {Epilepsy} {Comorbidity}}, - volume = {21}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - shorttitle = {Clinical {Spectrum} of {KCNA1} {Mutations}}, - url = {https://www.mdpi.com/1422-0067/21/8/2802}, - doi = {10.3390/ijms21082802}, - abstract = {Mutations in the KCNA1 gene, which encodes voltage-gated Kv1.1 potassium channel \α-subunits, cause a variety of human diseases, complicating simple genotype\–phenotype correlations in patients. KCNA1 mutations are primarily associated with a rare neurological movement disorder known as episodic ataxia type 1 (EA1). However, some patients have EA1 in combination with epilepsy, whereas others have epilepsy alone. KCNA1 mutations can also cause hypomagnesemia and paroxysmal dyskinesia in rare cases. Why KCNA1 variants are associated with such phenotypic heterogeneity in patients is not yet understood. In this review, literature databases (PubMed) and public genetic archives (dbSNP and ClinVar) were mined for known pathogenic or likely pathogenic mutations in KCNA1 to examine whether patterns exist between mutation type and disease manifestation. Analyses of the 47 deleterious KCNA1 mutations that were identified revealed that epilepsy or seizure-related variants tend to cluster in the S1/S2 transmembrane domains and in the pore region of Kv1.1, whereas EA1-associated variants occur along the whole length of the protein. In addition, insights from animal models of KCNA1 channelopathy were considered, as well as the possible influence of genetic modifiers on disease expressivity and severity. Elucidation of the complex relationship between KCNA1 variants and disease will enable better diagnostic risk assessment and more personalized therapeutic strategies for KCNA1 channelopathy.}, - language = {en}, - number = {8}, - urldate = {2021-06-10}, - journal = {International Journal of Molecular Sciences}, - author = {Paulhus, Kelsey and Ammerman, Lauren and Glasscock, Edward}, - month = jan, - year = {2020}, - keywords = {epilepsy, Kv1.1, episodic ataxia, \textit{KCNA1}}, - pages = {2802}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3RUJPZC5\\Paulhus et al. - 2020 - Clinical Spectrum of KCNA1 Mutations New Insights.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2MPBGHME\\Paulhus et al. - 2020 - Clinical Spectrum of KCNA1 Mutations New Insights.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9GT8A5DB\\2802.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7P5UI869\\2802.html:text/html}, -} - -@article{set_episodic_2017, - title = {Episodic {Ataxia} {Type} 1 ({K}-channelopathy) {Manifesting} as {Paroxysmal} {Nonkinesogenic} {Dyskinesia}: {Expanding} the {Phenotype}}, - volume = {4}, - copyright = {© 2017 International Parkinson and Movement Disorder Society}, - issn = {2330-1619}, - shorttitle = {Episodic {Ataxia} {Type} 1 ({K}-channelopathy) {Manifesting} as {Paroxysmal} {Nonkinesogenic} {Dyskinesia}}, - url = {https://movementdisorders.onlinelibrary.wiley.com/doi/abs/10.1002/mdc3.12518}, - doi = {10.1002/mdc3.12518}, - abstract = {View Supplementary Video 1}, - number = {5}, - urldate = {2021-06-10}, - journal = {Movement Disorders Clinical Practice}, - author = {Set, Kallol K. and Ghosh, Debabrata and Huq, A. H. M. and Luat, Aimee F.}, - year = {2017}, - keywords = {Phenotype, KCNA1 mutation, EA1, PNKD, Stiffness of limbs}, - pages = {784--786}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8267K2EZ\\Set et al. - 2017 - Episodic Ataxia Type 1 (K-channelopathy) Manifesti.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\CRH3B6AS\\mdc3.html:text/html}, -} - -@article{eunson_clinical_2000, - title = {Clinical, genetic, and expression studies of mutations in the potassium channel gene {KCNA1} reveal new phenotypic variability}, - volume = {48}, - copyright = {Copyright © 2000 American Neurological Association}, - issn = {1531-8249}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/1531-8249%28200010%2948%3A4%3C647%3A%3AAID-ANA12%3E3.0.CO%3B2-Q}, - doi = {10.1002/1531-8249(200010)48:4<647::AID-ANA12>3.0.CO;2-Q}, - abstract = {Episodic ataxia type 1 (EA1) is an autosomal dominant central nervous system potassium channelopathy characterized by brief attacks of cerebellar ataxia and continuous interictal myokymia. Point mutations in the voltage-gated potassium channel gene KCNA1 on chromosome 12p associate with EA1. We have studied 4 families and identified three new and one previously reported heterozygous point mutations in this gene. Affected members in Family A (KCNA1 G724C) exhibit partial epilepsy and myokymia but no ataxic episodes, supporting the suggestion that there is an association between mutations of KCNA1 and epilepsy. Affected members in Family B (KCNA1 C731A) exhibit myokymia alone, suggesting a new phenotype of isolated myokymia. Family C harbors the first truncation to be reported in KCNA1 (C1249T) and exhibits remarkably drug-resistant EA1. Affected members in Family D (KCNA1 G1210A) exhibit attacks typical of EA1. This mutation has recently been reported in an apparently unrelated family, although no functional studies were attempted. Heterologous expression of the proteins encoded by the mutant KCNA1 genes suggest that the four point mutations impair delayed-rectifier type potassium currents by different mechanisms. Increased neuronal excitability is likely to be the common pathophysiological basis for the disease in these families. The degree and nature of the potassium channel dysfunction may be relevant to the new phenotypic observations reported in this study. Ann Neurol 2000;48:647–656}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Annals of Neurology}, - author = {Eunson, L. H. and Rea, R. and Zuberi, S. M. and Youroukos, S. and Panayiotopoulos, C. P. and Liguori, R. and Avoni, P. and McWilliam, R. C. and Stephenson, J. B. P. and Hanna, M. G. and Kullmann, D. M. and Spauschus, A.}, - year = {2000}, - pages = {647--656}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CSQ3QRG7\\Eunson et al. - 2000 - Clinical, genetic, and expression studies of mutat.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XPEAQ4S9\\Eunson et al. - 2000 - Clinical, genetic, and expression studies of mutat.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\58MDSXY7\\Eunson et al. - 2000 - Clinical, genetic, and expression studies of mutat.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\QVKEEIBL\\Eunson et al. - 2000 - Clinical, genetic, and expression studies of mutat.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\969ZVVIV\\Eunson et al. - 2000 - Clinical, genetic, and expression studies of mutat.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H2F8BAC9\\1531-8249(200010)484647AID-ANA123.0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JGFRD96Y\\1531-8249(200010)484647AID-ANA123.0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\IDHMRKRZ\\1531-8249(200010)484647AID-ANA123.0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VK59I6UR\\1531-8249(200010)484647AID-ANA123.0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H8TX3NRK\\1531-8249(200010)484647AID-ANA123.0.html:text/html}, -} - -@article{yin_familial_2018, - title = {Familial paroxysmal kinesigenic dyskinesia is associated with mutations in the {KCNA1} gene}, - volume = {27}, - issn = {0964-6906}, - url = {https://doi.org/10.1093/hmg/ddx430}, - doi = {10.1093/hmg/ddx430}, - abstract = {Paroxysmal kinesigenic dyskinesia (PKD) is a heterogeneous movement disorder characterized by recurrent dyskinesia attacks triggered by sudden movement. PRRT2 has been identified as the first causative gene of PKD. However, it is only responsible for approximately half of affected individuals, indicating that other loci are most likely involved in the etiology of this disorder. To explore the underlying causative gene of PRRT2-negative PKD, we used a combination strategy including linkage analysis, whole-exome sequencing and copy number variations analysis to detect the genetic variants within a family with PKD. We identified a linkage locus on chromosome 12 (12p13.32–12p12.3) and detected a novel heterozygous mutation c.956 T\>G (p.319 L\>R) in the potassium voltage-gated channel subfamily A member 1, KCNA1. Whole-exome sequencing in another 58 Chinese patients with PKD who lacked mutations in PRRT2 revealed another novel mutation in the KCNA1 gene [c.765 C\>A (p.255 N\>K)] within another family. Biochemical analysis revealed that the L319R mutant accelerated protein degradation via the proteasome pathway and disrupted membrane expression of the Kv1.1 channel. Electrophysiological examinations in transfected HEK293 cells showed that both the L319R and N255K mutants resulted in reduced potassium currents and respective altered gating properties, with a dominant negative effect on the Kv1.1 wild-type channel. Our study suggests that these mutations in KCNA1 cause the Kv1.1 channel dysfunction, which leads to familial PKD. The current study further extended the genotypic spectrum of this disorder, indicating that Kv1.1 channel dysfunction maybe one of the underlying defects in PKD.}, - number = {4}, - urldate = {2021-06-10}, - journal = {Human Molecular Genetics}, - author = {Yin, Xiao-Meng and Lin, Jing-Han and Cao, Li and Zhang, Tong-Mei and Zeng, Sheng and Zhang, Kai-Lin and Tian, Wo-Tu and Hu, Zheng-Mao and Li, Nan and Wang, Jun-Ling and Guo, Ji-Feng and Wang, Ruo-Xi and Xia, Kun and Zhang, Zhuo-Hua and Yin, Fei and Peng, Jing and Liao, Wei-Ping and Yi, Yong-Hong and Liu, Jing-Yu and Yang, Zhi-Xian and Chen, Zhong and Mao, Xiao and Yan, Xin-Xiang and Jiang, Hong and Shen, Lu and Chen, Sheng-Di and Zhang, Li-Ming and Tang, Bei-Sha}, - month = feb, - year = {2018}, - pages = {625--637}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\LN32Z7CV\\Yin et al. - 2018 - Familial paroxysmal kinesigenic dyskinesia is asso.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\V9MKSTCY\\4779888.html:text/html}, -} - -@article{hasan_electromechanical_2020, - title = {Electromechanical coupling of the {Kv1}.1 voltage-gated {K}+ channel is fine-tuned by the simplest amino acid residue in the {S4}-{S5} linker}, - volume = {472}, - issn = {1432-2013}, - url = {https://doi.org/10.1007/s00424-020-02414-0}, - doi = {10.1007/s00424-020-02414-0}, - abstract = {Investigating the Shaker-related K+ channel Kv1.1, the dysfunction of which is responsible for episodic ataxia 1 (EA1), at the functional and molecular level provides valuable understandings on normal channel dynamics, structural correlates underlying voltage-gating, and disease-causing mechanisms. Most studies focused on apparently functional amino acid residues composing voltage-gated K+ channels, neglecting the simplest ones. Glycine at position 311 of Kv1.1 is highly conserved both evolutionarily and within the Kv channel superfamily, is located in a region functionally relevant (the S4-S5 linker), and results in overt disease when mutated (p.G311D). By mutating the G311 residue to aspartate, we show here that the channel voltage-gating, activation, deactivation, inactivation, and window currents are markedly affected. In silico, modeling shows this glycine residue is strategically placed at one end of the linker helix which must be free to both bend and move past other portions of the protein during the channel’s opening and closing. This is befitting of a glycine residue as its small neutral side chain allows for movement unhindered by interaction with any other amino acid. Results presented reveal the crucial importance of a distinct glycine residue, within the S4-S5 linker, in the voltage-dependent electromechanical coupling that control channel gating.}, - language = {en}, - number = {7}, - urldate = {2021-06-10}, - journal = {Pflügers Archiv - European Journal of Physiology}, - author = {Hasan, Sonia and Megaro, Alfredo and Cenciarini, Marta and Coretti, Lorena and Botti, Fabio Massimo and Imbrici, Paola and Steinbusch, Harry W. M. and Hunter, Therese and Hunter, Gary and Pessia, Mauro and D’Adamo, Maria Cristina}, - month = jul, - year = {2020}, - pages = {899--909}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WDRPGR8P\\Hasan et al. - 2020 - Electromechanical coupling of the Kv1.1 voltage-ga.pdf:application/pdf}, -} - -@article{hasan_channelopathy_2017, - title = {A channelopathy mutation in the voltage-sensor discloses contributions of a conserved phenylalanine to gating properties of {Kv1}.1 channels and ataxia}, - volume = {7}, - copyright = {2017 The Author(s)}, - issn = {2045-2322}, - url = {https://www.nature.com/articles/s41598-017-03041-z}, - doi = {10.1038/s41598-017-03041-z}, - abstract = {Channelopathy mutations prove informative on disease causing mechanisms and channel gating dynamics. We have identified a novel heterozygous mutation in the KCNA1 gene of a young proband displaying typical signs and symptoms of Episodic Ataxia type 1 (EA1). This mutation is in the S4 helix of the voltage-sensing domain and results in the substitution of the highly conserved phenylalanine 303 by valine (p.F303V). The contributions of F303 towards K+ channel voltage gating are unclear and here have been assessed biophysically and by performing structural analysis using rat Kv1.2 coordinates. We observed significant positive shifts of voltage-dependence, changes in the activation, deactivation and slow inactivation kinetics, reduced window currents, and decreased current amplitudes of both Kv1.1 and Kv1.1/1.2 channels. Structural analysis revealed altered interactions between F303V and L339 and I335 of the S5 helix of a neighboring subunit. The substitution of an aromatic phenylalanine with an aliphatic valine within the voltage-sensor destabilizes the open state of the channel. Thus, F303 fine-tunes the Kv1.1 gating properties and contributes to the interactions between the S4 segment and neighboring alpha helices. The resulting channel’s loss of function validates the clinical relevance of the mutation for EA1 pathogenesis.}, - language = {en}, - number = {1}, - urldate = {2021-06-10}, - journal = {Scientific Reports}, - author = {Hasan, Sonia and Bove, Cecilia and Silvestri, Gabriella and Mantuano, Elide and Modoni, Anna and Veneziano, Liana and Macchioni, Lara and Hunter, Therese and Hunter, Gary and Pessia, Mauro and D’Adamo, Maria Cristina}, - month = jul, - year = {2017}, - pages = {4583}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3TG7P5JQ\\Hasan et al. - 2017 - A channelopathy mutation in the voltage-sensor dis.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\VYQU4PW8\\Hasan et al. - 2017 - A channelopathy mutation in the voltage-sensor dis.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\K3MR8IE5\\s41598-017-03041-z.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GAJBVQIZ\\s41598-017-03041-z.html:text/html}, -} - -@article{simeone_respiratory_2018, - title = {Respiratory dysfunction progresses with age in {Kcna1}-null mice, a model of sudden unexpected death in epilepsy}, - volume = {59}, - copyright = {Wiley Periodicals, Inc. © 2018 International League Against Epilepsy}, - issn = {1528-1167}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/epi.13971}, - doi = {10.1111/epi.13971}, - abstract = {Objective Increased breathing rate, apnea, and respiratory failure are associated with sudden unexpected death in epilepsy (SUDEP). We recently demonstrated the progressive nature of epilepsy and mortality in Kcna1−/− mice, a model of temporal lobe epilepsy and SUDEP. Here we tested the hypothesis that respiratory dysfunction progresses with age in Kcna1−/− mice, thereby increasing risk of respiratory failure and sudden death (SD). Methods Respiratory parameters were determined in conscious mice at baseline and following increasing doses of methacholine (MCh) using noninvasive airway mechanics (NAM) systems. Kcna1+/+, Kcna1+/−, and Kcna1−/− littermates were assessed during 3 age ranges when up to 30\%, 55\%, and 90\% of Kcna1−/− mice have succumbed to SUDEP: postnatal day (P) 32-36, P40-46, and P48-56, respectively. Saturated arterial O2 (SaO2) was determined with pulse oximetry. Lung and brain tissues were isolated and Kcna1 gene and protein expression were evaluated by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Western blot techniques. Airway smooth muscle responsiveness was assessed in isolated trachea exposed to MCh. Results Kcna1−/− mice experienced an increase in basal respiratory drive, chronic oxygen desaturation, frequent apnea-hypopnea (A-H), an atypical breathing sequence of A-H-tachypnea-A-H, increased tidal volume, and hyperventilation induced by MCh. The MCh-provoked hyperventilation was dramatically attenuated with age. Of interest, only Kcna1−/− mice developed seizures following exposure to MCh. Seizures were provoked by lower concentrations of MCh as Kcna1−/− mice approached SD. MCh-induced seizures experienced by a subset of younger Kcna1−/− mice triggered death. Respiratory parameters of these younger Kcna1−/− mice resembled older near-SD Kcna1−/− mice. Kcna1 gene and protein were not expressed in Kcna1+/+ and Kcna1+/− lungs, and MCh-mediated airway smooth muscle contractions exhibited similar half-maximal effective concentration( EC50) in isolated Kcna1+/+ and Kcna1−/− trachea. Significance The Kcna1−/− model of SUDEP exhibits progressive respiratory dysfunction, which suggests a potential increased susceptibility for respiratory failure during severe seizures that may result in sudden death.}, - language = {en}, - number = {2}, - urldate = {2021-06-10}, - journal = {Epilepsia}, - author = {Simeone, Kristina A. and Hallgren, Jodi and Bockman, Charles S. and Aggarwal, Ankita and Kansal, Vikash and Netzel, Lauren and Iyer, Shruthi H. and Matthews, Stephanie A. and Deodhar, Malavika and Oldenburg, Peter J. and Abel, Peter W. and Simeone, Timothy A.}, - year = {2018}, - keywords = {seizures, apnea, hypopnea, Kv1.1 knockout, mortality, survival}, - pages = {345--357}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TXCY78DI\\Simeone et al. - 2018 - Respiratory dysfunction progresses with age in Kcn.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\HSMBD9RH\\epi.html:text/html}, -} - -@article{chun_ketogenic_2018, - title = {Ketogenic diet-induced extension of longevity in epileptic {Kcna1}-null mice is influenced by gender and age at treatment onset}, - volume = {140}, - issn = {0920-1211}, - url = {https://www.sciencedirect.com/science/article/pii/S092012111730342X}, - doi = {10.1016/j.eplepsyres.2017.11.005}, - abstract = {Sudden unexpected death in epilepsy (SUDEP) is a leading cause of premature mortality in patients with epilepsy, and has been linked to multiple risk factors, including gender and early age at seizure onset. Despite the lack of a targeted therapy for SUDEP, it has recently been shown that a high-fat, low carbohydrate ketogenic diet (KD) enhances longevity in the epileptic Kcna1-null (KO) mouse, a validated model of SUDEP. Here, we asked whether the KD-driven prolongation of lifespan in KO mice is dependent on sex and/or age at treatment onset. We found that as KO mice aged, their daily seizure frequency steadily increased, but had early demise by postnatal day (PD) 46.9±0.8. In KO mice started on the KD at PD30, longevity was extended to a mean of PD69.8±1.7, accompanied with improved seizure control. Interestingly, while seizure control on the KD was similar between male and female mice, KD-fed female KO mice survived longer than their male counterparts. Further, epileptic mice initiated on the KD at PD25 had longer lifespans compared to those placed on the KD starting at PD35. Collectively, these data further support the notion that the KD can retard disease progression and sudden death in KO mice, but that this beneficial action is influenced by gender and age at the start of treatment.}, - language = {en}, - urldate = {2021-06-10}, - journal = {Epilepsy Research}, - author = {Chun, Kyoung-chul and Ma, Shun-Chieh and Oh, Hyoungil and Rho, Jong M. and Kim, Do Young}, - month = feb, - year = {2018}, - keywords = {mice, Epilepsy, SUDEP, Treatment, Gender, Ketogenic diet, Longevity}, - pages = {53--55}, - file = {Accepted Version:C\:\\Users\\nilsk\\Zotero\\storage\\XA7NRMND\\Chun et al. - 2018 - Ketogenic diet-induced extension of longevity in e.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4D9TEP2Y\\S092012111730342X.html:text/html}, -} - -@article{dhaibar_cardiorespiratory_2019, - title = {Cardiorespiratory profiling reveals primary breathing dysfunction in {Kcna1}-null mice: {Implications} for sudden unexpected death in epilepsy}, - volume = {127}, - issn = {0969-9961}, - shorttitle = {Cardiorespiratory profiling reveals primary breathing dysfunction in {Kcna1}-null mice}, - url = {https://www.sciencedirect.com/science/article/pii/S096999611930097X}, - doi = {10.1016/j.nbd.2019.04.006}, - abstract = {Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related mortality, but the relative importance of underlying cardiac and respiratory mechanisms remains unclear. To illuminate the interactions between seizures, respiration, cardiac function, and sleep that contribute to SUDEP risk, here we developed a mouse epilepsy monitoring unit (EMU) to simultaneously record video, electroencephalography (EEG), electromyography (EMG), plethysmography, and electrocardiography (ECG) in a commonly used genetic model of SUDEP, the Kcna1 knockout (Kcna1−/−) mouse. During interictal periods, Kcna1−/− mice exhibited an abnormal absence of post-sigh apneas and a 3-fold increase in respiratory variability. During spontaneous convulsive seizures, Kcna1−/− mice displayed an array of aberrant breathing patterns that always preceded cardiac abnormalities. These findings support respiratory dysfunction as a primary risk factor for susceptibility to deleterious cardiorespiratory sequelae in epilepsy and reveal a new role for Kcna1-encoded Kv1.1 channels in the regulation of basal respiratory physiology.}, - language = {en}, - urldate = {2021-06-10}, - journal = {Neurobiology of Disease}, - author = {Dhaibar, Hemangini and Gautier, Nicole M. and Chernyshev, Oleg Y. and Dominic, Paari and Glasscock, Edward}, - month = jul, - year = {2019}, - keywords = {Sleep, Epilepsy, Kv1.1, Apnea, Respiratory variability, Sigh, Sudden unexpected death in epilepsy (SUDEP)}, - pages = {502--511}, - file = {Accepted Version:C\:\\Users\\nilsk\\Zotero\\storage\\LNJLV8G6\\Dhaibar et al. - 2019 - Cardiorespiratory profiling reveals primary breath.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2SFNY9PN\\S096999611930097X.html:text/html}, -} - -@article{hubert_ibotenic_1989, - title = {Ibotenic acid stimulates d-[{3H}]aspartate release from cultured cerebellar granule cells}, - volume = {96}, - issn = {0304-3940}, - url = {https://www.sciencedirect.com/science/article/pii/0304394089904035}, - doi = {10.1016/0304-3940(89)90403-5}, - abstract = {The release of d-[3H]aspartate from cultured cerebellar granule cells can be evoked by potassium depolarization or by superfusion with the exctitatory amino acids glutamic and aspartic acids. The latter phenomenon is not mediated by N-methyl-d-aspartate (NMDA)-, kainate- or quisqualate-preferring receptors, but is stimulated by ibotenic acid. Excitatory amino acid-stimulated d-[3H]aspartate release is antagonised by l-serine-O-phosphate and riluzole. These compounds did not block potassium-stimulated d-[3H]aspartate release. This pharmacology resembles an excitatory amino acid receptor coupled to inositol phosphate (PI) turnover.}, - language = {en}, - number = {3}, - urldate = {2021-06-10}, - journal = {Neuroscience Letters}, - author = {Hubert, J. P. and Doble, A.}, - month = jan, - year = {1989}, - keywords = {Glutamate, Ibotenic acid, Riluzole, Autoreceptor, Cell culture, Granule cell, Release}, - pages = {345--350}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\MRHZNLZU\\Hubert and Doble - 1989 - Ibotenic acid stimulates d-[3H]aspartate release f.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\U9JRMPIX\\0304394089904035.html:text/html}, -} - -@article{martin_neuroprotective_1993, - title = {The neuroprotective agent riluzole inhibits release of glutamate and aspartate from slices of hippocampal area {CA1}}, - volume = {250}, - issn = {0014-2999}, - url = {https://www.sciencedirect.com/science/article/pii/001429999390037I}, - doi = {10.1016/0014-2999(93)90037-I}, - abstract = {Riluzole is believed to exert its anticonvulsant and neuroprotective actions by reducing glutamate release. This study demonstrated that 10–30 μM riluzole reduces the K+-evoked release of glutamate and aspartate from slices of hippocampal area CA1. Only higher concentrations reduced γ-aminobutyrate (GABA) release. These actions of riluzole were not occluded by tetrodotoxin. Riluzole did not diminish the ability of glutamate analogues to depolarize CA1 pyramidal cells, as determined from grease-gap recordings. Therefore the anticonvulsant and neuroprotective actions of riluzole in the hippocampus may be at least partly explained by its ability to inhibit glutamate/aspartate release from synaptic terminals.}, - language = {en}, - number = {3}, - urldate = {2021-06-10}, - journal = {European Journal of Pharmacology}, - author = {Martin, David and Thompson, Michael A. and Nadler, J. Victor}, - month = dec, - year = {1993}, - keywords = {Glutamate, Hippocampus, Riluzole, Aspartate, Excitatory amino acid, Transmitter release}, - pages = {473--476}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GQA477PS\\Martin et al. - 1993 - The neuroprotective agent riluzole inhibits releas.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GRPN6QQM\\001429999390037I.html:text/html}, -} - -@article{cheramy_riluzole_1992, - title = {Riluzole inhibits the release of glutamate in the caudate nucleus of the cat in vivo}, - volume = {147}, - issn = {0304-3940}, - url = {https://www.sciencedirect.com/science/article/pii/030439409290597Z}, - doi = {10.1016/0304-3940(92)90597-Z}, - abstract = {When applied locally to the caudate nucleus of the halothane-anaesthetized cat, riluzole (10−5 M) markedly reduced (−57\%) the spontaneous release of glutamate. This effect seems to be specific, since the efflux of the other amino acids, including aspartate was not affected. Indicating further its selective inhibitory effect on the spontaneous release of glutamate, the prolonged (90 min) application of riluzole (10−5 M) enhanced the size of the potassium-releasable pool of glutamate, but not that of aspartate. This effect of riluzole was not noticed with classical anti-glutamatergic drugs, tested in the same conditions.}, - language = {en}, - number = {2}, - urldate = {2021-06-10}, - journal = {Neuroscience Letters}, - author = {Chéramy, André and Barbeito, Luis and Godeheu, Gérard and Glowinski, Jacques}, - month = dec, - year = {1992}, - keywords = {Riluzole, Caudate nucleus, Glutamate release, PK 26124, Presynaptic mechanism, Push-pull cannula}, - pages = {209--212}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XQERHSV5\\Chéramy et al. - 1992 - Riluzole inhibits the release of glutamate in the .pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VGAB8ZLN\\030439409290597Z.html:text/html}, -} - -@article{parker_periodic_1946, - title = {Periodic ataxia}, - volume = {38}, - issn = {0095-9677}, - language = {eng}, - journal = {Collected Papers of the Mayo Clinic and the Mayo Foundation. Mayo Clinic}, - author = {Parker, H. L.}, - year = {1946}, - keywords = {Humans, Ataxia, ATAXIA, Spinocerebellar Degenerations}, - pages = {642--645}, -} - -@article{knight_identification_2000, - title = {Identification of a novel missense mutation {L329I} in the episodic ataxia type 1 gene {KCNA1} —{A} challenging problem}, - volume = {16}, - copyright = {Copyright © 2000 Wiley-Liss, Inc.}, - issn = {1098-1004}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/1098-1004%28200010%2916%3A4%3C374%3A%3AAID-HUMU15%3E3.0.CO%3B2-4}, - doi = {10.1002/1098-1004(200010)16:4<374::AID-HUMU15>3.0.CO;2-4}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Human Mutation}, - author = {Knight, Melanie A. and Storey, Elsdon and Gardner, R. J. McKinlay and Hand, Peter and Forrest, Susan M.}, - year = {2000}, - keywords = {potassium channel, episodic ataxia type 1, KCNA1, mutation detection}, - pages = {374--374}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ETVDJ5IU\\Knight et al. - 2000 - Identification of a novel missense mutation L329I .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7G5N5QHW\\1098-1004(200010)164374AID-HUMU153.0.html:text/html}, -} - -@article{spauschus_functional_1999, - title = {Functional {Characterization} of a {Novel} {Mutation} in {KCNA1} in {Episodic} {Ataxia} {Type} 1 {Associated} with {Epilepsy}}, - volume = {868}, - issn = {1749-6632}, - url = {https://nyaspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1749-6632.1999.tb11310.x}, - doi = {10.1111/j.1749-6632.1999.tb11310.x}, - language = {en}, - number = {1}, - urldate = {2021-06-10}, - journal = {Annals of the New York Academy of Sciences}, - author = {Spauschus, Alexander and Eunson, Louise and Hanna, Michael G. and Kullmann, Dimitri M.}, - year = {1999}, - pages = {442--446}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\N5WDT2BW\\Spauschus et al. - 1999 - Functional Characterization of a Novel Mutation in.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\F8H25K8V\\j.1749-6632.1999.tb11310.html:text/html}, -} - -@article{scheffer_three_1998, - title = {Three novel {KCNA1} mutations in episodic ataxia type {I} families}, - volume = {102}, - issn = {1432-1203}, - url = {https://doi.org/10.1007/s004390050722}, - doi = {10.1007/s004390050722}, - abstract = {Hereditary paroxysmal ataxia, or episodic ataxia (EA), is a rare, genetically heterogeneous neurological disorder characterized by attacks of generalized ataxia. By direct sequence analysis, a different missense mutation of the potassium channel gene (KCNA1) has been identified in three families with EA.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Human Genetics}, - author = {Scheffer, H. and Brunt, E. R. P. and Mol, G. J. J. and van der Vlies, P. and {Stulp} and Verlind, E. and Mantel, G. and Averyanov, Y. N. and Hofstra, R. M. W. and Buys, C. H. C. M.}, - month = apr, - year = {1998}, - pages = {464--466}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\I5UBSRC2\\Scheffer et al. - 1998 - Three novel KCNA1 mutations in episodic ataxia typ.pdf:application/pdf}, -} - -@article{comu_episodic_1996, - title = {Episodic ataxia and myokymia syndrome: {A} new mutation of potassium channel gene {Kv1}.1}, - volume = {40}, - copyright = {Copyright © 1996 American Neurological Association}, - issn = {1531-8249}, - shorttitle = {Episodic ataxia and myokymia syndrome}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410400422}, - doi = {10.1002/ana.410400422}, - abstract = {Episodic ataxia and myokymia syndrome is an autosomal dominant disorder characterized by persistent myokymia and attacks of unsteadiness, slurred speech, and tremulousness. This disease has been associated with point mutations in the potassium channel gene Kv1.1 (KCNA1), located at chromosome 12p13. Here, we describe a novel mutation within this gene in a newly diagnosed family.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Annals of Neurology}, - author = {Çomu, Sinan and Narayanan, Vinodh and Giuliani, Michael}, - year = {1996}, - pages = {684--687}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\U6ZRYGXS\\Çomu et al. - 1996 - Episodic ataxia and myokymia syndrome A new mutat.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\IECUHDWU\\ana.html:text/html}, -} - -@article{hanson_contractures_1977, - title = {Contractures, continuous muscle discharges, and titubation}, - volume = {1}, - copyright = {Copyright © 1977 The American Neurological Association}, - issn = {1531-8249}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410010203}, - doi = {10.1002/ana.410010203}, - abstract = {A mother and 2 children had abnormally fixed postures of the hands and feet at birth. At adolescence, intermittent attacks of shaking and titubation with dysarthria and, rarely, abnormal hand posturing developed in all 3. Electromyographically, there were continuous muscle discharges inhibited only by curare. Muscle biopsy in the younger child showed a distinct population of small fibers staining intensely with oxidative enzymes and myosin adenosine triphosphatase after acid preincubation. The mother's biopsy specimen contained similar cells, occasionally split or grouped. The electron microscopical findings were unremarkable. It appears likely that a single physiological abnormality underlies the abnormal central and peripheral nervous system discharges. A pool of low-threshold neurons may account for the symptoms, with the abnormal discharge arising from the unusual muscle fibers seen on biopsy.}, - language = {en}, - number = {2}, - urldate = {2021-06-10}, - journal = {Annals of Neurology}, - author = {Hanson, Peggy A. and Martinez, Leonardo B. and Cassidy, Robert}, - year = {1977}, - pages = {120--124}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GZ8GH5PN\\Hanson et al. - 1977 - Contractures, continuous muscle discharges, and ti.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\RAVEXCFA\\ana.html:text/html}, -} - -@article{kinali_expanding_2004, - title = {Expanding the phenotype of potassium channelopathy: severe neuromyotonia and skeletal deformities without prominent {Episodic} {Ataxia}}, - volume = {14}, - issn = {0960-8966}, - shorttitle = {Expanding the phenotype of potassium channelopathy}, - url = {https://www.sciencedirect.com/science/article/pii/S0960896604001749}, - doi = {10.1016/j.nmd.2004.06.007}, - abstract = {We report an unusual family in which the same point mutation in the voltage-gated potassium channel gene KCNA1 resulted in markedly different clinical phenotypes. The propositus presented in infancy with marked muscle stiffness, motor developmental delay, short stature, skeletal deformities, muscle hypertrophy and muscle rippling on percussion. He did not experience episodic ataxia. His mother presented some years later with typical features of Episodic Ataxia type 1 (EA1), with episodes of ataxia lasting a few minutes provoked by exercise. On examination she had myokymia, joint contractures and mild skeletal deformities. A heterozygous point mutation in the voltage-gated K+ channel (KCNA1) gene (ACG-AGG, Thr226Arg) was found in both. We conclude that mutations in the potassium channel gene (KCNA1) can cause severe neuromyotonia resulting in marked skeletal deformities even if episodic ataxia is not prominent.}, - language = {en}, - number = {10}, - urldate = {2021-06-10}, - journal = {Neuromuscular Disorders}, - author = {Kinali, M. and Jungbluth, H. and Eunson, L. H. and Sewry, C. A. and Manzur, A. Y. and Mercuri, E. and Hanna, M. G. and Muntoni, F.}, - month = oct, - year = {2004}, - keywords = {K channel, KCNA1, Neuromyotonia}, - pages = {689--693}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WBGWTX7S\\Kinali et al. - 2004 - Expanding the phenotype of potassium channelopathy.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\KM43WQ89\\S0960896604001749.html:text/html}, -} - -@article{lubbers_hereditary_1995, - title = {Hereditary myokymia and paroxysmal ataxia linked to chromosome 12 is responsive to acetazolamide.}, - volume = {59}, - issn = {0022-3050, 1468-330X}, - url = {https://jnnp.bmj.com/content/59/4/400}, - doi = {10.1136/jnnp.59.4.400}, - abstract = {A sixth family with autosomal dominantly inherited myokymia and paroxysmal ataxia is described. The syndrome in this family is linked to the recently discovered locus for inherited myokymia and paroxysmal ataxia on the human chromosome 12p, and a missense mutation is shown in the KCNA1 gene. The attacks of ataxia in this family compare well with those of previously described families and similarly are precipitated by kinesigenic stimuli, exertion, and startle. Responsiveness of these attacks to low dose acetazolamide is confirmed, but some loss of efficacy occurs with prolonged treatment, and side effects are notable. Although not all affected family members showed myokymia on clinical examination, electromyography invariably showed myokymic discharges, in one patient only after a short provocation with regional ischaemia. One affected family member also had attacks of paroxysmal kinesigenic choreoathetosis, responsive to carbamazepine.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Journal of Neurology, Neurosurgery \& Psychiatry}, - author = {Lubbers, W. J. and Brunt, E. R. and Scheffer, H. and Litt, M. and Stulp, R. and Browne, D. L. and Weerden, T. W. van}, - month = oct, - year = {1995}, - pages = {400--405}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UHBZJKY5\\Lubbers et al. - 1995 - Hereditary myokymia and paroxysmal ataxia linked t.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ZQI2W6IL\\400.html:text/html}, -} - -@article{zhou_temperature-sensitive_1998, - title = {Temperature-{Sensitive} {Neuromuscular} {Transmission} in {Kv1}.1 {Null} {Mice}: {Role} of {Potassium} {Channels} under the {Myelin} {Sheath} in {Young} {Nerves}}, - volume = {18}, - copyright = {Copyright © 1998 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - shorttitle = {Temperature-{Sensitive} {Neuromuscular} {Transmission} in {Kv1}.1 {Null} {Mice}}, - url = {https://www.jneurosci.org/content/18/18/7200}, - doi = {10.1523/JNEUROSCI.18-18-07200.1998}, - abstract = {In mammalian myelinated nerves, the internodal axon that is normally concealed by the myelin sheath expresses a rich repertoire of K channel subtypes thought to be important in modulating action potential propagation. The function of myelin-covered K channels at transition zones, however, has remained unexplored. Here we show that deleting the voltage-sensitive potassium channel Kv1.1 from mice confers a marked temperature-sensitivity to neuromuscular transmission in postnatal day 14 (P14)–P21 mice. Using immunofluorescence and electrophysiology, we examined contributions of four regions of the peripheral nervous system to the mutant phenotype: the nerve trunk, the myelinated segment preceding the terminal, the presynaptic terminal membrane itself, and the muscle. We conclude that the temperature-sensitive neuromuscular transmission is accounted for solely by a deficiency in Kv1.1 normally concealed in the myelinated segments just preceding the terminal. This paper demonstrates that under certain situations of physiological stress, the functional role of myelin-covered K channels is dramatically enhanced as the transition zone at the neuromuscular junction is approached.}, - language = {en}, - number = {18}, - urldate = {2021-06-10}, - journal = {Journal of Neuroscience}, - author = {Zhou, Lei and Zhang, Chuan-Li and Messing, Albee and Chiu, Shing Yan}, - month = sep, - year = {1998}, - keywords = {mouse, end plate, homologous recombination, myelinated nerves, nerve conduction, potassium channel gene}, - pages = {7200--7215}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SCRRDKGM\\Zhou et al. - 1998 - Temperature-Sensitive Neuromuscular Transmission i.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FQBN6Q2X\\7200.html:text/html}, -} - -@article{zhang_specific_1999, - title = {Specific {Alteration} of {Spontaneous} {GABAergic} {Inhibition} in {Cerebellar} {Purkinje} {Cells} in {Mice} {Lacking} the {Potassium} {Channel} {Kv1}.1}, - volume = {19}, - copyright = {Copyright © 1999 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/19/8/2852}, - doi = {10.1523/JNEUROSCI.19-08-02852.1999}, - abstract = {In the cerebellum, the basket cell innervation on Purkinje cells provides a major GABAergic inhibitory control of the single efferent output from the cerebellum. The Shaker-type K channel Kv1.1 is localized at the axon arborization preceding the terminal of the basket cells and is therefore a potential candidate for regulating the GABAergic inhibition. In this study, we directly assess this role of Kv1.1 by electrophysiological analysis of Kv1.1 null mutant mice. Whole-cell patch-clamp recordings of spontaneous IPSCs (sIPSCs) were made from Purkinje cells in thin cerebellar slices from postnatal day (P)10–15 Kv1.1-null mutants using wild-type littermates as controls. The null mutation confers a very specific change in the sIPSC: the frequency increases about twofold, without accompanying changes in the mean and variance of its amplitude distribution. The frequency and amplitude of the miniature IPSCs (mIPSCs) are unaffected. Spontaneous firing rate of the basket cells is unaltered. Evoked IPSC does not show multiple activity in the mutants. Motor skills tests show that Kv1.1 null mice display a compromised ability to maintain balance on a thin stationary rod. We conclude that the Kv1.1 null mutation results in a persistent elevation of the tonic inhibitory tone on the cerebellum Purkinje cell efferent and that this is not fully compensated for by residual Shaker-type channels. We further suggest that the increase in inhibitory tone in the mutants might underlie the behavioral deficits. At the cellular level, we propose that Kv1.1 deletion enhances excitability of the basket cells by selectively enhancing the likelihood of action potential propagation past axonal branch points.}, - language = {en}, - number = {8}, - urldate = {2021-06-10}, - journal = {Journal of Neuroscience}, - author = {Zhang, Chuan-Li and Messing, Albee and Chiu, Shing Yan}, - month = apr, - year = {1999}, - keywords = {mouse, GABA, cerebellum, Purkinje cell, homologous recombination, potassium channel gene}, - pages = {2852--2864}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CAKAQZ6X\\Zhang et al. - 1999 - Specific Alteration of Spontaneous GABAergic Inhib.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8MH5FK92\\2852.html:text/html}, -} - -@article{browne_identification_1995, - title = {Identification of two new {KCNA1} mutations in episodic ataxia/myokymia families}, - volume = {4}, - issn = {0964-6906}, - url = {https://doi.org/10.1093/hmg/4.9.1671}, - doi = {10.1093/hmg/4.9.1671}, - number = {9}, - urldate = {2021-06-10}, - journal = {Human Molecular Genetics}, - author = {Browne, D.L. and Brunt, E.R.P. and Griggs, R.C. and Nutt, J.G. and Gancher, S.T. and Smith, E.A. and Litt, M.}, - month = sep, - year = {1995}, - pages = {1671--1672}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\X8R57337\\Browne et al. - 1995 - Identification of two new KCNA1 mutations in episo.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\X8SUGSSL\\635268.html:text/html}, -} - -@article{maylie_episodic_2002, - title = {Episodic {Ataxia} {Type} 1 {Mutations} in the {Human} {Kv1}.1 {Potassium} {Channel} {Alter} {hKvβ1}-{Induced} {N}-{Type} {Inactivation}}, - volume = {22}, - copyright = {Copyright © 2002 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/22/12/4786}, - doi = {10.1523/JNEUROSCI.22-12-04786.2002}, - abstract = {Episodic ataxia type 1 (EA1) is an autosomal dominant neurological disorder affecting both central and peripheral nerve function, causing attacks of imbalance and uncontrolled movements. Genetic linkage studies have identified mutations in the gene encoding the voltage-gated delayed rectifier potassium channel Kv1.1 as underlying EA1. The EA1 mutations E325D and V408A, residing near the cytoplasmic ends of S5 and S6, respectively, induce an unstable open state, resulting in an ∼10-fold increase in deactivation rates compared with wild-type (WT) channels. Coexpression of EA1 mutations with human Kvβ1 (hKvβ1) subunits in Xenopusoocytes yielded channels with altered rapid N-type inactivation. Compared with WT channels, inactivation was approximately twofold slower for homomeric E325D or V408A channels and 1.5-fold slower for heteromeric channels composed of two WT and two E325D or V408A subunits. Recovery from inactivation was ∼10-fold faster for homomeric E325D or V408A channels and threefold to fourfold faster for heteromeric WT and E325D or V408A channels compared with WT channels. Currents during successive pulses 3 msec in duration given at a rate of 40 kHz decayed e-fold in approximately four pulses for homomeric E325D or V408A and ∼2.5 pulses for heteromeric channels compared with approximately one pulse for WT channels. These results show that channels containing E325D or V408A subunits, which destabilize the open state, increase the rate of recovery from inactivation. The slower onset and more rapid recovery of hKvβ1-induced inactivation in channels containing these EA1 subunits may affect temporal integration of action potential firing rates.}, - language = {en}, - number = {12}, - urldate = {2021-06-10}, - journal = {Journal of Neuroscience}, - author = {Maylie, Brooke and Bissonnette, Erinne and Virk, Michael and Adelman, John P. and Maylie, James G.}, - month = jun, - year = {2002}, - keywords = {potassium channel, episodic ataxia type 1, Kv1.1, inactivation, Kvβ1, recovery from inactivation}, - pages = {4786--4793}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\EJ5LULPE\\Maylie et al. - 2002 - Episodic Ataxia Type 1 Mutations in the Human Kv1..pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GJIQDS53\\4786.html:text/html}, -} - -@article{smart_deletion_1998, - title = {Deletion of the {KV1}.1 {Potassium} {Channel} {Causes} {Epilepsy} in {Mice}}, - volume = {20}, - issn = {0896-6273}, - url = {https://www.sciencedirect.com/science/article/pii/S0896627300810181}, - doi = {10.1016/S0896-6273(00)81018-1}, - abstract = {Mice lacking the voltage-gated potassium channel α subunit, KV1.1, display frequent spontaneous seizures throughout adult life. In hippocampal slices from homozygous KV1.1 null animals, intrinsic passive properties of CA3 pyramidal cells are normal. However, antidromic action potentials are recruited at lower thresholds in KV1.1 null slices. Furthermore, in a subset of slices, mossy fiber stimulation triggers synaptically mediated long-latency epileptiform burst discharges. These data indicate that loss of KV1.1 from its normal localization in axons and terminals of the CA3 region results in increased excitability in the CA3 recurrent axon collateral system, perhaps contributing to the limbic and tonic–clonic components of the observed epileptic phenotype. Axonal action potential conduction was altered as well in the sciatic nerve—a deficit potentially related to the pathophysiology of episodic ataxia/myokymia, a disease associated with missense mutations of the human KV1.1 gene.}, - language = {en}, - number = {4}, - urldate = {2021-06-10}, - journal = {Neuron}, - author = {Smart, Sharon L. and Lopantsev, Valeri and Zhang, C. L. and Robbins, Carol A. and Wang, Hao and Chiu, S. Y. and Schwartzkroin, Philip A. and Messing, Albee and Tempel, Bruce L.}, - month = apr, - year = {1998}, - pages = {809--819}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BWWW4ZL8\\Smart et al. - 1998 - Deletion of the KV1.1 Potassium Channel Causes Epi.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\A7QYCC6F\\S0896627300810181.html:text/html}, -} - -@article{wang_localization_1994, - title = {Localization of {Kv1}.1 and {Kv1}.2, two {K} channel proteins, to synaptic terminals, somata, and dendrites in the mouse brain}, - volume = {14}, - copyright = {© 1994 by Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/14/8/4588}, - doi = {10.1523/JNEUROSCI.14-08-04588.1994}, - abstract = {Multiple voltage-gated potassium (K) channel gene products are likely to be involved in regulating neuronal excitability of any single neuron in the mammalian brain. Here we show that two closely related voltage- gated K channel proteins, mKv1.1 and mKv1.2, are present in multiple subcellular locations including cell somata, juxta-paranodal regions of myelinated axons, synaptic terminals, unmyelinated axons, specialized junctions among axons, and proximal dendrites. Staining patterns of the two channel polypeptides overlap in some areas of the brain, yet each has a unique pattern of expression. For example, in the hippocampus, both mKv1.1 and mKv1.2 proteins are present in axons, often near or at synaptic terminals in the middle molecular layer of the dentate gyrus, while only mKv1.1 is detected in axons and synaptic terminals in the hilar/CA3 region. In the cerebellum, both channel proteins are localized to axon terminals and specialized junctions among axons in the plexus region of basket cells. Strong differential staining is observed in the olfactory bulb, where mKv1.2 is localized to cell somata and axons, as well as to proximal dendrites of the mitral cells. This overlapping yet differential pattern of expression and specific subcellular localization may contribute to the unique profile of excitability displayed by a particular neuron.}, - language = {en}, - number = {8}, - urldate = {2021-06-10}, - journal = {Journal of Neuroscience}, - author = {Wang, H. and Kunkel, D. D. and Schwartzkroin, P. A. and Tempel, B. L.}, - month = aug, - year = {1994}, - pages = {4588--4599}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8W3QSPJ8\\Wang et al. - 1994 - Localization of Kv1.1 and Kv1.2, two K channel pro.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XW29S3YF\\4588.html:text/html}, -} - -@article{adelman_episodic_1995, - title = {Episodic ataxia results from voltage-dependent potassium channels with altered functions}, - volume = {15}, - issn = {0896-6273}, - url = {https://www.sciencedirect.com/science/article/pii/0896627395900225}, - doi = {10.1016/0896-6273(95)90022-5}, - abstract = {Episodic ataxia (EA) is an autosomal dominant human disorder that produces persistent myokymia and attacks of generalized ataxia. Recently, familial EA has been linked to the voltage-dependent delayed rectifier, Kv1.1, on chromosome 12. Six EA families have been identified that carry distinct Kv1.1 missense mutations; all individuals are heterozygous. Expression in Xenopus oocytes demonstrates that two of the EA subunits form homomeric channels with altered gating properties. V408A channels have voltage dependence similar to that of wild-type channels, but with faster kinetics and increased C-type inactivation, while the voltage dependence of F1 84C channels is shifted 20 mV positive. The other four EA subunits do not produce functional homomeric channels but reduce the potassium current when coassembled with wild-type subunits. The results suggest a cellular mechanism underlying EA in which the affected nerve cells cannot efficiently repolarize following an action potential because of altered delayed rectifier function.}, - language = {en}, - number = {6}, - urldate = {2021-06-10}, - journal = {Neuron}, - author = {Adelman, John P. and Bond, Chris T. and Pessia, Mauro and Mayliet, James}, - month = dec, - year = {1995}, - pages = {1449--1454}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UHEYHJP3\\Adelman et al. - 1995 - Episodic ataxia results from voltage-dependent pot.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\UW5AMZAR\\0896627395900225.html:text/html}, -} - -@article{rea_variable_2002, - title = {Variable {K}+ channel subunit dysfunction in inherited mutations of {KCNA1}}, - volume = {538}, - copyright = {© 2002 The Journal of Physiology © 2002 The Physiological Society}, - issn = {1469-7793}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.2001.013242}, - doi = {10.1113/jphysiol.2001.013242}, - abstract = {Mutations of KCNA1, which codes for the K+ channel subunit hKv1.1, are associated with the human autosomal dominant disease episodic ataxia type 1 (EA1). Five recently described mutations are associated with a broad range of phenotypes: neuromyotonia alone or with seizures, EA1 with seizures, or very drug-resistant EA1. Here we investigated the consequences of each mutation for channel assembly, trafficking, gating and permeation. We related data obtained from co-expression of mutant and wild-type hKv1.1 to the results of expressing mutant-wild-type fusion proteins, and combined electrophysiological recordings in Xenopus oocytes with a pharmacological discrimination of the contribution of mutant and wild-type subunits to channels expressed at the membrane. We also applied confocal laser scanning microscopy to measure the level of expression of either wild-type or mutant subunits tagged with green fluorescent protein (GFP). R417stop truncates most of the C-terminus and is associated with severe drug-resistant EA1. Electrophysiological and pharmacological measurements indicated that the mutation impairs both tetramerisation of R417stop with wild-type subunits, and membrane targeting of heterotetramers. This conclusion was supported by confocal laser scanning imaging of enhanced GFP (EGFP)-tagged hKv1.1 subunits. Co-expression of R417stop with wild-type hKv1.2 subunits yielded similar results to co-expression with wild-type hKv1.1. Mutations associated with typical EA1 (V404I) or with neuromyotonia alone (P244H) significantly affected neither tetramerisation nor trafficking, and only altered channel kinetics. Two other mutations associated with a severe phenotype (T226R, A242P) yielded an intermediate result. The phenotypic variability of KCNA1 mutations is reflected in a wide range of disorders of channel assembly, trafficking and kinetics.}, - language = {en}, - number = {1}, - urldate = {2021-06-10}, - journal = {The Journal of Physiology}, - author = {Rea, Ruth and Spauschus, Alexander and Eunson, Louise H. and Hanna, Michael G. and Kullmann, Dimitri M.}, - year = {2002}, - pages = {5--23}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9THMANRQ\\Rea et al. - 2002 - Variable K+ channel subunit dysfunction in inherit.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\87H99RLA\\jphysiol.2001.html:text/html}, -} - -@article{beckh_members_1990, - title = {Members of the {RCK} potassium channel family are differentially expressed in the rat nervous system.}, - volume = {9}, - issn = {0261-4189}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC551736/}, - abstract = {mRNAs encoding four members of the RCK potassium channel family, named RCK1, RCK3, RCK4 and RCK5 have been analyzed by RNA blot hybridization experiments using specific RNA probes. Each probe recognizes a single mRNA species, their sizes ranging from approximately 4600 nucleotides up to approximately 11,000 nucleotides. The expression of RCK mRNAs as well as their developmental appearance in different regions of the central and peripheral rat nervous system has been investigated. The two most abundant RCK potassium channel mRNAs (RCK1 and RCK5) are predominantly expressed in the adult nervous system. RCK3 and RCK4 mRNAs are present throughout all developmental stages studied. The temporal and regional patterns observed are specific for each RCK potassium channel mRNA indicating that specific regulation of expression occurs. Differential mRNA expression might provide one mechanism for the generation of potassium channel diversity in vivo.}, - number = {3}, - urldate = {2021-06-10}, - journal = {The EMBO Journal}, - author = {Beckh, S and Pongs, O}, - month = mar, - year = {1990}, - pages = {777--782}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SSPWSKB7\\Beckh and Pongs - 1990 - Members of the RCK potassium channel family are di.pdf:application/pdf}, -} - -@article{morales-villagran_protection_1996, - title = {Protection by {NMDA} receptor antagonists against seizures induced by intracerebral administration of 4-aminopyridine}, - volume = {305}, - issn = {0014-2999}, - url = {https://www.sciencedirect.com/science/article/pii/0014299996001574}, - doi = {10.1016/0014-2999(96)00157-4}, - abstract = {The effects of NMDA receptor antagonists on the convulsant action of the administration of 4-aminopyridine in the rat lateral cerebral ventricle (i.c.v. injection) and motor cerebral cortex (i.cx. injection) were studied. 4-Aminopyridine administration in both regions induced various preconvulsive symptoms, such as salivation, tremors, chewing and rearing, followed by continuous clonic convulsions and, only after i.c.v. injection, running fits and generalized tonic convulsions. This behavioral pattern appeared 5–9 min after administration of 4-aminopyridine and persisted for 100–150 min. 4-Aminopyridine also generated epileptiform electroencephalographic (EEG) discharges characterized by isolated spikes, poly-spikes and spike-wave complexes, which began some seconds after administration of the drug and were present for more than 2 h. The NMDA receptor antagonists (±)-3-(2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP), (±)-2-amino-7-phosphono-heptanoic acid (AP7) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) clearly protected against some of the behavioral alterations induced by i.c.v. 4-aminopyridine, particularly the tonic convulsions, but were less effective against those produced by i.cx. 4-aminopyridine. These antagonists also delayed the appearance of EEG epileptiform discharges, reduced its amplitude, frequency and duration, and blocked their propagation to other cortical regions after i.cx. 4-aminopyridine. These results, together with previous data showing that 4-aminopyridine stimulates the release of glutamate in vivo, suggest that an excessive glutamatergic neurotransmission involving NMDA receptors is implicated in 4-aminopyridine-induced seizures.}, - language = {en}, - number = {1}, - urldate = {2021-06-12}, - journal = {European Journal of Pharmacology}, - author = {Morales-Villagrán, Alberto and Ureña-Guerrero, Mónica E. and Tapia, Ricardo}, - month = jun, - year = {1996}, - keywords = {Seizure, 4-Aminopyridine, Excitatory amino acid neurotransmission, NMDA receptor antagonist}, - pages = {87--93}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CIJQBWZV\\Morales-Villagrán et al. - 1996 - Protection by NMDA receptor antagonists against se.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9EDF8NNK\\0014299996001574.html:text/html}, -} - -@article{awiszus_effects_1990, - title = {Effects of paranodal potassium permeability on repetitive activity of mammalian myelinated nerve fiber models}, - volume = {64}, - issn = {1432-0770}, - url = {https://doi.org/10.1007/BF00203632}, - doi = {10.1007/BF00203632}, - abstract = {Almost all potassium channels within mammalian myelinated nerve fibers are covered by the myelin sheath and their majority is concentrated in a small paranodal region. In order to investigate effects of this paranodal potassium permeability on nerve fiber behavior via a simulation approach, a myelinated fiber model is required that treats myelin sheath and internodal axolemma as separate entities. Such a fiber description was developed by Blight (1985) and his model was used to investigate the effects paranodal potassium channels have on the ability of maintaining repetitive firing in response to a constant current injected into the fiber. It was found that increasing the potassium channel density at the paranode from low to moderate values widened the range of injected currents with a repetitive response. This promotion of repetitive activity by the introduction of additional potassium channels occurred up to an “optimal” value beyond which a further increase in paranodal potassium permeability narrowed the range of currents with a repetitive response. Finally, if a certain limit in paranodal potassium channel density was exceeded, repetitive activity was abolished completely. These results were obtained regardless of the assumptions about the electrical resistance of the myelin sheath. On the other hand, in the absence of potassium channels repetitive firing could be observed only when a high resistance myelin sheath was assumed, whereas a nerve fiber model with electrical properties inferred from intracellular recordings needed at least some potassium channels within the paranodal region for repetitive firing in response to an injected current.}, - language = {en}, - number = {1}, - urldate = {2021-06-12}, - journal = {Biological Cybernetics}, - author = {Awiszus, F.}, - month = nov, - year = {1990}, - pages = {69--76}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7HCDKD8U\\Awiszus - 1990 - Effects of paranodal potassium permeability on rep.pdf:application/pdf}, -} - -@article{baker_function_1987, - title = {Function and distribution of three types of rectifying channel in rat spinal root myelinated axons.}, - volume = {383}, - copyright = {© 1987 The Physiological Society}, - issn = {1469-7793}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1987.sp016395}, - doi = {10.1113/jphysiol.1987.sp016395}, - abstract = {1. The nature, distribution and function of rectifying channels in rat spinal root myelinated axons has been assessed with selective blocking agents and a variety of intracellular and extracellular recording techniques. 2. The electrotonic responses of roots poisoned with tetrodotoxin (TTX) to constant current pulses had fast (rise time much less than 1 ms) and slow components, which were interpreted in terms of Barrett \& Barrett's (1982) revised cable model for myelinated nerve. Depolarization evoked a rapid outward rectification (time constant, tau approximately 0.5 ms), selectively blocked by 4-aminopyridine (4AP, 1 mM), and a slow outward rectification (tau approximately 15 ms), selectively blocked by tetraethylammonium (TEA, 1 mM) or Ba2+ (0.5 mM). Hyperpolarization evoked an even slower inward rectification, selectively blocked by Cs+ (3 mM) but not by Ba2+. 3. From the different effects of the blocking agents on the fast and slow components of electrotonus, it was deduced (a) that the inward rectification is a property of the internodal axon, (b) that the slow outward rectifier is present at the nodes, and probably the internodes as well, and (c) that the 4AP-sensitive channels have a minor nodal and a major internodal representation. 4. TEA and Ba2+ reduced the accommodation of roots and fibres not poisoned with TTX to long current pulses, whereas 4AP facilitated short bursts of impulses in response to a single brief stimulus. 5. TEA and Ba2+ also abolished a late hyperpolarizing after-potential (peaking at 20-80 ms), while 4AP enhanced the depolarizing after-potential in normal fibres, and abolished an early hyperpolarizing after-potential (peaking at 1-3 ms) in depolarized fibres. Corresponding to the later after-potentials were post-spike changes in excitability and conduction velocity, which were affected similarly by the blocking agents. Cs+ increased the post-tetanic depression attributable to electrogenic hyperpolarization. 6. The physiological roles of the three different rectifying conductances are discussed. It is also argued that the prominent ohmic 'leak conductance', usually ascribed to the nodal axon, must arise in an extracellular pathway in series with the rectifying internodal axon.}, - language = {en}, - number = {1}, - urldate = {2021-06-12}, - journal = {The Journal of Physiology}, - author = {Baker, M. and Bostock, H. and Grafe, P. and Martius, P.}, - year = {1987}, - pages = {45--67}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\QXD6ZG6S\\Baker et al. - 1987 - Function and distribution of three types of rectif.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7WNTMVLH\\jphysiol.1987.html:text/html}, -} - -@article{barrett_intracellular_1982, - title = {Intracellular recording from vertebrate myelinated axons: mechanism of the depolarizing afterpotential}, - volume = {323}, - copyright = {© 1982 The Physiological Society}, - issn = {1469-7793}, - shorttitle = {Intracellular recording from vertebrate myelinated axons}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.1982.sp014064}, - doi = {10.1113/jphysiol.1982.sp014064}, - abstract = {1. Electrophysiological techniques are described which allow intracellular recording from peripheral myelinated axons of lizards and frogs for up to several hours. The sciatic and intramuscular axons studied here have resting potentials of -60 to -80 mV and action potentials (evoked by stimulation of the proximal nerve trunk) of 50-90 mV. They show a prominent depolarizing afterpotential (d.a.p.), which is present both in isolated axons and in axons still attached to their peripheral terminals. This d.a.p. has a peak amplitude of 5-20 mV at the resting potential, and decays with a half-time of 20-100 msec. 2. The peak amplitude of the d.a.p. is voltage-sensitive, increasing to up to 26 mV with membrane hyperpolarization. The d.a.p. disappears as the axon is depolarized to -60 to -45 mV, and does not appear to reverse with further depolarization. 3. The d.a.p. is not reduced when bath Ca is replaced by 2-10 m m divalent Mn or Ni. The d.a.p. is not reversed when axons depleted of Cl (by prolonged exposure to Cl-deficient, SO4-enriched solutions) are bathed in Cl-rich solutions. These results suggest that the d.a.p. is not mediated by a conductance change specific for Ca or Cl ions. Partial substitution of tetramethylammonium for bath Na, or addition of 10−5 m-tetrodotoxin to the normal bathing solution, reduces the amplitude of both the action potential and the d.a.p. 4. The amplitude of the d.a.p. is not sensitive to bath [K] over the range 1-7·5 m m, provided that all measurements are made at the same holding potential. This result argues that the d.a.p. is not mediated by accumulation of K outside the active axon. 5. Treatments expected to inhibit the Na—K exchange pump (cooling from 25 to 10 °C, or 0·15 m m-ouabain) do not enlarge or prolong the d.a.p., although they do abolish a slower hyperpolarizing afterpotential seen following repetitive stimulation. 6. The passive voltage response of the axon to small injected pulses of depolarizing or hyperpolarizing current shows a prominent, slowly decaying component with a time course similar to that of the d.a.p. Depolarizing current reduces the input resistance of the axon, and increases the rate of decay of both the passive voltage response and the d.a.p. There is a slight conductance increase during the peak of the d.a.p., but the same conductance increase can be produced by a comparable passive depolarization. 7. We conclude that the d.a.p. is due mainly to a passive capacitative current, probably resulting from discharge of the internodal axonal membrane capacitance through a resistive current pathway beneath or through the myelin sheath. We suggest that this slow capacitative discharge becomes evident as soon as most of the nodal ionic channels activated during the action potential have closed. An electrical model of the myelinated axon that incorporates the postulated internodal leakage pathway can account both for the prolonged d.a.p. recorded inside the axon, and for the potential profile recorded extra-axonally in or near the internodal periaxonal space.}, - language = {en}, - number = {1}, - urldate = {2021-06-12}, - journal = {The Journal of Physiology}, - author = {Barrett, Ellen F. and Barrett, John N.}, - year = {1982}, - pages = {117--144}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8H8D6NAV\\Barrett and Barrett - 1982 - Intracellular recording from vertebrate myelinated.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\M3R6C6J8\\jphysiol.1982.html:text/html}, -} - -@article{jonas_regulation_1996, - title = {Regulation of potassium channels by protein kinases}, - volume = {6}, - issn = {0959-4388}, - url = {https://www.sciencedirect.com/science/article/pii/S0959438896801140}, - doi = {10.1016/S0959-4388(96)80114-0}, - abstract = {Studies of the role of protein phosphorylation in the modulation of neuronal excitability are beginning to identify specific sites on ion channels that are substrates for serine/threonine kinases and that contribute to short-term and long-term regulation of current amplitude and kinetics. In addition, it is becoming apparent that phosphorylation of tyrosine residues may produce acute changes in the characteristics of ion channels. These recent findings are best illustrated by examining the Shaker superfamily of potassium channels.}, - language = {en}, - number = {3}, - urldate = {2021-06-12}, - journal = {Current Opinion in Neurobiology}, - author = {Jonas, Elizabeth A and Kaczmarek, Leonard K}, - month = jun, - year = {1996}, - pages = {318--323}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3GZJ4IP9\\Jonas and Kaczmarek - 1996 - Regulation of potassium channels by protein kinase.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\M3UBSIZQ\\S0959438896801140.html:text/html}, -} - -@article{kocsis_maturation_1983, - title = {Maturation of mammalian myelinated fibers: changes in action-potential characteristics following 4-aminopyridine application}, - volume = {50}, - issn = {0022-3077}, - shorttitle = {Maturation of mammalian myelinated fibers}, - url = {https://journals.physiology.org/doi/abs/10.1152/jn.1983.50.2.449}, - doi = {10.1152/jn.1983.50.2.449}, - number = {2}, - urldate = {2021-06-12}, - journal = {Journal of Neurophysiology}, - author = {Kocsis, J. D. and Ruiz, J. A. and Waxman, S. G.}, - month = aug, - year = {1983}, - pages = {449--463}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\XCMMY9LD\\Kocsis et al. - 1983 - Maturation of mammalian myelinated fibers changes.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\6V4W7V73\\jn.1983.50.2.html:text/html}, -} - -@article{rasband_potassium_1998, - title = {Potassium {Channel} {Distribution}, {Clustering}, and {Function} in {Remyelinating} {Rat} {Axons}}, - volume = {18}, - copyright = {Copyright © 1998 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/18/1/36}, - doi = {10.1523/JNEUROSCI.18-01-00036.1998}, - abstract = {The K+ channel α-subunits Kv1.1 and Kv1.2 and the cytoplasmic β-subunit Kvβ2 were detected by immunofluorescence microscopy and found to be colocalized at juxtaparanodes in normal adult rat sciatic nerve. After demyelination by intraneural injection of lysolecithin, and during remyelination, the subcellular distributions of Kv1.1, Kv1.2, and Kvβ2 were reorganized. At 6 d postinjection (dpi), axons were stripped of myelin, and K+ channels were found to be dispersed across zones that extended into both nodal and internodal regions; a few days later they were undetectable. By 10 dpi, remyelination was underway, but Kv1.1 immunoreactivity was absent at newly forming nodes of Ranvier. By 14 dpi, K+ channels were detected but were in the nodal gap between Schwann cells. By 19 dpi, most new nodes had Kv1.1, Kv1.2, and Kvβ2, which precisely colocalized. However, this nodal distribution was transient. By 24 dpi, the majority of K+ channels was clustered within paranodal regions of remyelinated axons, leaving a gap that overlapped with Na+ channel immunoreactivity. Inhibition of Schwann cell proliferation delayed both remyelination and the development of the K+ channel distributions described. Conduction studies indicate that neither 4-aminopyridine (4-AP) nor tetraethylammonium alters normal nerve conduction. However, during remyelination, 4-AP profoundly increased both compound action potential amplitude and duration. The level of this effect matched closely the nodal presence of these voltage-dependent K+channels. Our results suggest that K+ channels may have a significant effect on conduction during remyelination and that Schwann cells are important in K+ channel redistribution and clustering.}, - language = {en}, - number = {1}, - urldate = {2021-06-12}, - journal = {Journal of Neuroscience}, - author = {Rasband, Matthew N. and Trimmer, James S. and Schwarz, Thomas L. and Levinson, S. Rock and Ellisman, Mark H. and Schachner, Melitta and Shrager, Peter}, - month = jan, - year = {1998}, - keywords = {potassium channels, axons, demyelination, node of Ranvier, remyelination, Schwann cells}, - pages = {36--47}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YUJXICV4\\Rasband et al. - 1998 - Potassium Channel Distribution, Clustering, and Fu.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WHY8YIG9\\Rasband et al. - 1998 - Potassium Channel Distribution, Clustering, and Fu.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9CL8VFNA\\36.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\6H58N8YY\\36.html:text/html}, -} - -@article{rhodes_association_1997, - title = {Association and {Colocalization} of the {Kvβ1} and {Kvβ2} β-{Subunits} with {Kv1} α-{Subunits} in {Mammalian} {Brain} {K}+{Channel} {Complexes}}, - volume = {17}, - copyright = {Copyright © 1997 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/17/21/8246}, - doi = {10.1523/JNEUROSCI.17-21-08246.1997}, - abstract = {The differential expression and association of cytoplasmic β-subunits with pore-forming α-subunits may contribute significantly to the complexity and heterogeneity of voltage-gated K+ channels in excitable cells. Here we examined the association and colocalization of two mammalian β-subunits, Kvβ1 and Kvβ2, with the K+ channel α-subunits Kv1.1, Kv1.2, Kv1.4, Kv1.6, and Kv2.1 in adult rat brain. Reciprocal coimmunoprecipitation experiments using subunit-specific antibodies indicated that Kvβ1 and Kvβ2 associate with all the Kv1 α-subunits examined, and with each other, but not with Kv2.1. A much larger portion of the total brain pool of Kv1-containing channel complexes was found associated with Kvβ2 than with Kvβ1. Single- and multiple-label immunohistochemical staining indicated that Kvβ1 codistributes extensively with Kv1.1 and Kv1.4 in cortical interneurons, in the hippocampal perforant path and mossy fiber pathways, and in the globus pallidus and substantia nigra. Kvβ2 codistributes extensively with Kv1.1 and Kv1.2 in all brain regions examined and was strikingly colocalized with these α-subunits in the juxtaparanodal region of nodes of Ranvier as well as in the axons and terminals of cerebellar basket cells. Taken together, these data provide a direct demonstration that Kvβ1 and Kvβ2 associate and colocalize with Kv1 α-subunits in native tissues and provide a biochemical and neuroanatomical basis for the differential contribution of Kv1 α- and β-subunits to electrophysiologically diverse neuronal K+ currents.}, - language = {en}, - number = {21}, - urldate = {2021-06-12}, - journal = {Journal of Neuroscience}, - author = {Rhodes, Kenneth J. and Strassle, Brian W. and Monaghan, Michael M. and Bekele-Arcuri, Zewditu and Matos, Maria F. and Trimmer, James S.}, - month = nov, - year = {1997}, - keywords = {immunohistochemistry, striatum, cerebellum, epilepsy, ion channel, central nervous system, immunofluorescence, immunoprecipitation}, - pages = {8246--8258}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DDCV55HF\\Rhodes et al. - 1997 - Association and Colocalization of the Kvβ1 and Kvβ.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\878Z2IN2\\8246.html:text/html}, -} - -@article{isacoff_evidence_1990, - title = {Evidence for the formation of heteromultimeric potassium channels in {Xenopus} oocytes}, - volume = {345}, - copyright = {1990 Nature Publishing Group}, - issn = {1476-4687}, - url = {https://www.nature.com/articles/345530a0}, - doi = {10.1038/345530a0}, - abstract = {POTASSIUM channels show a wide range of functional diversity1–3. Nerve cells typically express a number of K+. channels that differ in their kinetics, single-channel conductance, pharmacology, and sensitivity to voltage and second messengers. The cloning of the Shaker gene in Drosophila4–7, and of related genes8–14, has revealed that the encoded K+ channel polypeptides resemble one of the four internally homologous domains of the α-subunits of Na+ channels and Ca2+ channels15–18, indicating that K+ channels may form by the co-assembly of several polypeptides. In this report we provide evidence that the Shaker A-type K+ channels expressed in Xenopus oocytes contain several Shaker polypeptides, that heteromultimeric channels may form through assembly of different channel polypeptides, that the kinetics or pharmacology of some heteromultimeric channels differ from those of homomultimeric channels, and that channel polypeptides from the fruit fly can co-assemble with homologous polypeptides from the rat. We suggest that heteromultimer formation may increase K+ channel diversity beyond even the level expected from the large number of K+ channel genes and alternative splicing products4,5,19–25.}, - language = {en}, - number = {6275}, - urldate = {2021-06-12}, - journal = {Nature}, - author = {Isacoff, Ehud Y. and Jan, Yuh Nung and Jan, Lily Yeh}, - month = jun, - year = {1990}, - pages = {530--534}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7W7QWWF8\\Isacoff et al. - 1990 - Evidence for the formation of heteromultimeric pot.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4S7NC3QA\\345530a0.html:text/html}, -} - -@article{ruppersberg_heteromultimeric_1990, - title = {Heteromultimeric channels formed by rat brain potassium-channel proteins}, - volume = {345}, - copyright = {1990 Nature Publishing Group}, - issn = {1476-4687}, - url = {https://www.nature.com/articles/345535a0}, - doi = {10.1038/345535a0}, - abstract = {AN important step towards understanding the molecular basis of the functional diversity of voltage-gated K+ channels in the mammalian brain has been the discovery of a family of genes encoding rat brain K+ channel-forming (RCK) proteins1–6. All species of these RCK proteins form homomultimeric voltage-gated K+ channels with distinct functional characteristics in Xenopus laevis oocytes following injection of the respective cRNAs2. RCK-specific mRNAs are coexpressed in several regions of the brain7, suggesting that RCK proteins also assemble into heteromultimeric K+ channels. In addition expression experiments with fractionated poly(A)+ mRNA have suggested that heteromultimeric K+ channels may occur in mammalian brain8. We report here that heteromultimeric K+ channels composed of two different RCK proteins (RCK1 and RCK4) assemble after cotransfection of HeLa cells with the corresponding cDNAs and after coinjection of the corresponding cRNAs into Xenopus oocytes. The heteromultimeric RCK1, 4 channel mediates a transient potassium outward current, similar to the RCK4 channel but inactivates more slowly, has a larger conductance and is more sensitive to block by dendrotoxin and tetraethylammonium chloride.}, - language = {en}, - number = {6275}, - urldate = {2021-06-12}, - journal = {Nature}, - author = {Ruppersberg, J. Peter and Schröter, Klaus H. and Sakmann, Bert and Stocker, Martin and Sewing, Sabine and Pongs, Olaf}, - month = jun, - year = {1990}, - pages = {535--537}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9MTQJWHB\\Ruppersberg et al. - 1990 - Heteromultimeric channels formed by rat brain pota.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8TLMQMQM\\345535a0.html:text/html}, -} - -@article{mi_differential_1995, - title = {Differential distribution of closely related potassium channels in rat {Schwann} cells}, - volume = {15}, - copyright = {© 1995 by Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/15/5/3761}, - doi = {10.1523/JNEUROSCI.15-05-03761.1995}, - abstract = {Closely related K+ channels can coassemble to form heteromultimers in expression systems, as well as in vivo. Whether in vivo this coassembly is random and inevitable or whether highly homologous channels can be segregated and targeted independently within a given cell has not been determined. In this study, we address these questions by characterizing and localizing voltage-dependent K+ channels in Schwann cells. Transcripts for three closely related members of the Shaker-like family of K+ channels are found in adult rat sciatic nerve: Kv1.1, Kv1.2, and Kv1.5. We have examined two of these and observed that both Kv1.1 and Kv1.5 proteins are expressed in Schwann cells but differ in their distributions. Kv1.5 is localized on the Schwann cell membrane at the nodes of Ranvier and in bands that run along the outer surface of the myelin. It is also seen intracellularly in the vicinity of the nucleus. Schwann cell staining for Kv1.1, on the other hand, was seen only in perinuclear, intracellular compartments. These results provide evidence that closely related channels from the same family need not coassemble and can be localized differentially in the same cell. In addition, Kv1.1 was highly concentrated in the axonal membrane at juxtaparanodal regions. The distributions of these K+ channels in myelinated nerve highlight the elaborate molecular specializations of these membranes.}, - language = {en}, - number = {5}, - urldate = {2021-06-12}, - journal = {Journal of Neuroscience}, - author = {Mi, H. and Deerinck, T. J. and Ellisman, M. H. and Schwarz, T. L.}, - month = may, - year = {1995}, - pages = {3761--3774}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\X25NUETT\\Mi et al. - 1995 - Differential distribution of closely related potas.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8H5UHTR9\\3761.html:text/html}, -} - -@article{bulman_phenotype_1997, - title = {Phenotype {Variation} and {Newcomers} in {Ion} {Channel} {Disorders}}, - volume = {6}, - issn = {0964-6906}, - url = {https://doi.org/10.1093/hmg/6.10.1679}, - doi = {10.1093/hmg/6.10.1679}, - abstract = {Ion channels are part of a large family of macromolecules whose functions include the control and maintenance of electrical potential across cell membranes, secretion and signal transduction. Close inspection of the physiological processes involved in channel function and the secondary structure of various ion channels has served as a basis for subdividing ion channels into a number of superfamilies. The voltage-gated ion channels are one of these superfamilies. Recent work has shown that mutations in various ion channel genes are responsible for a number of neuromuscular and neurological disorders. Correlation of the various mutations with the clinical phenotype is providing us with insight into the pathophysiology of these channel proteins. Interestingly, different mutations within the same gene may cause quite distinct clinical disorders, while mutations in different channel genes may result in very similar phenotypes (genetic heterogeneity). Examples of phenotypic variation and genetic heterogeneity are presented in the context of the periodic paralytic disorders of skeletal muscle, episodic ataxia, migraine, long QT syndrome and paroxysmal dyskinesia. Some of these disorders are known to be caused by mutations in ion channel genes, while in the episodic movement disorders, ion channel genes are considered excellent candidate genes.}, - number = {10}, - urldate = {2021-06-12}, - journal = {Human Molecular Genetics}, - author = {Bulman, Dennis E.}, - month = sep, - year = {1997}, - pages = {1679--1685}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7EPY8RLC\\Bulman - 1997 - Phenotype Variation and Newcomers in Ion Channel D.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JFM4AKW6\\587073.html:text/html}, -} - -@article{ashizawa_dominantly_1983, - title = {A dominantly inherited syndrome with continuous motor neuron discharges}, - volume = {13}, - copyright = {Copyright © 1983 American Neurological Association}, - issn = {1531-8249}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/ana.410130310}, - doi = {10.1002/ana.410130310}, - abstract = {A distinct syndrome with continuous motor neuron discharges apparently developed in seven members of a single family, involving both sexes and spanning three generations. Persistent vermiform twitching and episodic stiffness predominantly in lower extremity muscles occurred in early childhood and tended to be less severe in adulthood. In 2 patients the clinical manifestations improved with oral phenytoin and carbamazepine but not with parenteral diazepam. Insertional activity was normal, and continuous, rhythmical, normal-appearing muscle discharges were observed on electromyography. The cerebrospinal fluid levels of homovanillic acid and 5-hydroxyindoleacetic acid were increased in the proband. The disappearance of continuous muscle discharges during spinal anesthesia and the lack of response to diazepam indicated generation of the discharges from the proximal portion of the motor unit.}, - language = {en}, - number = {3}, - urldate = {2021-06-12}, - journal = {Annals of Neurology}, - author = {Ashizawa, Tetsuo and Butler, Ian J. and Harati, Yadollah and Roongta, Suresh M.}, - year = {1983}, - pages = {285--290}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ICITHZ5G\\Ashizawa et al. - 1983 - A dominantly inherited syndrome with continuous mo.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AKWKEXZ8\\ana.html:text/html}, -} - -@article{campomanes_kv_2002, - title = {Kvβ {Subunit} {Oxidoreductase} {Activity} and {Kv1} {Potassium} {Channel} {Trafficking}}, - volume = {277}, - issn = {0021-9258}, - url = {https://www.sciencedirect.com/science/article/pii/S0021925819364324}, - doi = {10.1074/jbc.M110276200}, - abstract = {Voltage-gated Kv1 potassium channels consist of pore-forming α subunits and cytoplasmic Kvβ subunits. The latter play diverse roles in modulating the gating, stability, and trafficking of Kv1 channels. The crystallographic structure of the Kvβ2 subunit revealed surprising structural homology with aldo-keto reductases, including a triosephosphate isomerase barrel structure, conservation of key catalytic residues, and a bound NADP+ cofactor (Gulbis, J. M., Mann, S., and MacKinnon, R. (1999) Cell 90, 943–952). Each Kv1-associated Kvβ subunit (Kvβ1.1, Kvβ1.2, Kvβ2, and Kvβ3) shares striking amino acid conservation in key catalytic and cofactor binding residues. Here, by a combination of structural modeling and biochemical and cell biological analyses of structure-based mutations, we investigate the potential role for putative Kvβ subunit enzymatic activity in the trafficking of Kv1 channels. We found that all Kvβ subunits promote cell surface expression of coexpressed Kv1.2 α subunits in transfected COS-1 cells. Kvβ1.1 and Kvβ2 point mutants lacking a key catalytic tyrosine residue found in the active site of all aldo-keto reductases have wild-type trafficking characteristics. However, mutations in residues within the NADP+ binding pocket eliminated effects on Kv1.2 trafficking. In cultured hippocampal neurons, Kvβ subunit coexpression led to axonal targeting of Kv1.2, recapitulating the Kv1.2 localization observed in many brain neurons. Similar to the trafficking results in COS-1 cells, mutations within the cofactor binding pocket reduced axonal targeting of Kv1.2, whereas those in the catalytic tyrosine did not. Together, these data suggest that NADP+ binding and/or the integrity of the binding pocket structure, but not catalytic activity, of Kvβ subunits is required for intracellular trafficking of Kv1 channel complexes in mammalian cells and for axonal targeting in neurons.}, - language = {en}, - number = {10}, - urldate = {2021-06-12}, - journal = {Journal of Biological Chemistry}, - author = {Campomanes, Claire R. and Carroll, Karen I. and Manganas, Louis N. and Hershberger, Marcia E. and Gong, Belvin and Antonucci, Dana E. and Rhodes, Kenneth J. and Trimmer, James S.}, - month = mar, - year = {2002}, - pages = {8298--8305}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DQE5VCME\\Campomanes et al. - 2002 - Kvβ Subunit Oxidoreductase Activity and Kv1 Potass.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8SLAS8NP\\S0021925819364324.html:text/html}, -} - -@article{litt_gene_1994, - title = {A gene for episodic ataxia/myokymia maps to chromosome 12p13.}, - volume = {55}, - issn = {0002-9297}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1918305/}, - abstract = {Episodic ataxia (EA) is a rare, familial disorder producing attacks of generalized ataxia, with normal or near-normal neurological function between attacks. Families with autosomal dominant EA represent at least two distinct clinical syndromes. One clinical type of EA (MIM 160120) includes individuals who have episodes of ataxia and dysarthria lasting seconds to minutes. In addition, myokymia (rippling of muscles, diagnosable by electromyography) is evident during and between attacks. Since K+ channel genes are candidate genes for EA, we tested markers near known K+ channel genes for linkage. Using a group of Genethon markers from one such region--chromosome 12p--we found evidence of linkage in four EA/myokymia families. A maximum combined lod score of 13.6 was obtained at theta = 0, with the marker D12S99. A human Ca++ channel gene, CACNL1A1, and three human K+ channel genes--KCNA5, KCNA6, and KCNA1--map close to D12S99, but the Ca++ channel gene is unlikely to be the site of the defect, because crossovers have been observed to occur between the disease gene and a CA-repeat marker located close to this gene. Studies of a large EA family with a different clinical phenotype (MIM 108500), which lacks myokymia but is associated with nystagmus, have excluded the gene causing that disease from the chromosome 12p locus.}, - number = {4}, - urldate = {2021-06-12}, - journal = {American Journal of Human Genetics}, - author = {Litt, M. and Kramer, P. and Browne, D. and Gancher, S. and Brunt, E. R. and Root, D. and Phromchotikul, T. and Dubay, C. J. and Nutt, J.}, - month = oct, - year = {1994}, - pages = {702--709}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3HJRZ6XY\\Litt et al. - 1994 - A gene for episodic ataxiamyokymia maps to chromo.pdf:application/pdf}, -} - -@article{manganas_identification_2001, - title = {Identification of a trafficking determinant localized to the {Kv1} potassium channel pore}, - volume = {98}, - copyright = {Copyright © 2001, The National Academy of Sciences}, - issn = {0027-8424, 1091-6490}, - url = {https://www.pnas.org/content/98/24/14055}, - doi = {10.1073/pnas.241403898}, - abstract = {The repertoire of Kv1 potassium channels expressed in presynaptic terminals of mammalian central neurons is shaped by intrinsic trafficking signals that determine surface-expression efficiencies of homomeric and heteromeric Kv1 channel complexes. Here, we show that a determinant controlling surface expression of Kv1 channels is localized to the highly conserved pore region. Point-mutation analysis revealed two residues as critical for channel trafficking, one in the extracellular “turret” domain and one in the region distal to the selectivity filter. Interestingly, these same residues also form the binding sites for polypeptide neurotoxins. Our findings demonstrate a previously uncharacterized function for the channel-pore domain as a regulator of channel trafficking.}, - language = {en}, - number = {24}, - urldate = {2021-06-12}, - journal = {Proceedings of the National Academy of Sciences}, - author = {Manganas, Louis N. and Wang, Qiang and Scannevin, Robert H. and Antonucci, Dana E. and Rhodes, Kenneth J. and Trimmer, James S.}, - month = nov, - year = {2001}, - pages = {14055--14059}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\USC4WDPI\\Manganas et al. - 2001 - Identification of a trafficking determinant locali.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9M7UBRBX\\14055.html:text/html}, -} - -@article{shi_subunits_1996, - title = {β{Subunits} {Promote} {K}+ {Channel} {Surface} {Expression} through {Effects} {Early} in {Biosynthesis}}, - volume = {16}, - issn = {0896-6273}, - url = {https://www.sciencedirect.com/science/article/pii/S089662730080104X}, - doi = {10.1016/S0896-6273(00)80104-X}, - abstract = {Voltage-gated K+ channels are protein complexes composed of ion-conducting integral membrane α subunits and cytoplasmic β subunits. Here, we show that, in transfected mammalian cells, the predominant β subunit isoform in brain, Kvβ2, associates with the Kv1.2 α subunit early in channel biosynthesis and that Kvβ2 exerts multiple chaperone-like effects on associated Kv1.2 including promotion of cotranslational N-linked glycosylation of the nascent Kv1.2 polypeptide, increased stability of Kvβ2/Kv1.2 complexes, and increased efficiency of cell surface expression of Kv1.2. Taken together, these results indicate that while some cytoplasmic K+ channel β subunits affect the inactivation kinetics of α subunits, a more general, and perhaps more fundamental, role is to mediate the biosynthetic maturation and surface expression of voltage-gated K+ channel complexes. These findings provide a molecular basis for recent genetic studies indicating that β subunits are key determinants of neuronal excitability.}, - language = {en}, - number = {4}, - urldate = {2021-06-12}, - journal = {Neuron}, - author = {Shi, Gongyi and Nakahira, Kensuke and Hammond, Scott and Rhodes, Kenneth J and Schechter, Lee E and Trimmer, James S}, - month = apr, - year = {1996}, - pages = {843--852}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BV27M2UF\\Shi et al. - 1996 - βSubunits Promote K+ Channel Surface Expression th.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9LQS5KPD\\S089662730080104X.html:text/html}, -} - -@article{tsaur_differential_1992, - title = {Differential expression of {K}+ channel {mRNAs} in the rat brain and down-regulation in the hippocampus following seizures}, - volume = {8}, - issn = {0896-6273}, - url = {https://www.sciencedirect.com/science/article/pii/089662739290127Y}, - doi = {10.1016/0896-6273(92)90127-Y}, - abstract = {K+ channels are major determinants of membrane excitability. Differences in neuronal excitability within the nervous system may arise from differential expression of K+ channel genes, regulated spatially in a cell type-specific manner, or temporally in response to neuronal activity. We have compared the distribution of mRNAs of three K+ channel genes, Kv1.1, Kv1.2, and Kv4.2 in rat brain, and examined activity-dependent changes following treatment with the convulsant drug pentylenetetrazole. Both regional and cell type-specific differences of K+ channel gene expression were found. In addition, seizure activity caused a reduction of Kv1.2 and Kv4.2 mRNAs in the dentate granule cells of the hippocampus, raising the possibility that K+ channel gene regulation may play a role in long-term neuronal plasticity.}, - language = {en}, - number = {6}, - urldate = {2021-06-12}, - journal = {Neuron}, - author = {Tsaur, Meei-Ling and Sheng, Morgan and Lowenstein, Daniel H. and Jan, Yuh Nung and Jan, Lily Yeh}, - month = jun, - year = {1992}, - pages = {1055--1067}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\AV3MLGZ2\\Tsaur et al. - 1992 - Differential expression of K+ channel mRNAs in the.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\BAQZSPTI\\089662739290127Y.html:text/html}, -} - -@article{xu_kv2_1997, - title = {Kvβ2 {Inhibits} the {Kvβ1}-mediated {Inactivation} of {K}+ {Channels} in {Transfected} {Mammalian} {Cells}}, - volume = {272}, - issn = {0021-9258}, - url = {https://www.sciencedirect.com/science/article/pii/S0021925818405091}, - doi = {10.1074/jbc.272.18.11728}, - abstract = {Cloned auxiliary β-subunits (e.g.Kvβ1) modulate the kinetic properties of the pore-forming α-subunits of a subset of Shaker-like potassium channels. Coexpression of the α-subunit and Kvβ2, however, induces little change in channel properties. Since more than one β-subunit has been found in individual K+ channel complexes and expression patterns of different β-subunits overlap in vivo, it is important to test the possible physical and/or functional interaction(s) between different β-subunits. In this report, we show that both Kvβ2 and Kvβ1 recognize the same region on the pore-forming α-subunits of the Kv1 Shaker-like potassium channels. In the absence of α-subunits the Kvβ2 polypeptide interacts with additional β-subunit(s) to form either a homomultimer with Kvβ2 or a heteromultimer with Kvβ1. When coexpressing α-subunits and Kvβ1 in the presence of Kvβ2, we find that Kvβ2 is capable of inhibiting the Kvβ1-mediated inactivation. Using deletion analysis, we have localized the minimal interaction region that is sufficient for Kvβ2 to associate with both α-subunits and Kvβ1. This mapped minimal interaction region is necessary and sufficient for inhibiting the Kvβ1-mediated inactivation, consistent with the notion that the inhibitory activity of Kvβ2 results from the coassembly of Kvβ2 with compatible α-subunits and possibly with Kvβ1. Together, these results provide biochemical evidence that Kvβ2 may profoundly alter the inactivation activity of another β-subunit by either differential subunit assembly or by competing for binding sites on α-subunits, which indicates that Kvβ2 is capable of serving as an important determinant in regulating the kinetic properties of K+currents.}, - language = {en}, - number = {18}, - urldate = {2021-06-12}, - journal = {Journal of Biological Chemistry}, - author = {Xu, Jia and Li, Min}, - month = may, - year = {1997}, - pages = {11728--11735}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RVNNHGE9\\Xu and Li - 1997 - Kvβ2 Inhibits the Kvβ1-mediated Inactivation of K+.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EG8EMIEK\\S0021925818405091.html:text/html}, -} - -@article{zerr_episodic_1998, - title = {Episodic {Ataxia} {Mutations} in {Kv1}.1 {Alter} {Potassium} {Channel} {Function} by {Dominant} {Negative} {Effects} or {Haploinsufficiency}}, - volume = {18}, - copyright = {Copyright © 1998 Society for Neuroscience}, - issn = {0270-6474, 1529-2401}, - url = {https://www.jneurosci.org/content/18/8/2842}, - doi = {10.1523/JNEUROSCI.18-08-02842.1998}, - abstract = {Subunits of the voltage-gated potassium channel Kv1.1 containing mutations responsible for episodic ataxia (EA), a human inherited neurological disease, were expressed in Xenopus oocytes. Five EA subunits formed functional homomeric channels with lower current amplitudes and altered gating properties compared with wild type. Two EA mutations located in the first cytoplasmic loop, R239S and F249I, yielded minimal or no detectable current, and Western blot analysis showed reduced protein levels. Coinjection of equal amounts of EA and wild-type mRNAs, mimicking the heterozygous condition, resulted in current amplitudes and gating properties that were intermediate between wild-type and EA homomeric channels, suggesting that heteromeric channels are formed with a mixed stoichiometry of EA and wild-type subunits. To examine the relative contribution of EA subunits in forming heteromeric EA and wild-type channels, each EA subunit was made insensitive to TEA, TEA-tagged, and coexpressed with wild-type subunits. TEA-tagged R239S and F249I induced the smallest shift in TEA sensitivity compared with homomeric wild-type channels, whereas the other TEA-tagged EA subunits yielded TEA sensitivities similar to coexpression of wild-type and TEA-tagged wild-type subunits. Taken together, these results show that the different mutations in Kv1.1 affect channel function and indicate that both dominant negative effects and haplotype insufficiency may result in the symptoms of EA.}, - language = {en}, - number = {8}, - urldate = {2021-06-12}, - journal = {Journal of Neuroscience}, - author = {Zerr, Patricia and Adelman, John P. and Maylie, James}, - month = apr, - year = {1998}, - keywords = {K channel, episodic ataxia, dominant negative effects, haploinsufficiency, neurological disease, oocyte expression}, - pages = {2842--2848}, - file = {Episodic Ataxia Mutations in Kv1.1 Alter Potassium Channel Function by Dominant Negative Effects or Haploinsufficiency | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\G6QWTYDT\\2842.html:text/html;Episodic Ataxia Mutations in Kv1.1 Alter Potassium Channel Function by Dominant Negative Effects or Haploinsufficiency | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\EBVKAILN\\2842.html:text/html;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\G3IIMY97\\Zerr et al. - 1998 - Episodic Ataxia Mutations in Kv1.1 Alter Potassium.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\M4MA84QX\\2842.html:text/html}, -} - -@article{zerr_characterization_1998, - title = {Characterization of three episodic ataxia mutations in the human {Kv1}.1 potassium channel}, - volume = {431}, - copyright = {FEBS Letters 431 (1998) 1873-3468 © 2015 Federation of European Biochemical Societies}, - issn = {1873-3468}, - url = {https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/S0014-5793%2898%2900814-X}, - doi = {10.1016/S0014-5793(98)00814-X}, - abstract = {Episodic ataxia (EA) is a rare inherited neurological disorder due to mutation in the voltage-dependent Kv1.1 potassium channel. In nine unrelated families, a different missense point mutation at highly conserved positions has been reported. We have previously characterized six of the EA mutants. In this study, three recently identified mutations were introduced into the human Kv1.1 cDNA and expressed in Xenopus oocytes. Compared to wild type, T226A and T226M reduced the current amplitude by {\textgreater}95\%, shifted the voltage dependence by 15 mV, and slowed activation and deactivation kinetics. Currents from G311S were ∼25\% of wild type, less steeply voltage-dependent and had more pronounced C-type inactivation. These altered gating properties will reduce the delayed-rectifier potassium current which may underlie the symptoms of EA.}, - language = {en}, - number = {3}, - urldate = {2021-06-12}, - journal = {FEBS Letters}, - author = {Zerr, Patricia and Adelman, John P. and Maylie, James}, - year = {1998}, - keywords = {Kv1.1, Ataxia, Inherited disease, Potassium channel}, - pages = {461--464}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KK4I4HPY\\Zerr et al. - 1998 - Characterization of three episodic ataxia mutation.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\AJH7YY93\\Zerr et al. - 1998 - Characterization of three episodic ataxia mutation.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5GC8SL6L\\S0014-5793(98)00814-X.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\HPZW8884\\S0014-5793(98)00814-X.html:text/html}, -} - -@article{dadamo_episodic_1998, - title = {Episodic ataxia type-1 mutations in the {hKv1}.1 cytoplasmic pore region alter the gating properties of the channel}, - volume = {17}, - issn = {0261-4189}, - url = {https://www.embopress.org/doi/full/10.1093/emboj/17.5.1200}, - doi = {10.1093/emboj/17.5.1200}, - abstract = {Episodic ataxia type-1 is a rare human neurological syndrome which occurs during childhood and persists through the whole life of affected patients. Several heterozygous point mutations have been found in the coding sequence of the voltage-gated potassium channel gene hKv1.1 of different affected families. V408A and E325D mutations are located in the cytoplasmic putative pore region of hKv1.1 channels and profoundly alter their gating properties. V408A channels showed increased kinetic rates of activation, deactivation and C-type inactivation. Expression of E325D channels in Xenopus oocytes led to an ?13-fold current amplitude reduction and to a 52.4 mV positive shift in the voltage dependence of activation. Moreover, the E325D mutation altered the kinetics of activation, deactivation, C-type inactivation and channel open probability. Heteromeric channels composed of two wild-type and two mutated subunits, linked as dimers, showed gating properties intermediate between channels formed from four normal or four mutated subunits. The results demonstrate that the highly conserved residues Val408 and Glu325 play a pivotal role in several gating processes of a human potassium channel, and suggest a pathogenetic mechanism by which the impairment of the delayed-rectifier function of affected neurons is related to the type and number of mutated subunits which make up the hKv1.1 channels.}, - number = {5}, - urldate = {2021-06-12}, - journal = {The EMBO Journal}, - author = {D'Adamo, Maria Cristina and Liu, Zhaoping and Adelman, John P. and Maylie, James and Pessia, Mauro}, - month = mar, - year = {1998}, - keywords = {potassium channel, gating, episodic ataxia type-1, hKv1.1 channels, mutation}, - pages = {1200--1207}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\65BKUWQM\\D'Adamo et al. - 1998 - Episodic ataxia type-1 mutations in the hKv1.1 cyt.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4ZQ529AL\\17.5.html:text/html}, -} - -@article{gancher_autosomal_1986, - title = {Autosomal dominant episodic ataxia: {A} heterogeneous syndrome}, - volume = {1}, - copyright = {Copyright © 1986 Movement Disorder Society}, - issn = {1531-8257}, - shorttitle = {Autosomal dominant episodic ataxia}, - url = {https://movementdisorders.onlinelibrary.wiley.com/doi/abs/10.1002/mds.870010404}, - doi = {10.1002/mds.870010404}, - abstract = {We describe six kindreds with autosomal dominant episodic ataxia, apparently representing three distinct syndromes. Four kindreds were characterized by episodic ataxia and response to acetazolamide, and in three, interictal nystagmus. One kindred was characterized by paroxysmal ataxia and in one member, paroxysmal choreoathetosis. The last kindred had brief attacks of ataxia and interictal neuromyotonia. The age of onset and severity of the disorder varied within each kindred. These kindreds illustrate the heterogenity of episodic ataxia as well as the variable expressivity within each kindred.}, - language = {en}, - number = {4}, - urldate = {2021-06-12}, - journal = {Movement Disorders}, - author = {Gancher, Stephen T. and Nutt, John G.}, - year = {1986}, - pages = {239--253}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\S5THTLSD\\Gancher and Nutt - 1986 - Autosomal dominant episodic ataxia A heterogeneou.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\PZI6LUN7\\mds.html:text/html}, -} - -@article{pongs_voltage-gated_1999, - title = {Voltage-gated potassium channels: from hyperexcitability to excitement}, - volume = {452}, - copyright = {FEBS Letters 452 (1999) 1873-3468 © 2015 Federation of European Biochemical Societies}, - issn = {1873-3468}, - shorttitle = {Voltage-gated potassium channels}, - url = {https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/S0014-5793%2899%2900535-9}, - doi = {10.1016/S0014-5793(99)00535-9}, - abstract = {The superfamily of voltage-activated potassium channels may express structurally and functionally diverse voltage-activated potassium channels in the nervous system. The roles of some voltage-activated potassium channel types, e.g. rapidly inactivating (transiently active type) channels and muscarine sensitive muscarine sensitive channels, are beginning to be understood. They may significantly influence dendritic action-potential back-propagation, signal to noise ratios in presynaptic excitability or the responsiveness of a neuron to synaptic input. Inherited disorders related to changes in excitability (episodic ataxia, epilepsy, heart arrhythmia) or to defects in sensory perception (hearing loss) have been associated with mutations in a few voltage-activated potassium channel genes. Most likely, more voltage-activated potassium channel genes will be linked to related disorders in the near future.}, - language = {en}, - number = {1-2}, - urldate = {2021-06-12}, - journal = {FEBS Letters}, - author = {Pongs, Olaf}, - year = {1999}, - keywords = {Hyperexcitability, Action-potential, Hearing loss, Voltage-activated potassium channel}, - pages = {31--35}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9F6L4W3Z\\Pongs - 1999 - Voltage-gated potassium channels from hyperexcita.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\93UCLB3A\\S0014-5793(99)00535-9.html:text/html}, -} - -@article{coleman_subunit_1999, - title = {Subunit {Composition} of {Kv1} {Channels} in {Human} {CNS}}, - volume = {73}, - issn = {1471-4159}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1471-4159.1999.0730849.x}, - doi = {10.1046/j.1471-4159.1999.0730849.x}, - abstract = {: The α subunits of Shaker-related K+ channels (Kv1.X) show characteristic distributions in mammalian brain and restricted coassembly. Despite the functional importance of these voltage-sensitive K+ channels and involvement in a number of diseases, little progress has been achieved in deciphering the subunit composition of the (α)4(β)4 oligomers occurring in human CNS. Thus, the association of α and β subunits was investigated in cerebral grey and white matter and spinal cord from autopsy samples. Immunoblotting established the presence of Kv1.1, 1.2, and 1.4 in all the tissues, with varying abundance. Sequential immunoprecipitations identified the subunits coassembled. A putative tetramer of Kv1.3/1.4/1.1/1.2 was found in grey matter. Both cerebral white matter and spinal cord contained the heterooligomers Kv1.1/1.4 and Kv1.1/1.2, similar to grey matter, but both lacked Kv1.3 and the Kv1.4/1.2 combination. An apparent Kv1.4 homooligomer was detected in all the samples, whereas only the brain tissue possessed a putative Kv1.2 homomer. In grey matter, Kvβ2.1 was coassociated with the Kv1.1/1.2 combination and Kv1.2 homooligomer. In white matter, Kvβ2.1 was associated with Kv1.2 only, whereas Kvβ1.1 coprecipitated with all the α subunits present. This represents the first description of Kv1 subunit complexes in the human CNS and demonstrates regional variations, indicative of functional specialisation.}, - language = {en}, - number = {2}, - urldate = {2021-06-12}, - journal = {Journal of Neurochemistry}, - author = {Coleman, Sarah K. and Newcombe, Jia and Pryke, Jonathan and Dolly, J. Oliver}, - year = {1999}, - keywords = {Human, Potassium channel, Axolemma, CNS, Delayed rectifier, Immunoprecipitation.}, - pages = {849--858}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9N6K9G2L\\Coleman et al. - 1999 - Subunit Composition of Kv1 Channels in Human CNS.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\54GLRDQU\\j.1471-4159.1999.0730849.html:text/html}, -} - -@article{boland_episodic_1999, - title = {Episodic ataxia/myokymia mutations functionally expressed in the {Shaker} potassium channel}, - volume = {91}, - issn = {0306-4522}, - url = {https://www.sciencedirect.com/science/article/pii/S0306452298007180}, - doi = {10.1016/S0306-4522(98)00718-0}, - abstract = {Episodic ataxia type 1 is a rare, autosomal dominant neurological disorder caused by missense mutations of the Kv1.1 gene from the Shaker K+ channel subfamily. To study the functional effects of the disease-causing mutations in a robust K+ channel background, we introduced seven different episodic ataxia type 1 substitutions into the corresponding, conserved residues of the Shaker K+ channel. K+ channel currents expressed in Xenopus oocytes were studied by electrophysiology. All episodic ataxia type 1 mutations produced functional K+ channels. In a Shaker N-terminal deletion mutant with fast inactivation removed, current amplitudes were significantly reduced in channels harboring an episodic ataxia type 1 mutation. Six of the seven mutations also showed depolarizing shifts (+9 to +36mV) in the conductance voltage dependence. One mutation (F307I) shifted the midpoint of the conductance–voltage relationship by 23mV in the hyperpolarizing direction. Episodic ataxia type 1 mutations were also expressed in ShakerH4 with intact N-terminal inactivation. In this construct, current amplitudes for episodic ataxia type 1 mutants were not significantly different from wild-type channels. All mutations altered the voltage range of steady-state inactivation; most changes were coupled to the changes in activation gating. Some episodic ataxia type 1 mutants also caused significant changes in the kinetics of N-type (F307I, E395D) or C-type (F307I, E395D, V478A) inactivation. These results suggest that episodic ataxia type 1 mutations may change K+ channel function by two mechanisms: (i) reduced channel expression and (ii) altered channel gating.}, - language = {en}, - number = {4}, - urldate = {2021-06-12}, - journal = {Neuroscience}, - author = {Boland, L. M and Price, D. L and Jackson, K. A}, - month = jul, - year = {1999}, - keywords = {voltage clamp, K channel, episodic ataxia type 1, inactivation, activation}, - pages = {1557--1564}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SQTJL7N7\\Boland et al. - 1999 - Episodic ataxiamyokymia mutations functionally ex.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\HMLLQ5V3\\S0306452298007180.html:text/html}, -} - -@article{rho_developmental_1999, - title = {Developmental {Seizure} {Susceptibility} of {Kv1}.1 {Potassium} {Channel} {Knockout} {Mice}}, - volume = {21}, - issn = {0378-5866, 1421-9859}, - url = {https://www.karger.com/Article/FullText/17381}, - doi = {10.1159/000017381}, - abstract = {Potassium channels play a critical role in limiting neuronal excitability. Mutations in certain voltage-gated potassium channels have been associated with hyperexcitable phenotypes in both humans and animals. However, only recently have mutations in potassium channel genes (i.e. \textit{KCNQ2} and \textit{KCNQ3}) been discovered in a human epilepsy, benign familial neonatal convulsions. Recently, it has been reported that mice lacking the voltage-gated Shaker-like potassium channel Kv1.1 α-subunit develop recurrent spontaneous seizures early in postnatal development. The clinical relevance of the Kv1.1 knockout mouse has been underscored by a recent report of epilepsy occurring in a family affected by mutations in the \textit{KCNA1} locus (the human homologue of Kv1.1) which typically cause episodic ataxia and myokymia. Here we summarize preliminary studies characterizing the developmental changes in seizure susceptibility and neuronal activation in the three genotypes of Kv1.1 mice (–/–, +/–, +/+). Using behavioral and immediate-early gene indicators of regional brain excitability, we have found that a seizure-sensitive predisposition exists in Kv1.1 –/– animals at a very young age (P10), before either spontaneous seizure activity or changes in c-fos mRNA expression can be demonstrated. Kv1.1 +/– mice, although behaviorally indistinguishable from wild types, also have an increased susceptibility to seizures at a similar early age. The Kv1.1 knockout mouse possesses many features desirable in a developmental animal epilepsy model and represents a clinically relevant model of early-onset epilepsies.}, - language = {english}, - number = {3-5}, - urldate = {2021-06-14}, - journal = {Developmental Neuroscience}, - author = {Rho, Jong M. and Szot, Patricia and Tempel, Bruce L. and Schwartzkroin, Philip A.}, - year = {1999}, - pages = {320--327}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\QHECJ4SU\\Rho et al. - 1999 - Developmental Seizure Susceptibility of Kv1.1 Pota.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\P5FU9TYH\\17381.html:text/html}, -} - -@article{van_brederode_evidence_2001, - title = {Evidence of altered inhibition in layer {V} pyramidal neurons from neocortex of {Kcna1}-null mice}, - volume = {103}, - issn = {0306-4522}, - url = {https://www.sciencedirect.com/science/article/pii/S0306452201000410}, - doi = {10.1016/S0306-4522(01)00041-0}, - abstract = {Mice lacking the potassium channel subunit KCNA1 exhibit a severe epileptic phenotype beginning at an early postnatal age. The precise cellular physiological substrates for these seizures are unclear, as is the site of origin. Since KCNA1 mRNA in normal mice is expressed in the neocortex, we asked whether neurons in the neocortex of three to four week-old Kcna1-null mutants exhibit evidence of hyperexcitability. Layer V pyramidal neurons were directly visualized in brain slices with infrared differential-interference contrast microscopy and evaluated with cellular electrophysiological techniques. There were no significant differences in intrinsic membrane properties and action potential shape between Kcna1-null and wild-type mice, consistent with previous findings in hippocampal slice recordings. However, the frequency of spontaneous post-synaptic currents was significantly higher in Kcna1-null compared to wild-type mice. The frequency of spontaneous inhibitory post-synaptic currents and miniature (action-potential-independent) inhibitory post-synaptic currents was also significantly higher in Kcna1-null compared to wild-type mice. However, the frequency of spontaneous and miniature excitatory post-synaptic currents was not different in these two groups of animals. Comparison of the amplitude and kinetics of miniature inhibitory and excitatory post-synaptic currents revealed differences in amplitude, rise time and half-width between Kcna1-null and wild-type mice. Our data indicate that the inhibitory drive onto layer V pyramidal neurons is increased in Kcna1 knockout mice, either directly through an increased spontaneous release of GABA from presynaptic terminals contacting layer V pyramidal neurons, or an enhanced excitatory synaptic input to inhibitory interneurons.}, - language = {en}, - number = {4}, - urldate = {2021-06-14}, - journal = {Neuroscience}, - author = {van Brederode, J. F. M. and Rho, J. M. and Cerne, R. and Tempel, B. L and Spain, W. J.}, - month = apr, - year = {2001}, - keywords = {epilepsy, potassium channel, Kv1.1, knockout, seizure}, - pages = {921--929}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\VXJ3N53E\\van Brederode et al. - 2001 - Evidence of altered inhibition in layer V pyramida.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AG6SXGLJ\\S0306452201000410.html:text/html}, -} - -@article{brew_hyperexcitability_2003, - title = {Hyperexcitability and reduced low threshold potassium currents in auditory neurons of mice lacking the channel subunit {Kv1}.1}, - volume = {548}, - copyright = {© 2003 The Journal of Physiology © 2003 The Physiological Society}, - issn = {1469-7793}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1111/j..2003.t01-1-00001.x}, - doi = {10.1111/j..2003.t01-1-00001.x}, - abstract = {A low voltage-activated potassium current, IKL, is found in auditory neuron types that have low excitability and precisely preserve the temporal pattern of activity present in their presynaptic inputs. The gene Kcna1 codes for Kv1.1 potassium channel subunits, which combine in expression systems to produce channel tetramers with properties similar to those of IKL, including sensitivity to dendrotoxin (DTX). Kv1.1 is strongly expressed in neurons with IKL, including auditory neurons of the medial nucleus of the trapezoid body (MNTB). We therefore decided to investigate how the absence of Kv1.1 affected channel properties and function in MNTB neurons from mice lacking Kcna1. We used the whole cell version of the patch clamp technique to record from MNTB neurons in brainstem slices from Kcna1-null (−/−) mice and their wild-type (+/+) and heterozygous (+/−) littermates. There was an IKL in voltage-clamped −/− MNTB neurons, but it was about half the amplitude of the IKL in +/+ neurons, with otherwise similar properties. Consistent with this, −/− MNTB neurons were more excitable than their +/+ counterparts; they fired more than twice as many action potentials (APs) during current steps, and the threshold current amplitude required to generate an AP was roughly halved. +/− MNTB neurons had excitability and IKL amplitudes identical to the +/+ neurons. The IKL remaining in −/− neurons was blocked by DTX, suggesting the underlying channels contained subunits Kv1.2 and/or Kv1.6 (also DTX-sensitive). DTX increased excitability further in the already hyperexcitable −/− MNTB neurons, suggesting that −/−IKL limited excitability despite its reduced amplitude in the absence of Kv1.1 subunits.}, - language = {en}, - number = {1}, - urldate = {2021-06-14}, - journal = {The Journal of Physiology}, - author = {Brew, Helen M. and Hallows, Janice L. and Tempel, Bruce L.}, - year = {2003}, - pages = {1--20}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KHZTN5RA\\Brew et al. - 2003 - Hyperexcitability and reduced low threshold potass.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\SRKME4BH\\j..2003.t01-1-00001.html:text/html}, -} - -@article{ristori_riluzole_2010, - title = {Riluzole in cerebellar ataxia: {A} randomized, double-blind, placebo-controlled pilot trial}, - volume = {74}, - copyright = {© 2010}, - issn = {0028-3878, 1526-632X}, - shorttitle = {Riluzole in cerebellar ataxia}, - url = {https://n.neurology.org/content/74/10/839}, - doi = {10.1212/WNL.0b013e3181d31e23}, - abstract = {Background: The pleiotropic effects of riluzole may antagonize common mechanisms underlying chronic cerebellar ataxia, a debilitating and untreatable consequence of various diseases. -Methods: In a randomized, double-blind, placebo-controlled pilot trial, 40 patients presenting with cerebellar ataxias of different etiologies were randomly assigned to riluzole (100 mg/day) or placebo for 8 weeks. The following outcome measures were compared: proportion of patients with a decrease of at least 5 points in the International Cooperative Ataxia Rating Scale (ICARS) total score after 4 and 8 weeks compared with the baseline score; mean changes from the baseline to posttreatment ICARS (total score and subscores at 8 weeks); and occurrence of adverse events. -Results: Riluzole and placebo groups did not differ in baseline characteristics. The number of patients with a 5-point ICARS drop was significantly higher in the riluzole group than in the placebo group after 4 weeks (9/19 vs 1/19; odds ratio [OR] = 16.2; 95\% confidence interval [CI ] 1.8–147.1) and 8 weeks (13/19 vs 1/19; OR = 39.0; 95\% CI 4.2–364.2). The mean change in the riluzole group ICARS after treatment revealed a decrease (p {\textless} 0.001) in the total score (−7.05 [4.96] vs 0.16 [2.65]) and major subscores (−2.11 [2.75] vs 0.68 [1.94] for static function, −4.11 [2.96] vs 0.37 [2.0] for kinetic function, and −0.74 [0.81] vs 0.05 [0.40] for dysarthria). Sporadic, mild adverse events occurred. -Conclusions: These findings indicate the potential effectiveness of riluzole as symptomatic therapy in diverse forms of cerebellar ataxia. -Classification of evidence: This study provides Class I evidence that riluzole reduces, by at least 5 points, the ICARS score in patients with a wide range of disorders that cause cerebellar ataxia (risk difference 63.2\%, 95\% CI 33.5\%–79.9\%).}, - language = {en}, - number = {10}, - urldate = {2021-06-14}, - journal = {Neurology}, - author = {Ristori, G. and Romano, S. and Visconti, A. and Cannoni, S. and Spadaro, M. and Frontali, M. and Pontieri, F. E. and Vanacore, N. and Salvetti, M.}, - month = mar, - year = {2010}, - pages = {839--845}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FHUH2W7Y\\Ristori et al. - 2010 - Riluzole in cerebellar ataxia A randomized, doubl.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B3EKSN68\\839.html:text/html}, -} - -@article{maciver_riluzole_1996, - title = {Riluzole {Anesthesia}: {Use}-{Dependent} {Block} of {Presynaptic} {Glutamate} {Fibers}}, - volume = {85}, - issn = {0003-3022}, - shorttitle = {Riluzole {Anesthesia}}, - url = {https://doi.org/10.1097/00000542-199609000-00023}, - doi = {10.1097/00000542-199609000-00023}, - abstract = {Riluzole (RP 54274) is an experimental benzothiazole with anesthetic properties, but little is known about its synaptic or cellular actions.The authors investigated riluzole effects on synaptic response of CA 1 pyramidal neurons in rat hippocampal brain slices. Electrophysiologic recordings of population spikes (PS), excitatory postsynaptic potentials (EPSP), and fiber volleys were studied. Paired pulse stimulation (120 ms interpulse interval) was used to measure effects on gamma-amino butyric acid (GABA)-mediated synaptic inhibition, and stimulus trains (33 Hz) were used to test for use-dependent effects.Synaptically evoked PS discharge was blocked in a concentration-dependent manner by riluzole (2.0-20 microM), similar to effects produced by other anesthetics. Paired pulse inhibition was not altered by riluzole. In contrast, 20 microM thiopental produced a marked increase in paired pulse inhibition. Riluzole (5.0 microM) produced a 46.6 +/- 19.8\% depression of glutamate-mediated EPSPs, which could account for most of the mate-mediated EPSPs, which could account for most of the depression of PS discharge (54.2 +/- 12.6\%) produced by this concentration. Riluzole produced a 36 +/- 17\% depression of fiver volley amplitudes, which, based on input/output analysis, could completely account for the depression of EPSPs. The depression of fiber volley amplitudes showed a marked use-dependence; the second and subsequent action potentials in a train were progressively depressed by riluzole to a greater extent than the first action potential.Riluzole produced a potent block of excitatory synaptic transmission via depression of presynaptic conduction in glutamatergic nerve fibers. The use-dependent depression observed resembled that produced by some local anesthetics on nerve conduction and sodium channels. The presynaptic action, together with a lack of effect on gamma-amino butyric acid-mediated inhibition, provides a unique mechanism of action for a general anesthetic.}, - number = {3}, - urldate = {2021-06-14}, - journal = {Anesthesiology}, - author = {MacIver, M. Bruce and Amagasu, Shanti M. and Mikulec, Anthony A. and Monroe, Frances A.}, - month = sep, - year = {1996}, - pages = {626--634.}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GD9A2BVV\\MacIver et al. - 1996 - Riluzole Anesthesia Use-Dependent Block of Presyn.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4TM9UY4P\\Riluzole-AnesthesiaUse-Dependent-Block-of.html:text/html}, -} - -@article{hassani_riluzole_2001, - title = {Riluzole reduces hyperactivity of subthalamic neurons induced by unilateral 6-{OHDA} lesion in the rat brain}, - volume = {16}, - copyright = {Copyright © 2001 Movement Disorder Society}, - issn = {1531-8257}, - url = {https://movementdisorders.onlinelibrary.wiley.com/doi/abs/10.1002/mds.1219}, - doi = {10.1002/mds.1219}, - abstract = {An abnormal increase in the activity of neurons of the subthalamic nucleus is a key pathophysiological feature of Parkinson's disease. We sought to determine whether riluzole, a sodium channel inhibitor that interferes with glutamatergic neurotransmission, affects neuronal activity in this brain region. Intravenous administration of riluzole reduced the discharge rate of subthalamic neurons in rats with 6-OHDA-induced lesions of the midbrain. By contrast, no effect was observed in nonlesioned control animals. This property may contribute to the neuroprotective effects of riluzole in animal models of PD through the modulation of the glutamatergic inputs these neurons feedback to nigral dopaminergic neurons. © 2001 Movement Disorder Society.}, - language = {en}, - number = {6}, - urldate = {2021-06-14}, - journal = {Movement Disorders}, - author = {Hassani, Oum-Kaltoum and Mouroux, Mireille and Bohme, Georg Andrees and Stutzmann, Jean-Marie and Féger, Jean}, - year = {2001}, - keywords = {Parkinson's disease, basal ganglia, neuroprotection, excitotoxicity, glutamate release, neurodegenerative diseases, sodium channels blockers}, - pages = {1110--1114}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WHE2MS5U\\Hassani et al. - 2001 - Riluzole reduces hyperactivity of subthalamic neur.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8BLBCUTL\\mds.html:text/html}, -} - -@article{siniscalchi_effects_1997, - title = {Effects of riluzole on rat cortical neurones: an in vitro electrophysiological study}, - volume = {120}, - copyright = {1997 British Pharmacological Society}, - issn = {1476-5381}, - shorttitle = {Effects of riluzole on rat cortical neurones}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1038/sj.bjp.0700905}, - doi = {10.1038/sj.bjp.0700905}, - abstract = {The electrophysiological effects of riluzole on rat prefrontal and frontal cortical neurones were investigated by using both extracellular (field) and intracellular recording techniques in brain slices. Bath applied riluzole (3–200 μm) depressed the cortico-cortical stimulus-evoked field potential in a concentration-related manner (EC50=29.5 μm). Riluzole (3–100 μm) reduced the tonic firing of the neocortical neurones which was caused by intracellular current injection, while it did not have any effect on the resting membrane potential and apparent input resistance of these cells. In the presence of tetrodotoxin (1 μm) and tetraethylammonium (30 mm), the injection of a depolarizing current step generated a calcium spike in the neocortical neurones. Riluzole (30 μm) abolished this calcium-dependent action potential. However, when the amount of the depolarizing current was increased the calcium-dependent regenerative potential was evoked again. The depolarization of the membrane (10–20 mV) caused by brief (8–15 s) bath applications of glutamate (300 μm–1 mm) were not changed in the presence of riluzole (30 μm). It is concluded that riluzole has direct actions on rat neocortical neurones: (a) it blocks the repetitive discharge of sodium action potentials and (b) it increases the threshold for the generation of the calcium spike. These two cellular mechanisms might at least in part account for the depression of the cortico-cortical field potential caused by this drug. British Journal of Pharmacology (1997) 120, 225–230; doi:10.1038/sj.bjp.0700905}, - language = {en}, - number = {2}, - urldate = {2021-06-14}, - journal = {British Journal of Pharmacology}, - author = {Siniscalchi, Antonio and Bonci, Antonello and Mercuri, Nicola B. and Bernardi, Giorgio}, - year = {1997}, - keywords = {epilepsy, brain slices, field potentials, Neuroprotection, repetitive firing, sodium and calcium spikes}, - pages = {225--230}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\G3DCB8J5\\Siniscalchi et al. - 1997 - Effects of riluzole on rat cortical neurones an i.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2PF8NB84\\Siniscalchi et al. - 1997 - Effects of riluzole on rat cortical neurones an i.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\SYC79VEF\\sj.bjp.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\P7KBDLEY\\sj.bjp.html:text/html}, -} - -@article{lamanauskas_riluzole_2008, - title = {Riluzole blocks persistent {Na}+ and {Ca2}+ currents and modulates release of glutamate via presynaptic {NMDA} receptors on neonatal rat hypoglossal motoneurons in vitro}, - volume = {27}, - copyright = {© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd}, - issn = {1460-9568}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.2008.06211.x}, - doi = {10.1111/j.1460-9568.2008.06211.x}, - abstract = {The neuroprotective agent riluzole is used for the symptomatic treatment of motoneuron disease, which strongly affects the brainstem nucleus hypoglossus. The mechanism of action of riluzole was investigated using, as a model, patch-clamp recording from hypoglossal motoneurons of the neonatal rat brainstem slice preparation. In the presence of riluzole (10 µm), theta-rhythm oscillations evoked by nicotine continued even though the persistent inward current (comprising sodium and calcium components) was halved, but they disappeared when the high frequency of spontaneous glutamatergic currents waned. Riluzole fully inhibited the persistent sodium current and partly depressed a tetrodotoxin (TTX)-insensitive slow current antagonized by Mn2+ or Cd2+. Repetitive firing was inhibited by riluzole without changing single action potentials. In the presence of TTX, riluzole depressed miniature glutamatergic currents occurring at high rate. Synaptic transmission with low release probability became sensitive to riluzole if release was stimulated by high potassium solution. Miniature current frequency was depressed by the N-methyl-d-aspartic acid (NMDA) receptor antagonist d-amino-phosphonovaleriate (50 µm), which fully occluded the action of riluzole. As riluzole is a protein kinase C (PKC) inhibitor, the PKC antagonist chelerythrine (2.5 µm) mimicked the effect of riluzole and prevented it. In summary, riluzole blocked the persistent sodium current fully, and the calcium one partly, plus it decreased glutamatergic transmission probably via inhibition of PKC that regulated presynaptic NMDA receptors having a facilitatory effect on glutamate release. Controlling NMDA receptor function and, thus, excitatory transmitter release via modulation of PKC suggests a novel potential target to contrast glutamate excitotoxicity in this motor nucleus.}, - language = {en}, - number = {10}, - urldate = {2021-06-14}, - journal = {European Journal of Neuroscience}, - author = {Lamanauskas, Nerijus and Nistri, Andrea}, - year = {2008}, - keywords = {brainstem, oscillation, riluzole, NMDA receptors, persistent inward current}, - pages = {2501--2514}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GS9LB5ZE\\Lamanauskas and Nistri - 2008 - Riluzole blocks persistent Na+ and Ca2+ currents a.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\J3GR54ZV\\j.1460-9568.2008.06211.html:text/html}, -} - -@article{jehle_effects_2000, - title = {Effects of riluzole on electrically evoked neurotransmitter release}, - volume = {130}, - copyright = {2000 British Pharmacological Society}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1038/sj.bjp.0703424}, - doi = {10.1038/sj.bjp.0703424}, - abstract = {The main purpose of the present study was to investigate the effects of the neuroprotective agent riluzole on the electrically evoked release of [3H]-glutamate ([3H]-Glu) in mouse neocortical slices. The reported selectivity of riluzole for excitatory amino acids was tested in release experiments with further neurotransmitters. Also distinct species, mouse, rat and man were compared. [3H]-Glu was formed endogenously during incubation of slices with [3H]-glutamine ([3H]-Gln). Released [3H]-Glu and tissue [3H]-Glu was separated by anion exchange chromatography. Electrically evoked [3H]-Glu release was strongly diminished by tetrodotoxin (TTX) and Ca2+-withdrawal. Riluzole (100 μM) depressed the release of [3H]-Glu up to 77\% (IC50=19.5 μM). Riluzole was also able to inhibit strongly the electrically evoked release of [3H]-acetylcholine ([3H]-ACh) (at 100 μM by 92\%, IC50=3.3 μM, and [3H]-dopamine ([3H]-DA) (at 32 μM by 72\%, IC50=6.8 μM). However, the release of [3H]-serotonin ([3H]-5-HT) was less diminished (at 100 μM by 53\%, IC50=39.8 μM). Riluzole up to 100 μM did not affect [3H]-noradrenaline ([3H]-NA) release. Between species, i.e. in mouse, rat and human neocortex, no significant differences between the effects of riluzole could be observed. The NMDA-receptor blocker MK-801 (1 μM) and the AMPA/Kainate-receptor blocker NBQX (1 μM) did neither affect the electrically evoked [3H]-ACh release nor its inhibition by riluzole, indicating that effects of riluzole on transmitter release were neither due to modulation of ionotropic Glu receptors, nor due to indirect inhibition of Glu release through these receptors. Taken together, riluzole inhibits the release of distinct neurotransmitters differently, but is not selective for the excitatory amino acid Glu. British Journal of Pharmacology (2000) 130, 1227–1234; doi:10.1038/sj.bjp.0703424}, - language = {en}, - number = {6}, - urldate = {2021-06-14}, - journal = {British Journal of Pharmacology}, - author = {Jehle, T. and Bauer, J. and Blauth, E. and Hummel, A. and Darstein, M. and Freiman, T. M. and Feuerstein, T. J.}, - year = {2000}, - keywords = {rat, riluzole, human, mouse neocortex, neurotransmitter release, Superfusion}, - pages = {1227--1234}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4YYCSVDB\\Jehle et al. - 2000 - Effects of riluzole on electrically evoked neurotr.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\QYG8T7UI\\sj.bjp.html:text/html}, -} - -@article{fumagalli_riluzole_2008, - title = {Riluzole enhances the activity of glutamate transporters {GLAST}, {GLT1} and {EAAC1}}, - volume = {578}, - issn = {0014-2999}, - url = {https://www.sciencedirect.com/science/article/pii/S0014299907011818}, - doi = {10.1016/j.ejphar.2007.10.023}, - abstract = {Riluzole exerts a neuroprotective effect through different mechanisms, including action on glutamatergic transmission. We investigated whether this drug affects glutamate transporter-mediated uptake, using clonal cell lines stably expressing the rat glutamate transporters GLAST, GLT1 or EAAC1. We found that riluzole significantly increased glutamate uptake in a dose-dependent manner; kinetic analysis indicated that the apparent affinity of glutamate for the transporters was significantly increased, with similar effects in the three cell lines. This may facilitate the buffering of excessive extracellular glutamate under pathological conditions suggesting that riluzole's neuroprotective action might be partly mediated by its activating effect on glutamate uptake.}, - language = {en}, - number = {2}, - urldate = {2021-06-14}, - journal = {European Journal of Pharmacology}, - author = {Fumagalli, Elena and Funicello, Marcella and Rauen, Thomas and Gobbi, Marco and Mennini, Tiziana}, - month = jan, - year = {2008}, - keywords = {Riluzole, Cell lines, Glutamate transporter, Synaptosomes, Uptake}, - pages = {171--176}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\QXAB6QMJ\\Fumagalli et al. - 2008 - Riluzole enhances the activity of glutamate transp.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2ZAIK4PM\\S0014299907011818.html:text/html}, -} - -@article{boraud_effects_2000, - title = {Effects of riluzole on the electrophysiological activity of pallidal neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated monkey}, - volume = {281}, - issn = {0304-3940}, - url = {https://www.sciencedirect.com/science/article/pii/S0304394000007801}, - doi = {10.1016/S0304-3940(00)00780-1}, - abstract = {The effect of riluzole administration, an antiglutamatergic compound, on the electrophysiological activity of the pallidal complex of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated monkeys is compared with those induced by two dosages of levodopa (l-DOPA), the first affording the best clinical alleviation, the second sufficient to induce dyskinesias. Both dosages of l-DOPA reduced sharply the firing frequency of globus pallidus pars internalis (GPi) neurons (respectively, 43.8±23.0 and 27.4±20.2 vs. 111.2±31.4 Hz), decreased the percentage of bursting cells (respectively, 60.7 and 50.0 vs. 80.3\%) and augmented the number of regular cells (respectively, 6.5 and 33.0 vs. 4.8\%). Riluzole restored the firing frequency (75.0±26.9 Hz) and the firing pattern of the GPi (39.7\% bursting, 9.5\% regular and 50.8\% irregular). These results suggest that the emergence of dyskinesia may well be due to a modification of the neuronal messages transmitted from the GPi to the motor nuclei of the thalamus. Riluzole would represent an interesting alternative to dopamine therapy in Parkinson's disease since it regularizes firing but does not cause dyskinesia.}, - language = {en}, - number = {2}, - urldate = {2021-06-14}, - journal = {Neuroscience Letters}, - author = {Boraud, Th and Bezard, E and Stutzmann, J. M and Bioulac, B and Gross, C. E}, - month = mar, - year = {2000}, - keywords = {Parkinson’s disease, Dyskinesia, Globus pallidus, Levodopa, Single unit recordings}, - pages = {75--78}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4UUPWMS3\\Boraud et al. - 2000 - Effects of riluzole on the electrophysiological ac.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7QM3ZMTK\\S0304394000007801.html:text/html}, -} - -@article{umemiya_inhibition_1995, - title = {Inhibition by riluzole of glycinergic postsynaptic currents in rat hypoglossal motoneurones}, - volume = {116}, - copyright = {1995 British Pharmacological Society}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1476-5381.1995.tb15128.x}, - doi = {10.1111/j.1476-5381.1995.tb15128.x}, - abstract = {1 Riluzole has been shown to have beneficial effects in motoneurone disease, yet its effect on motoneurones is not known. To address this question, we investigated synaptic modulation by riluzole in hypoglossal motoneurones by recording glycinergic inhibitory postsynaptic currents evoked by stimulation of nearby single interneurones. 2 Glycinergic inhibitory postsynaptic currents were evoked by electrical stimulation of single interneurones and were recorded from visually identified hypoglossal motoneurones. Riluzole (10 μm) inhibited mean amplitude of evoked glycinergic inhibitory postsynaptic currents by 87\%. 3 We found that riluzole suppressed sodium currents in brainstem interneurones by 23.8\%. Riluzole did not modulate barium currents through voltage-activated calcium channels (98\% of control). Therefore, the effect of riluzole on synaptic transmission may be mediated, in part, by stabilizing presynaptic neurones through inhibition of voltage-activated sodium currents. 4 In the presence of tetrodotoxin (0.5 μm), riluzole reduced the frequency (1.2 Hz in control to 0.6 Hz in riluzole) of spontaneous transmitter release recorded in motoneurones. 5 Riluzole was found to have no effect on mean miniature inhibitory postsynaptic current amplitude, therefore the reduction in spontaneous transmitter release cannot be due to an action on postsynaptic glycine receptors. 6 We conclude that riluzole inhibits synaptic transmission presynaptically, independent of a reduction in the excitation of presynaptic neurones.}, - language = {en}, - number = {8}, - urldate = {2021-06-14}, - journal = {British Journal of Pharmacology}, - author = {Umemiya, Masashi and Berger, Albert J.}, - year = {1995}, - keywords = {brainstem, glycine, amyotrophic lateral sclerosis, miniature i.p.s.cs, synaptic modulation, voltage-activated calcium channel, Voltage-activated sodium channel}, - pages = {3227--3230}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BLN8P7VC\\Umemiya and Berger - 1995 - Inhibition by riluzole of glycinergic postsynaptic.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VLMQUN6Y\\j.1476-5381.1995.tb15128.html:text/html}, -} - -@article{romano_riluzole_2015, - title = {Riluzole in patients with hereditary cerebellar ataxia: a randomised, double-blind, placebo-controlled trial}, - volume = {14}, - issn = {1474-4422}, - shorttitle = {Riluzole in patients with hereditary cerebellar ataxia}, - url = {https://www.sciencedirect.com/science/article/pii/S147444221500201X}, - doi = {10.1016/S1474-4422(15)00201-X}, - abstract = {Background -Our previous study in patients with cerebellar ataxias of different causes showed significant benefit of riluzole after 8 weeks. We aimed to confirm these results in patients with spinocerebellar ataxia or Friedreich's ataxia in a 1-year trial. -Methods -Patients with spinocerebellar ataxia or Friedreich's ataxia (2:1 ratio) from three Italian neurogenetic units were enrolled in this multicentre, double-blind, placebo-controlled trial, and randomly assigned to riluzole (50 mg orally, twice daily) or placebo for 12 months. The randomisation list was computer-generated and a centralised randomisation system was implemented. Participants and assessing neurologists were masked to treatment allocation. The primary endpoint was the proportion of patients with improved Scale for the Assessment and Rating of Ataxia (SARA) score (a drop of at least one point) at 12 months. An intention-to-treat analysis was done. This trial is registered at ClinicalTrials.gov, number NCT01104649. -Findings -Between May 22, 2010, and Feb 25, 2013, 60 patients were enrolled. Two patients in the riluzole group and three in the placebo group withdrew their consent before receiving treatment, so the intention-to-treat analysis was done on 55 patients (19 with spinocerebellar ataxia and nine with Friedreich's ataxia in the riluzole group, and 19 with spinocerebellar ataxia and eight with Friedreich's ataxia in the placebo group). The proportion with decreased SARA score was 14 (50\%) of 28 patients in the riluzole group versus three (11\%) of 27 in the placebo group (OR 8·00, 95\% CI 1·95–32·83; p=0·002). No severe adverse events were recorded. In the riluzole group, two patients had an increase in liver enzymes (less than two times above normal limits). In two participants in the riluzole group and two participants in the placebo group, sporadic mild adverse events were reported. -Interpretation -Our findings lend support to the idea that riluzole could be a treatment for cerebellar ataxia. Longer studies and disease-specific trials are needed to confirm whether these findings can be applied in clinical practice. -Funding -Agenzia Italiana del Farmaco.}, - language = {en}, - number = {10}, - urldate = {2021-06-14}, - journal = {The Lancet Neurology}, - author = {Romano, Silvia and Coarelli, Giulia and Marcotulli, Christian and Leonardi, Luca and Piccolo, Francesca and Spadaro, Maria and Frontali, Marina and Ferraldeschi, Michela and Vulpiani, Maria Chiara and Ponzelli, Federica and Salvetti, Marco and Orzi, Francesco and Petrucci, Antonio and Vanacore, Nicola and Casali, Carlo and Ristori, Giovanni}, - month = oct, - year = {2015}, - pages = {985--991}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RLHWJKPJ\\Romano et al. - 2015 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\WNAERBYR\\Romano et al. - 2015 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\BRRU6MK6\\S147444221500201X.html:text/html;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\J3W2RKZC\\S147444221500201X.html:text/html}, -} - -@article{abbasi_power_2017, - title = {Power {Spectral} {Density} {Analysis} of {Purkinje} {Cell} {Tonic} and {Burst} {Firing} {Patterns} {From} a {Rat} {Model} of {Ataxia} and {Riluzole} {Treated}}, - volume = {8}, - issn = {2008-126X}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5396175/}, - doi = {10.15412/J.BCN.03080108}, - abstract = {Introduction: -Purkinje Cell (PC) output displays a complex firing pattern consisting of high frequency sodium spikes and low frequency calcium spikes, and disruption in this firing behavior may contribute to cerebellar ataxia. Riluzole, neuroprotective agent, has been demonstrated to have neuroprotective effects in cerebellar ataxia. Here, the spectral analysis of PCs firing in control, 3-acetylpyridine (3-AP), neurotoxin agent, treated alone and riluzole plus 3-AP treated were investigated to determine changes in the firing properties. Difference in the power spectra of tonic and burst firing was assessed. Furthermore, the role of calcium-activated potassium channels in the power spectra was evaluated. - -Methods: -Analysis was performed using Matlab. Power spectral density (PSD) of PCs output were obtained. Peak frequencies were extracted from the spectrum and statistical comparisons were done. In addition, a multi-compartment computational model of a Purkinje cell was used. This computational stimulation allowed us to study the changes in the power spectral density of the PC output as a result of alteration in ion channels. - -Results: -Spectral analysis showed that in the spectrum of tonic and burst firing pattern only high sodium frequency and low calcium frequency was seen, respectively. In addition, there was a significant difference between the frequency components of PCs firing obtained from normal, ataxia and riluzole treated rats. Results indicated that sodium firing frequency of normal, ataxic and treated PCs occurred in approximate frequency of 22.53±5.49, 6.46±0.23, and 31.34±4.07 Hz, respectively; and calcium frequency occurred in frequency of 4.22±2.02, 1.52±1.19, and 3.88±1.37 Hz, respectively. The simulation results demonstrated that blockade of calcium-activated potassium channels in the PC model changed the PSD of the PC model firing activity. This change was similar to PSD changes in ataxia condition. - -Conclusion: -These alterations in the spectrum of PC output may be a basis for developing possible new treatment strategies to improve cerebellar ataxia.}, - number = {1}, - urldate = {2021-06-14}, - journal = {Basic and Clinical Neuroscience}, - author = {Abbasi, Samira and Abbasi, Ataollah and Sarbaz, Yashar and Janahmadi, Mahyar}, - month = jan, - year = {2017}, - pages = {61--68}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\M3AESXWI\\Abbasi et al. - 2017 - Power Spectral Density Analysis of Purkinje Cell T.pdf:application/pdf}, -} - -@article{abbasi_computational_2013, - title = {Computational insights into the neuroprotective action of riluzole on 3-acetylpyridine-induced ataxia in rats}, - volume = {15}, - issn = {2228-5806}, - abstract = {OBJECTIVE: Intra-peritoneal administration of riluzole has been shown to preserve the membrane properties and firing characteristics of Purkinje neurons in a rat model of cerebellar ataxia induced by 3-acetylpyridine (3-AP). However, the exact mechanism(s) by which riluzole restores the normal electrophysiological properties of Purkinje neurons is not completely understood. Changes in the conductance of several ion channels, including the BK channels, have been proposed as a neuro protective target of riluzole. In this study, the possible cellular effects of riluzole on Purkinje cells from 3-AP-induced ataxic rats that could be responsible for its neuro protective action have been investigated by computer simulations. -MATERIALS AND METHODS: This is a computational stimulation study. The simulation environment enabled a change in the properties of the specific ion channels as the possible mechanism of action of riluzole. This allowed us to study the resulted changes in the firing activity of Purkinje cells without concerns about its other effects and interfering parameters in the experiments. Simulations were performed in the NEURON environment (Version 7.1) in a time step of 25 μs; analyses were conducted using MATLAB r2010a (The Mathworks). Data were given as mean ± SEM. Statistical analyses were performed by the student's t test, and differences were considered significant if p{\textless} 0.05. -RESULTS: The computational findings demonstrated that modulation of an individual ion channel current, as suggested by previous experimental studies, should not be considered as the only possible target for the neuro protective effects of riluzole to restore the normal firing activity of Purkinje cells from ataxic rats. -CONCLUSION: Changes in the conductance of several potassium channels, including voltage- gated potassium (Kv1, Kv4) and big Ca(2+)-activated K(+) (BK) channels may be responsible for the neuro protective effect of riluzole against 3-AP induced alterations in the firing properties of Purkinje cells in a rat model of ataxia.}, - language = {eng}, - number = {2}, - journal = {Cell Journal}, - author = {Abbasi, Samira and Edrisi, Mehdi and Mahnam, Amin and Janahmadi, Mahyar}, - year = {2013}, - keywords = {Potassium Channels, Riluzole, Ataxia, Neuroprotection, Computer Simulation}, - pages = {98--107}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BGTFITYK\\Abbasi et al. - 2013 - Computational Insights into The Neuroprotective Ac.pdf:application/pdf}, -} - -@misc{noauthor_inhibitory_nodate, - title = {Inhibitory effects of riluzole on the spontaneous discharges of chronically compressed {A}-type dorsal root ganglion neurons with different firing patterns--《{Chinese} {Journal} of {Neuroanatomy}》2010年03期}, - url = {https://en.cnki.com.cn/Article_en/CJFDTotal-SJJP201003001.htm}, - urldate = {2021-06-14}, - file = {Inhibitory effects of riluzole on the spontaneous discharges of chronically compressed A-type dorsal root ganglion neurons with different firing patterns--《Chinese Journal of Neuroanatomy》2010年03期:C\:\\Users\\nilsk\\Zotero\\storage\\VKY96WEF\\CJFDTotal-SJJP201003001.html:text/html;Inhibitory effects of riluzole on the spontaneous discharges of chronically compressed A-type dorsal root ganglion neurons with different firing patterns--《Chinese Journal of Neuroanatomy》2010年03期:C\:\\Users\\nilsk\\Zotero\\storage\\HQH2YRR5\\CJFDTotal-SJJP201003001.html:text/html}, -} - -@article{schuster_effect_2012, - title = {Effect of prolonged riluzole exposure on cultured motoneurons in a mouse model of {ALS}}, - volume = {107}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00714.2011}, - doi = {10.1152/jn.00714.2011}, - abstract = {Riluzole is the only FDA-approved drug to treat amyotrophic lateral sclerosis, but its long-term effects on motoneurons are unknown. Therefore, we treated primary mouse spinal cord cultures with 2 μM riluzole for 4–9 days and then used whole cell patch clamp to record the passive and active properties of both wild-type and SOD1G93A motoneurons. At this concentration, riluzole blocks {\textgreater}50\% of the sodium component of a persistent inward current that plays a major role in determining motoneuron excitability. Prolonged riluzole treatment significantly decreased the amplitude of the persistent inward current. This effect was specific for SOD1G93A motoneurons, where the amplitude decreased by 55.4\%. In addition, prolonged treatment hyperpolarized the resting membrane potential as well as the voltage onset and voltage maximum of the persistent inward current (∼2–3 mV in each case). These effects appeared to offset one another and resulted in no change in the firing properties. In a subset of cells, acute reapplication of 2 μM riluzole during the recording decreased repetitive firing and the persistent inward current, which is consistent with the normal effects of riluzole. The downregulation of the persistent inward current in response to prolonged riluzole administration is in contrast to the strong upregulation of this same current after descending neuromodulatory drive to the cord is lost following spinal injury. This dichotomy suggests that decreased activation of G protein-coupled pathways can induce upregulation in the persistent inward current but that direct channel block is ineffective.}, - number = {1}, - urldate = {2021-06-14}, - journal = {Journal of Neurophysiology}, - author = {Schuster, J. E. and Fu, R. and Siddique, T. and Heckman, C. J.}, - month = jan, - year = {2012}, - pages = {484--492}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\J64GVUAM\\Schuster et al. - 2012 - Effect of prolonged riluzole exposure on cultured .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\T524IHA6\\jn.00714.html:text/html}, -} - -@article{han_riluzole_2015, - title = {Riluzole is a {Promising} {Pharmacological} {Inhibitor} of {Bilirubin}-{Induced} {Excitotoxicity} in the {Ventral} {Cochlear} {Nucleus}}, - volume = {21}, - copyright = {© 2014 John Wiley \& Sons Ltd}, - issn = {1755-5949}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/cns.12355}, - doi = {10.1111/cns.12355}, - abstract = {Background and purpose Bilirubin encephalopathy as a result of hyperbilirubinemia is a devastating neurological disorder that occurs mostly in the neonatal period. To date, no effective drug treatment is available. Glutamate-mediated excitotoxicity is likely an important factor causing bilirubin encephalopathy. Thus, drugs suppressing the overrelease of glutamate may protect the brain against bilirubin excitotoxicity. Riluzole is a prescription drug known for its antiglutamatergic function. This study was conducted in the rat's ventral cochlear nucleus, a structure highly sensitive to bilirubin toxicity, to find whether riluzole can be used to inhibit bilirubin toxicity. Experimental approach Electrophysiology changes were detected by perforated patch clamp technique. Calcium imaging using Rhod-2-AM as an indicator was used to study the intracellular calcium. Cell apoptosis and necrosis were measured by PI/Hoechst staining. Key results In the absence of bilirubin, riluzole effectively decreased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) and suppressed neuronal firing but did not change the amplitude of sEPSC and glutamate-activated currents (IGlu). Moreover, riluzole inhibited bilirubin-induced increases in the frequency of sEPSC and neuronal firing. Riluzole could prevent the bilirubin-induced increase in intracellular calcium, mediated by AMPA and NMDA receptors. Furthermore, riluzole significantly reduced bilirubin-induced cell death. Conclusions and implications These data suggest that riluzole can protect neurons in the ventral cochlear nucleus from bilirubin-induced hyperexcitation and excitotoxicity through reducing presynaptic glutamate release.}, - language = {en}, - number = {3}, - urldate = {2021-06-14}, - journal = {CNS Neuroscience \& Therapeutics}, - author = {Han, Guo-Ying and Li, Chun-Yan and Shi, Hai-Bo and Wang, Ji-Ping and Su, Kai-Ming and Yin, Xin-Lu and Yin, Shan-Kai}, - year = {2015}, - keywords = {Riluzole, Bilirubin, Bilirubin encephalopathy, Excitatory postsynaptic current (EPSC), Excitotoxicity, Spontaneous action potential}, - pages = {262--270}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\PQALWVNG\\Han et al. - 2015 - Riluzole is a Promising Pharmacological Inhibitor .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\NMQETZQY\\cns.html:text/html}, -} - -@article{stutzmann_riluzole_1991, - title = {Riluzole prevents hyperexcitability produced by the mast cell degranulating peptide and dendrotoxin {I} in the rat}, - volume = {193}, - issn = {0014-2999}, - url = {https://www.sciencedirect.com/science/article/pii/001429999190040W}, - doi = {10.1016/0014-2999(91)90040-W}, - abstract = {Using electroencephalographic (EEG) recordings in freely moving rats and extracellular neuronal firing-rate recordings in hippocampal slices, we examined the effects of riluzole (RP 54274), a compound with anti-glutamate properties, against the convulsive seizures and the cellular hyperexcitability produced by the mast-cell degranulating peptide (MCD), dendrotoxin I (DTXi) and 4-aminopyridine (4-AP). I.c.v. administration of riluzole (10 nmol) prevented the seizures induced by MCD, and to a lesser extent those due to DIXi, whilst leaving 4-AP seizures unaffected. This effect was also present after oral administration of the compound (4 mg kg−1) and lasted for approximately 6 h. Electrophysiological recordings in vitro confirmed that riluzole dose dependently and reversibly abolished the sustained increase in firing rate induced by both MCD and DTXi in the hippocampus. These results indicate that the anti-epileptic spectrum of riluzole in this model has similarities with, but is not identical to, that of classical potassium channel openers, and differs from that of calcium channel blockers or other glutamate antagonists such as D(−)-2-amino-5-phosphono-valeric acid. However, since MCD releases glutamate, the preventive effect of riluzole in this model may involve direct or indirect interaction with glutamatergic processes.}, - language = {en}, - number = {2}, - urldate = {2021-06-14}, - journal = {European Journal of Pharmacology}, - author = {Stutzmann, Jean-Marie and Böhme, Georg Andrees and Gandolfo, Gabriel and Gottesmann, Claude and Lafforgue, Joséphine and Blanchard, Jean-Charles and Laduron, Pierre M. and Lazdunski, Michel}, - month = feb, - year = {1991}, - keywords = {Electroencephalography, Anticonvulsants, Antiglutamate, Dendrotoxin I (DTX), Hippocampal slices, Mast-cell degranulating peptide (MCD)}, - pages = {223--229}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P7BLR8WL\\Stutzmann et al. - 1991 - Riluzole prevents hyperexcitability produced by th.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\6E5FCHQT\\001429999190040W.html:text/html}, -} - -@article{wang_riluzole-induced_2008, - title = {Riluzole-induced block of voltage-gated {Na}+ current and activation of {BKCa} channels in cultured differentiated human skeletal muscle cells}, - volume = {82}, - issn = {0024-3205}, - url = {https://www.sciencedirect.com/science/article/pii/S0024320507007813}, - doi = {10.1016/j.lfs.2007.10.015}, - abstract = {Riluzole is known to be of therapeutic use in the management of amyotrophic lateral sclerosis. In this study, we investigated the effects of riluzole on ion currents in cultured differentiated human skeletal muscle cells (dHSkMCs). Western blotting revealed the protein expression of α-subunits for both large-conductance Ca2+-activated K+ (BKCa) channel and Na+ channel (Nav1.5) in these cells. Riluzole could reduce the frequency of spontaneous beating in dHSkMCs. In whole-cell configuration, riluzole suppressed voltage-gated Na+ current (INa) in a concentration-dependent manner with an IC50 value of 2.3 μM. Riluzole (10 μM) also effectively increased Ca2+-activated K+ current (IK(Ca)) which could be reversed by iberiotoxin (200 nM) and paxilline (1 μM), but not by apamin (200 nM). In inside-out patches, when applied to the inside of the cell membrane, riluzole (10 μM) increased BKCa-channel activity with a decrease in mean closed time. Simulation studies also unraveled that both decreased conductance of INa and increased conductance of IK(Ca) utilized to mimic riluzole actions in skeletal muscle cells could combine to decrease the amplitude of action potentials and increase the repolarization of action potentials. Taken together, inhibition of INa and stimulation of BKCa-channel activity caused by this drug are partly, if not entirely, responsible for its muscle relaxant actions in clinical setting.}, - language = {en}, - number = {1}, - urldate = {2021-06-14}, - journal = {Life Sciences}, - author = {Wang, Ya-Jean and Lin, Ming-Wei and Lin, An-An and Wu, Sheng-Nan}, - month = jan, - year = {2008}, - keywords = {Riluzole, Ca-activated K current, Human skeletal muscle cell, Large-conductance Ca-activated K channel, Voltage-gated Na current}, - pages = {11--20}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\HQ7FKRB2\\Wang et al. - 2008 - Riluzole-induced block of voltage-gated Na+ curren.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WEI2C3EK\\S0024320507007813.html:text/html}, -} - -@article{saute_riluzole_2016, - title = {Riluzole in patients with hereditary cerebellar ataxia}, - volume = {15}, - issn = {1474-4422}, - url = {https://www.sciencedirect.com/science/article/pii/S1474442216001289}, - doi = {10.1016/S1474-4422(16)00128-9}, - language = {en}, - number = {8}, - urldate = {2021-06-14}, - journal = {The Lancet Neurology}, - author = {Saute, Jonas Alex Morales and Jardim, Laura Bannach}, - month = jul, - year = {2016}, - pages = {788--789}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5VRI4G3W\\Saute and Jardim - 2016 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\QYGA23U7\\S1474442216001289.html:text/html}, -} - -@article{wood_repurposing_2015, - title = {Repurposing riluzole to treat hereditary cerebellar ataxia}, - volume = {11}, - copyright = {2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.}, - issn = {1759-4766}, - url = {https://www.nature.com/articles/nrneurol.2015.161}, - doi = {10.1038/nrneurol.2015.161}, - language = {en}, - number = {10}, - urldate = {2021-06-14}, - journal = {Nature Reviews Neurology}, - author = {Wood, Heather}, - month = oct, - year = {2015}, - pages = {547--547}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UWUF4E4V\\Wood - 2015 - Repurposing riluzole to treat hereditary cerebella.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\LD88H9FG\\nrneurol.2015.html:text/html}, -} - -@article{romano_riluzole_2016, - title = {Riluzole in patients with hereditary cerebellar ataxia – {Authors}' reply}, - volume = {15}, - issn = {1474-4422}, - url = {https://www.sciencedirect.com/science/article/pii/S1474442216001174}, - doi = {10.1016/S1474-4422(16)00117-4}, - language = {en}, - number = {8}, - urldate = {2021-06-14}, - journal = {The Lancet Neurology}, - author = {Romano, Silvia and Coarelli, Giulia and Vanacore, Nicola and Salvetti, Marco and Ristori, Giovanni}, - month = jul, - year = {2016}, - pages = {789}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\X4B8HVG9\\Romano et al. - 2016 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5GLFU8FA\\Romano et al. - 2016 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\BUDE2WGD\\S1474442216001174.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ZJZTKXVZ\\fulltext.html:text/html}, -} - -@article{andreev_synthesis_2020, - title = {Synthesis and {Analysis} of the {Fixed}-{Point} {Hodgkin}–{Huxley} {Neuron} {Model}}, - volume = {9}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - url = {https://www.mdpi.com/2079-9292/9/3/434}, - doi = {10.3390/electronics9030434}, - abstract = {In many tasks related to realistic neurons and neural network simulation, the performance of desktop computers is nowhere near enough. To overcome this obstacle, researchers are developing FPGA-based simulators that naturally use fixed-point arithmetic. In these implementations, little attention is usually paid to the choice of numerical method for the discretization of the continuous neuron model. In our study, the implementation accuracy of a neuron described by simplified Hodgkin\–Huxley equations in fixed-point arithmetic is under investigation. The principle of constructing a fixed-point neuron model with various numerical methods is described. Interspike diagrams and refractory period analysis are used for the experimental study of the synthesized discrete maps of the simplified Hodgkin\–Huxley neuron model. We show that the explicit midpoint method is much better suited to simulate the neuron dynamics on an FPGA than the explicit Euler method which is in common use.}, - language = {en}, - number = {3}, - urldate = {2021-06-17}, - journal = {Electronics}, - author = {Andreev, Valery and Ostrovskii, Valerii and Karimov, Timur and Tutueva, Aleksandra and Doynikova, Elena and Butusov, Denis}, - month = mar, - year = {2020}, - keywords = {Hodgkin–Huxley model, discrete chaotic systems, fixed-point arithmetic, FPGA, nonlinear dynamics, scaling}, - pages = {434}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3KVT9AH8\\Andreev et al. - 2020 - Synthesis and Analysis of the Fixed-Point Hodgkin–.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\I7XHIMLY\\434.html:text/html}, -} - -@phdthesis{jacquerie_sensitivity_2018, - title = {Sensitivity and robustness analysis of thalamic neuron models at the cellular and network levels}, - url = {https://orbi.uliege.be/handle/2268/246896}, - language = {en}, - urldate = {2021-06-17}, - school = {Université de Liège, ​Liège, ​​Belgique}, - author = {Jacquerie, Kathleen}, - month = jun, - year = {2018}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2WFX7TLC\\246896.html:text/html}, -} - -@article{schweighofer_electrophysiological_1999, - title = {Electrophysiological {Properties} of {Inferior} {Olive} {Neurons}: {A} {Compartmental} {Model}}, - volume = {82}, - issn = {0022-3077}, - shorttitle = {Electrophysiological {Properties} of {Inferior} {Olive} {Neurons}}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.1999.82.2.804}, - doi = {10.1152/jn.1999.82.2.804}, - abstract = {As a step in exploring the functions of the inferior olive, we constructed a biophysical model of the olivary neurons to examine their unique electrophysiological properties. The model consists of two compartments to represent the known distribution of ionic currents across the cell membrane, as well as the dendritic location of the gap junctions and synaptic inputs. The somatic compartment includes a low-threshold calcium current (ICa\_l), an anomalous inward rectifier current (Ih), a sodium current (INa), and a delayed rectifier potassium current (IK\_dr). The dendritic compartment contains a high-threshold calcium current (ICa\_h), a calcium-dependent potassium current (IK\_Ca), and a current flowing into other cells through electrical coupling (Ic). First, kinetic parameters for these currents were set according to previously reported experimental data. Next, the remaining free parameters were determined to account for both static and spiking properties of single olivary neurons in vitro. We then performed a series of simulated pharmacological experiments using bifurcation analysis and extensive two-parameter searches. Consistent with previous studies, we quantitatively demonstrated the major role ofICa\_l in spiking excitability. In addition,Ih had an important modulatory role in the spike generation and period of oscillations, as previously suggested by Bal and McCormick. Finally, we investigated the role of electrical coupling in two coupled spiking cells. Depending on the coupling strength, the hyperpolarization level, and theICa\_l and Ihmodulation, the coupled cells had four different synchronization modes: the cells could be in-phase, phase-shifted, or anti-phase or could exhibit a complex desynchronized spiking mode. Hence these simulation results support the counterintuitive hypothesis that electrical coupling can desynchronize coupled inferior olive cells.}, - number = {2}, - urldate = {2021-06-17}, - journal = {Journal of Neurophysiology}, - author = {Schweighofer, Nicolas and Doya, Kenji and Kawato, Mitsuo}, - month = aug, - year = {1999}, - pages = {804--817}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\99Z4IGZW\\Schweighofer et al. - 1999 - Electrophysiological Properties of Inferior Olive .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\APYUXNQI\\jn.1999.82.2.html:text/html}, -} - -@article{verma_computational_2020, - title = {Computational analysis of a {9D} model for a small {DRG} neuron}, - volume = {48}, - issn = {1573-6873}, - url = {https://doi.org/10.1007/s10827-020-00761-6}, - doi = {10.1007/s10827-020-00761-6}, - abstract = {Small dorsal root ganglion (DRG) neurons are primary nociceptors which are responsible for sensing pain. Elucidation of their dynamics is essential for understanding and controlling pain. To this end, we present a numerical bifurcation analysis of a small DRG neuron model in this paper. The model is of Hodgkin-Huxley type and has 9 state variables. It consists of a Nav1.7 and a Nav1.8 sodium channel, a leak channel, a delayed rectifier potassium, and an A-type transient potassium channel. The dynamics of this model strongly depend on the maximal conductances of the voltage-gated ion channels and the external current, which can be adjusted experimentally. We show that the neuron dynamics are most sensitive to the Nav1.8 channel maximal conductance (\${\textbackslash}overline \{g\}\_\{1.8\}\$). Numerical bifurcation analysis shows that depending on \${\textbackslash}overline \{g\}\_\{1.8\}\$and the external current, different parameter regions can be identified with stable steady states, periodic firing of action potentials, mixed-mode oscillations (MMOs), and bistability between stable steady states and stable periodic firing of action potentials. We illustrate and discuss the transitions between these different regimes. We further analyze the behavior of MMOs. As the external current is decreased, we find that MMOs appear after a cyclic limit point. Within this region, bifurcation analysis shows a sequence of isolated periodic solution branches with one large action potential and a number of small amplitude peaks per period. For decreasing external current, the number of small amplitude peaks is increasing and the distance between the large amplitude action potentials is growing, finally tending to infinity and thereby leading to a stable steady state. A closer inspection reveals more complex concatenated MMOs in between these periodic MMO branches, forming Farey sequences. Lastly, we also find small solution windows with aperiodic oscillations which seem to be chaotic. The dynamical patterns found here—as consequences of bifurcation points regulated by different parameters—have potential translational significance as repetitive firing of action potentials imply pain of some form and intensity; manipulating these patterns by regulating the different parameters could aid in investigating pain dynamics.}, - language = {en}, - number = {4}, - urldate = {2021-06-17}, - journal = {Journal of Computational Neuroscience}, - author = {Verma, Parul and Kienle, Achim and Flockerzi, Dietrich and Ramkrishna, Doraiswami}, - month = nov, - year = {2020}, - pages = {429--444}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8VBIHVFQ\\Verma et al. - 2020 - Computational analysis of a 9D model for a small D.pdf:application/pdf}, -} - -@article{arhem_channel_2006, - title = {Channel {Density} {Regulation} of {Firing} {Patterns} in a {Cortical} {Neuron} {Model}}, - volume = {90}, - issn = {0006-3495}, - url = {https://www.sciencedirect.com/science/article/pii/S0006349506726169}, - doi = {10.1529/biophysj.105.077032}, - abstract = {Modifying the density and distribution of ion channels in a neuron (by natural up- and downregulation or by pharmacological intervention or by spontaneous mutations) changes its activity pattern. In this investigation we analyzed how the impulse patterns are regulated by the density of voltage-gated channels in a neuron model based on voltage-clamp measurements of hippocampal interneurons. At least three distinct oscillatory patterns, associated with three distinct regions in the Na-K channel density plane, were found. A stability analysis showed that the different regions are characterized by saddle-node, double-orbit, and Hopf-bifurcation threshold dynamics, respectively. Single, strongly graded action potentials occur in an area outside the oscillatory regions, but less graded action potentials occur together with repetitive firing over a considerable range of channel densities. The relationship found here between channel densities and oscillatory behavior may partly explain the difference between the principal spiking patterns previously described for crab axons (class 1 and 2) and cortical neurons (regular firing and fast spiking).}, - language = {en}, - number = {12}, - urldate = {2021-06-17}, - journal = {Biophysical Journal}, - author = {{\AA}rhem, P. and Klement, G. and Blomberg, C.}, - month = jun, - year = {2006}, - pages = {4392--4404}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SLH52KA5\\Århem et al. - 2006 - Channel Density Regulation of Firing Patterns in a.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\3DT52SAC\\S0006349506726169.html:text/html}, -} - -@article{tawfik_nonlinear_1994, - title = {Nonlinear parameter estimation by linear association: {Application} to a five-parameter passive neuron model}, - volume = {41}, - issn = {1558-2531}, - shorttitle = {Nonlinear parameter estimation by linear association}, - doi = {10.1109/10.293221}, - abstract = {Linear associative memories (LAM) have been intensely used in the areas of pattern recognition and parallel processing for the past two decades. Application of LAM to nonlinear parameter estimation, however, has only been recently attempted. The process consists in converting the nonlinear function in the parameters into a set of linear algebraic equations. The nature of the linearized system and the factors influencing the accuracy of the parameter estimates have not yet been fully investigated. Here, LAM is applied to a nonlinear five-parameter model of the neuron. Ill-conditioning, which is often exhibited in LAM, is treated with the method of regularization as well as by the singular value decomposition (SVD). Simulation results indicate that the parameters estimated by LAM exhibit a remarkable robustness against additive white noise in comparison with the classical gradient optimization technique. Moreover, it is shown that regularization can be superior to SVD under certain conditions. The authors' results suggest that LAM can be used both as a noise reduction technique and as a stand-alone nonlinear parameter estimation algorithm. The comparison between LAM and a gradient technique show that, for this estimation problem, the LAM method can give more reliable estimates. Further improvements in estimation quality may still be achieved by the use of other forms of regularizing functions.{\textless}{\textgreater}}, - number = {5}, - journal = {IEEE Transactions on Biomedical Engineering}, - author = {Tawfik, B. and Durand, D.M.}, - month = may, - year = {1994}, - keywords = {Neurons, Additive white noise, Associative memory, Noise reduction, Noise robustness, Nonlinear equations, Parallel processing, Parameter estimation, Pattern recognition, Singular value decomposition}, - pages = {461--469}, - file = {IEEE Xplore Abstract Record:C\:\\Users\\nilsk\\Zotero\\storage\\DJST9XTX\\293221.html:text/html}, -} - -@article{weaver_sensitivity_2010, - title = {Sensitivity analyses of a precerebellar neuron model predict a morphologic mechanism for plasticity of neuronal function}, - volume = {11}, - issn = {1471-2202}, - url = {https://doi.org/10.1186/1471-2202-11-S1-P137}, - doi = {10.1186/1471-2202-11-S1-P137}, - number = {1}, - urldate = {2021-06-17}, - journal = {BMC Neuroscience}, - author = {Weaver, Christina M. and Yadav, Aniruddha and Gamkrelidze, Georgi N. and Baker, Robert}, - month = jul, - year = {2010}, - keywords = {Dendritic Morphology, Distal Dendrite, Efferent Copy, Sensitive Direction, Velocity Motor}, - pages = {P137}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\MV9CZGDV\\Weaver et al. - 2010 - Sensitivity analyses of a precerebellar neuron mod.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\RMG5HTZR\\1471-2202-11-S1-P137.html:text/html}, -} - -@phdthesis{boatin_characterization_2005, - type = {Thesis}, - title = {Characterization of neuron models}, - url = {https://smartech.gatech.edu/handle/1853/36536}, - abstract = {Modern neuron models are large, complex entities. The ability to better simulate these complex models has been iven by the development of ever more powerful and cheap computers. The capacity to manage and understand the models has lagged behind improvements in simulation ability almost from the inception of neuron modeling. Despite the computing power currently available, more powerful simulation platforms and strategies are needed to cope with current and next generation neuron models. -This thesis develops methodologies aimed at better characterizing motoneuron models. The hypothesis presented is that relationships between model outputs in addition to the relationships between model inputs (parameters) and outputs (behaviors) provide a characteristic description of the model that describes the model in a more useful way than just model behaviors. This description can be used to compare a model to different implementations of the same motoneuron and to experiment data. -Data mining and data reduction techniques were used to process the data. Principal component analysis was used to indicate a significant, consistent reduction in dimensionality in an intermediate, mechanistic layer between model inputs and outputs. This layer represents the non-linear relationships between input and output, implying that if the non-linear relationships of a model were better understood and accessible, a model could be manipulated by varying the mechanism layer members, or rather the model parameters that primarily affect a mechanism layer member. - Hierarchical cluster analysis showed similarity between sensitivity analyses data from models with random parameter sets. A main cluster represented the main region of model behavior with outlying clusters representing non-physiological behavior. This indicates that sensitivity analysis data is a good candidate for a model signature. -The results demonstrate the usefulness of cluster analysis in identifying the similarities between data used as a model characterization metric or model signature. Its application is also valuable in identifying the main region of useful activity of a model, thus helping to identify a potential 'average' parameter set. Furthermore, factor analysis also proves functional in identifying members of the mechanism layer as well as the degree to which model outputs are affected by these members.}, - language = {en\_US}, - urldate = {2021-06-17}, - school = {Georgia Institute of Technology}, - author = {Boatin, William}, - month = jul, - year = {2005}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Q9VRGPQV\\36536.html:text/html}, -} - -@article{golowasch_failure_2002, - title = {Failure of {Averaging} in the {Construction} of a {Conductance}-{Based} {Neuron} {Model}}, - volume = {87}, - issn = {0022-3077}, - url = {https://journals.physiology.org/doi/full/10.1152/jn.00412.2001}, - doi = {10.1152/jn.00412.2001}, - abstract = {Parameters for models of biological systems are often obtained by averaging over experimental results from a number of different preparations. To explore the validity of this procedure, we studied the behavior of a conductance-based model neuron with five voltage-dependent conductances. We randomly varied the maximal conductance of each of the active currents in the model and identified sets of maximal conductances that generate bursting neurons that fire a single action potential at the peak of a slow membrane potential depolarization. A model constructed using the means of the maximal conductances of this population is not itself a one-spike burster, but rather fires three action potentials per burst. Averaging fails because the maximal conductances of the population of one-spike bursters lie in a highly concave region of parameter space that does not contain its mean. This demonstrates that averages over multiple samples can fail to characterize a system whose behavior depends on interactions involving a number of highly variable components.}, - number = {2}, - urldate = {2021-06-17}, - journal = {Journal of Neurophysiology}, - author = {Golowasch, Jorge and Goldman, Mark S. and Abbott, L. F. and Marder, Eve}, - month = feb, - year = {2002}, - pages = {1129--1131}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3XUIS8H6\\Golowasch et al. - 2002 - Failure of Averaging in the Construction of a Cond.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\3PM5WXVV\\jn.00412.html:text/html}, -} - -@article{tabak_parameter_2000, - title = {Parameter {Estimation} {Methods} for {Single} {Neuron} {Models}}, - volume = {9}, - issn = {1573-6873}, - url = {https://doi.org/10.1023/A:1026531603628}, - doi = {10.1023/A:1026531603628}, - abstract = {With the advancement in computer technology, it has become possible to fit complex models to neuronal data. In this work, we test how two methods can estimate parameters of simple neuron models (passive soma) to more complex ones (neuron with one dendritic cylinder and two active conductances). The first method uses classical voltage traces resulting from current pulses injection (time domain), while the second uses measures of the neuron's response to sinusoidal stimuli (frequency domain). Both methods estimate correctly the parameters in all cases studied. However, the time-domain method is slower and more prone to estimation errors in the cable parameters than the frequency-domain method. Because with noisy data the goodness of fit does not distinguish between different solutions, we suggest that running the estimation procedure a large number of times might help find a good solution and can provide information about the interactions between parameters. Also, because the formulation used for the model's response in the frequency domain is analytical, one can derive a local sensitivity analysis for each parameter. This analysis indicates how well a parameter is likely to be estimated and helps choose an optimal stimulation protocol. Finally, the tests suggest a strategy for fitting single-cell models using the two methods examined.}, - language = {en}, - number = {3}, - urldate = {2021-06-17}, - journal = {Journal of Computational Neuroscience}, - author = {Tabak, Joël and Murphey, C. Richard and Moore, L.E.}, - month = nov, - year = {2000}, - pages = {215--236}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ZPMRAGNC\\Tabak et al. - 2000 - Parameter Estimation Methods for Single Neuron Mod.pdf:application/pdf}, -} - -@article{shirahata_effect_2014, - title = {Effect of sodium conductance variations on electrical behavior of a neocortical neuron model}, - volume = {65}, - issn = {0236-5383, 1588-256X}, - url = {https://akjournals.com/view/journals/018/65/4/article-p379.xml}, - doi = {10.1556/abiol.65.2014.4.2}, - abstract = {{\textless}section class="abstract"{\textgreater}{\textless}p{\textgreater}Neocortical pyramidal neurons are capable of intrinsic regenerative firing. A mathematical model introduced by Delord et al. [2] of these neurons based on the Hodgkin-Huxley formalism, varied the values of two parameters of the model, i.e. the maximal persistent sodium conductance ({\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{NaP}}$) and the leakage one ({\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{{\textless}em{\textgreater}l{\textless}/em{\textgreater}}}$), and revealed the ({\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{NaP}}$, {\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{{\textless}em{\textgreater}l{\textless}/em{\textgreater}}}$) parameter space supporting regenerative firing. The present study focused on another parameter of this model, i.e. the maximal fast sodium conductance ({\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{Na}}$), to investigate the ({\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{NaP}}$, {\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{Na}}$) parameter space involved in regenerative firing. When {\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{Na}}$ was completely blocked, regenerative firing was suppressed. In addition, the {\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{Na}}$ threshold necessary to induce regenerative firing was almost independent of the {\textless}em{\textgreater}g{\textless}/em{\textgreater}$_{\textrm{NaP}}$ level. Finally, our results were compared with those of other types of neurons.{\textless}/p{\textgreater}{\textless}/section{\textgreater}}, - language = {en\_US}, - number = {4}, - urldate = {2021-06-17}, - journal = {Acta Biologica Hungarica}, - author = {Shirahata, T.}, - month = dec, - year = {2014}, - pages = {379--384}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WAV5H68C\\article-p379.html:text/html}, -} - -@article{nowacki_sensitivity_2011, - title = {Sensitivity analysis to explain the excitability in a pyramidal neuron with application to {Alzheimer}’s disease}, - volume = {12}, - issn = {1471-2202}, - url = {https://doi.org/10.1186/1471-2202-12-S1-P342}, - doi = {10.1186/1471-2202-12-S1-P342}, - number = {1}, - urldate = {2021-06-17}, - journal = {BMC Neuroscience}, - author = {Nowacki, Jakub and Osinga, Hinke M. and Brown, Jon T. and Randall, Andrew D. and Tsaneva-Atanasova, Krasimira}, - month = jul, - year = {2011}, - keywords = {Model Behaviour, Parameter Sensitivity, Profound Impact, Pyramidal Cell, Pyramidal Neuron}, - pages = {P342}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\424E84U5\\Nowacki et al. - 2011 - Sensitivity analysis to explain the excitability i.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\IWNDRCC7\\1471-2202-12-S1-P342.html:text/html}, -} - -@article{marder_multiple_2011, - title = {Multiple models to capture the variability in biological neurons and networks}, - volume = {14}, - copyright = {2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.}, - issn = {1546-1726}, - url = {https://www.nature.com/articles/nn.2735}, - doi = {10.1038/nn.2735}, - abstract = {Experimental work suggests that synaptic and intrinsic neuronal properties vary considerably across identified neurons in different animals. The authors propose that instead of building a single model that captures the average behavior of a neuron or circuit, one could construct a population of models with different underlying structure and similar behaviors, as a way of investigating compensatory mechanisms that contribute to neuron and network function.}, - language = {en}, - number = {2}, - urldate = {2021-06-17}, - journal = {Nature Neuroscience}, - author = {Marder, Eve and Taylor, Adam L.}, - month = feb, - year = {2011}, - pages = {133--138}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P6AXF7KA\\Marder and Taylor - 2011 - Multiple models to capture the variability in biol.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8VI7UGLZ\\nn.html:text/html}, -} - -@article{brandsma_riluzole_2016, - title = {Riluzole in patients with hereditary cerebellar ataxia}, - volume = {15}, - issn = {1474-4422}, - url = {https://www.sciencedirect.com/science/article/pii/S1474442216001319}, - doi = {10.1016/S1474-4422(16)00131-9}, - language = {en}, - number = {8}, - urldate = {2021-06-17}, - journal = {The Lancet Neurology}, - author = {Brandsma, Rick and Kremer, Hubertus P H and Sival, Deborah A}, - month = jul, - year = {2016}, - pages = {788}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\IBV8YQW7\\Brandsma et al. - 2016 - Riluzole in patients with hereditary cerebellar at.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MDBW32WL\\S1474442216001319.html:text/html}, -} - -@article{durr_rare_2015, - title = {Rare inherited diseases merit disease-specific trials}, - volume = {14}, - issn = {1474-4465}, - doi = {10.1016/S1474-4422(15)00217-3}, - language = {eng}, - number = {10}, - journal = {The Lancet. Neurology}, - author = {Durr, Alexandra}, - month = oct, - year = {2015}, - keywords = {Male, Humans, Female, Riluzole, Excitatory Amino Acid Antagonists, Friedreich Ataxia, Spinocerebellar Ataxias}, - pages = {968--969}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\J3PGIMSP\\Durr - 2015 - Rare inherited diseases merit disease-specific tri.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XG77M2M4\\S1474442215002173.html:text/html}, -} - -@article{grunnet_pharmacological_2001, - title = {Pharmacological modulation of {SK3} channels}, - volume = {40}, - issn = {0028-3908}, - url = {https://www.sciencedirect.com/science/article/pii/S0028390801000284}, - doi = {10.1016/S0028-3908(01)00028-4}, - abstract = {Small-conductance, calcium-activated K+ channels (SK channels) are voltage-insensitive channels that have been identified molecularly within the last few years. As SK channels play a fundamental role in most excitable cells and participate in afterhyperpolarization (AHP) and spike-frequency adaptation, pharmacological modulation of SK channels may be of significant clinical importance. Here we report the functional expression of SK3 in HEK293 and demonstrate a broad pharmacological profile for these channels. Brain slice studies commonly employ 4-aminopyridine (4-AP) to block voltage-dependent K+ channels or a methyl derivative of bicuculline, a blocker of gamma-aminobutyric acid (GABA)-gated Cl− channels, in order to investigate the role of various synapses in specialized neural networks. However, in this study both 4-AP and bicuculline are shown to inhibit SK3 channels (IC50 values of 512 μM and 6 μM, respectively) at concentrations lower than those used for brain slice recordings. Riluzole, a potent neuroprotective drug with anti-ischemic, anticonvulsant and sedative effects currently used in the treatment of amyotrophic lateral sclerosis, activates SK3 channels at concentrations of 3 μM and above. Amitriptyline, a tricyclic antidepressive widely used clinically, inhibits SK3 channels with an IC50 of 39.1±10 μM (n=6).}, - language = {en}, - number = {7}, - urldate = {2021-06-20}, - journal = {Neuropharmacology}, - author = {Grunnet, Morten and Jespersen, Thomas and Angelo, Kamilla and Frøkjær-Jensen, Christian and Klaerke, Dan A and Olesen, Søren-Peter and Jensen, Bo Skaaning}, - month = jun, - year = {2001}, - keywords = {Bicuculline, 4-Aminopyridine, Riluzole, 1-Ethylbenzimidiazolone, Amitriptyline, Ca-activated K channel}, - pages = {879--887}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\UH7ED7J5\\S0028390801000284.html:text/html}, -} - -@article{yokoo_selective_1998, - title = {Selective inhibition by riluzole of voltage-dependent sodium channels and catecholamine secretion in adrenal chromaffin cells}, - volume = {357}, - issn = {1432-1912}, - url = {https://doi.org/10.1007/PL00005203}, - doi = {10.1007/PL00005203}, - abstract = {We examined the effects of riluzole, a neuroprotective drug, on voltage–dependent Na channels, nicotinic receptors, and voltage-dependent Ca channels, as well as catecholamine secretion, in comparison with those of verapamil and nicardipine, in primary cultures of bovine adrenal chromaffin cells. Riluzole inhibited veratridine-induced 22Na influx via voltage-dependent Na channels even in the presence of ouabain, an inhibitor of Na,K-ATPase. Blockade of Na channels by riluzole was concentration-dependent with an IC50 of 5.3 µM. It was associated with a similar concentration-related reduction of veratridine-induced 45Ca influx via voltage-dependent Ca channels, and of catecholamine secretion. Riluzole had no effect on 45Ca influx caused by high K, which directly activates voltage-dependent Ca channels, and on nicotine-induced 22Na influx, which passes through the nicotinic receptors. Verapamil and nicardipine attenuated 22Na influx caused by veratridine or nicotine at the same concentrations as they suppressed high K-induced 45Ca influx. The inhibitory effect of riluzole on veratridine-induced 22Na influx disappeared at high concentrations of veratridine. A potentiation of veratridine (site 2 toxin)-induced 22Na influx caused by α-scorpion venom (site 3 toxin), β-scorpion venom (site 4 toxin), or brevetoxin PbTx-3 (site 5 toxin), occurred in the presence of riluzole in the same manner as in control cells. These results suggest that riluzole binds to the veratridine site in voltage–dependent Na channels. It does not impair the cooperative interaction between the functional peptide segments of Na channels, but selectively inhibits gating of Na channels, thereby reducing Ca influx via Ca channels and catecholamine secretion. In contrast, verapamil and nicardipine suppress Na influx both Na channels and nicotinic receptors.}, - language = {en}, - number = {5}, - urldate = {2021-06-20}, - journal = {Naunyn-Schmiedeberg's Archives of Pharmacology}, - author = {Yokoo, Hiroki and Shiraishi, Seiji and Kobayashi, Hideyuki and Yanagita, Toshihiko and Yamamoto, Ryuichi and Wada, A.}, - month = may, - year = {1998}, - pages = {526--531}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TQ96RVFD\\Yokoo et al. - 1998 - Selective inhibition by riluzole of voltage-depend.pdf:application/pdf}, -} - -@article{mohammadi_interaction_2002, - title = {Interaction of high concentrations of riluzole with recombinant skeletal muscle sodium channels and adult-type nicotinic receptor channels}, - volume = {26}, - copyright = {Copyright © 2002 Wiley Periodicals, Inc.}, - issn = {1097-4598}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.10230}, - doi = {10.1002/mus.10230}, - abstract = {Riluzole is a neuroprotective drug that modulates glutamergic transmission but also blocks the inactivated state of voltage-gated neuronal sodium channels at very low concentrations (about 0.1 μM). After nausea, the most common adverse effect of riluzole is asthenia, which could be due to a block of muscle sodium channels or acetylcholine receptor channels. Using the patch-clamp technique, we applied riluzole on recombinant voltage-gated skeletal muscle sodium and adult nicotinic acetylcholine receptor channels expressed in a mammalian cell line (HEK 293). Riluzole blocked the inactivated state of voltage-gated skeletal muscle sodium channels, shifting the midpoint of the steady-state inactivation curve to more negative potentials, but only in comparatively high concentrations (≥ 0.1 mM). At these concentrations, riluzole also caused an open-channel block at acetylcholine receptor channels. We conclude that riluzole has only a mild blocking effect on the inactivated state of voltage-gated skeletal muscle sodium channels and nicotinic acetylcholine receptor channels. As the plasma concentration of riluzole in amyotrophic lateral sclerosis (ALS) patients approximates 2 μM, it seems unlikely that asthenia is caused by a block of skeletal muscle sodium channels or acetylcholine receptor channels by riluzole. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 539–545, 2002}, - language = {en}, - number = {4}, - urldate = {2021-06-20}, - journal = {Muscle \& Nerve}, - author = {Mohammadi, Bahram and Lang, Nicolas and Dengler, Reinhard and Bufler, Johannes}, - year = {2002}, - keywords = {sodium channels, amyotrophic lateral sclerosis, riluzole, nicotinic acetylcholine receptor channels, patch-clamp technique}, - pages = {539--545}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BGV8S8AY\\Mohammadi et al. - 2002 - Interaction of high concentrations of riluzole wit.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AAYC4D3Z\\mus.html:text/html}, -} - -@article{hebert_block_1994, - title = {Block of the rat brain {IIA} sodium channel alpha subunit by the neuroprotective drug riluzole.}, - volume = {45}, - number = {5}, - journal = {Molecular Pharmacology}, - author = {Hebert, T. and Drapeau, P. and Pradier, L. and Dunn, R. J.}, - month = may, - year = {1994}, - pages = {1055--1060}, - file = {Block of the rat brain IIA sodium channel alpha subunit by the neuroprotective drug riluzole. | Molecular Pharmacology:C\:\\Users\\nilsk\\Zotero\\storage\\BUDRSRH9\\1055.html:text/html}, -} - -@article{doeser_targeting_2015, - title = {Targeting pharmacoresistant epilepsy and epileptogenesis with a dual-purpose antiepileptic drug}, - volume = {138}, - issn = {0006-8950}, - url = {https://academic.oup.com/brain/article/138/2/371/291995}, - doi = {10.1093/brain/awu339}, - abstract = {Pharmacoresistance is common in epilepsy. Doeser et al. reveal that the active metabolite of eslicarbazepine acetate can overcome a common pharmacoresistance me}, - language = {en}, - number = {2}, - urldate = {2021-06-20}, - journal = {Brain}, - author = {Doeser, Anna and Dickhof, Gesa and Reitze, Margit and Uebachs, Mischa and Schaub, Christina and Pires, Nuno Miguel and Bonifácio, Maria João and Soares-da-Silva, Patrício and Beck, Heinz}, - month = feb, - year = {2015}, - pages = {371--387}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Y47ZKD5S\\Doeser et al. - 2015 - Targeting pharmacoresistant epilepsy and epileptog.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SWQLASGN\\Doeser et al. - 2015 - Targeting pharmacoresistant epilepsy and epileptog.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\75SUU5CC\\291995.html:text/html}, -} - -@article{sun_anticonvulsant_2000, - title = {The {Anticonvulsant} {SGB}-017 ({ADCI}) {Blocks} {Voltage}-{Gated} {Sodium} {Channels} in {Rat} and {Human} {Neurons}: {Comparison} with {Carbamazepine}}, - volume = {41}, - issn = {1528-1167}, - shorttitle = {The {Anticonvulsant} {SGB}-017 ({ADCI}) {Blocks} {Voltage}-{Gated} {Sodium} {Channels} in {Rat} and {Human} {Neurons}}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1528-1157.2000.tb00154.x}, - doi = {10.1111/j.1528-1157.2000.tb00154.x}, - abstract = {Summary: Purpose: SGB-017 (ADCI) is a novel anticonvul-sant that blocks both voltage-activated sodium channels and N-methyl-d-aspartate (NMDA)-receptor-gated channels. Results by Rogawski et al. suggested that SGB-017 produces its anticonvulsant action primarily by inhibition of NMDA-receptor channels. However, SGB-017 is effective in several animal models of epilepsy that are unresponsive to NMDA antagonists. These results indicate that block of NMDA-receptor channels is not the only mechanism contributing to its anticonvulsant activity. Thus the effects of SGB-017 on neu-ronal sodium channels were investigated. Methods: Whole cell voltage-clamp techniques were used to record sodium currents in freshly dissociated rat superior cervical ganglion (SCG) and hippocampal neurons and cultured human NT2 neurons. The effects of SGB-017 on the amplitude of sodium currents, elicited by a depolarizing pulse to 0 mV from different holding potentials, were measured and compared with those of carbamazepine (CBZ). Results: SGB-017 inhibited sodium currents in rat SCG and hippocampal neurons with a similar potency to CBZ. Like CBZ, the inhibition of sodium channels by SGB-017 was voltage dependent. Its median inhibitory concentration (IC50) for inhibition of sodium channels at depolarized holding potentials is similar to that for its inhibition of NMDA receptor channels. In human hNT2 neurons, SGB-017 was more potent than CBZ at inhibiting sodium currents. Conclusions: SGB-017 produces its anticonvulsant activity by blocking both sodium- and NMDA-receptor channels in a voltage- and use-dependent manner. The combination of these two mechanisms of action makes SGB-017 an effective AED in several different animal models of epilepsy.}, - language = {en}, - number = {3}, - urldate = {2021-06-20}, - journal = {Epilepsia}, - author = {Sun, Lucy and Lin, Stephen S.}, - year = {2000}, - keywords = {Anticonvulsant, Hippocampal, hNT2 neuron, SCG, Sodium current}, - pages = {263--270}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\D9YZ6WCU\\Sun and Lin - 2000 - The Anticonvulsant SGB-017 (ADCI) Blocks Voltage-G.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ELMBMFPJ\\j.1528-1157.2000.tb00154.html:text/html}, -} - -@article{sun_carbamazepine_2007, - title = {Carbamazepine and {Topiramate} {Modulation} of {Transient} and {Persistent} {Sodium} {Currents} {Studied} in {HEK293} {Cells} {Expressing} the {Nav1}.3 α–{Subunit}}, - volume = {48}, - issn = {1528-1167}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1528-1167.2007.01001.x}, - doi = {10.1111/j.1528-1167.2007.01001.x}, - abstract = {Summary: Purpose: The transient and the persistent Na+ current play a distinct role in neuronal excitability. Several antiepileptic drugs (AEDs) modulate the transient Na+ current and block the persistent Na+ current; both effects contribute to their antiepileptic properties. The interactions of the AEDs carbamazepine (CBZ) and topiramate (TPM) with the persistent and transient Na+ current were investigated. Methods: HEK293 cells stably expressing the α-subunit of the Na+ channel NaV1.3 were used to record Na+ currents under voltage-clamp by using the patch-clamp technique in whole-cell configuration and to investigate the effects of CBZ and TPM. Results: The persistent Na+ current was present in all cells and constituted 10.3 ± 3.8\% of the total current. CBZ partially blocked the persistent Na+ current in a concentration-dependent manner [median effective concentration (EC50), 16 ± 4 μM]. CBZ also shifted the steady-state inactivation of the transient Na+ current to negative potentials (EC50, 14 ± 11 μM). TPM partially blocked the persistent Na+ current with a much higher affinity (EC50, 61 ± 37 nM) than it affected the steady-state inactivation of the transient Na+ current (EC50, 3.2 ± 1.8 μM). For the latter effect, TPM was at most half as effective as CBZ. Conclusions: The persistent Na+ current flowing through the α-subunit of the NaV1.3 channel is partially blocked by CBZ at about the same therapeutic concentrations at which it modulates the transient Na+ current, adding a distinct aspect to its anticonvulsant profile. The TPM-induced partial block of the persistent Na+ current, already effective at low concentrations, could be the dominant action of this drug on the Na+ current.}, - language = {en}, - number = {4}, - urldate = {2021-06-20}, - journal = {Epilepsia}, - author = {Sun, Guang-chun and Werkman, Taco R. and Battefeld, Arne and Clare, Jeffrey J. and Wadman, Wytse J.}, - year = {2007}, - keywords = {Epilepsy, Antiepileptic drug, Na+ channel NaV1.3, Persistent Na+ current, Stable expression system, Whole-cell voltage clamp}, - pages = {774--782}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TG3KGLFN\\Sun et al. - 2007 - Carbamazepine and Topiramate Modulation of Transie.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\HWP76CXW\\j.1528-1167.2007.01001.html:text/html}, -} - -@article{bonifacio_interaction_2001, - title = {Interaction of the {Novel} {Anticonvulsant}, {BIA} 2-093, with {Voltage}-{Gated} {Sodium} {Channels}: {Comparison} with {Carbamazepine}}, - volume = {42}, - issn = {1528-1167}, - shorttitle = {Interaction of the {Novel} {Anticonvulsant}, {BIA} 2-093, with {Voltage}-{Gated} {Sodium} {Channels}}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1528-1157.2001.43600.x}, - doi = {10.1046/j.1528-1157.2001.43600.x}, - abstract = {Summary: Purpose: BIA 2-093 [(S)-(-)-10-acetoxy-10,11-dihydro-5H-dibenz/b,f/azepine-5-carboxamide] is endowed with an anticonvulsant potency similar to that of carbamazepine (CBZ), but produces less cognitive and motor impairment. This study evaluated whether voltage-gated sodium channels (VGSCs) are a primary locus for the action of BIA 2-093. Methods: We used the whole-cell voltage-clamp technique in the mouse neuroblastoma cell line N1E-115 to investigate the effects of BIA 2-093 and CBZ on VGSCs, displacement of [3H]-batrachotoxinin A 20-α-benzoate ([3H]-BTX), and [3H]-saxitoxin to define their relative potency to bind to rat brain sodium channels, and inhibition of uptake of 22Na by rat brain cortical synaptosomes stimulated by veratridine as a measure of sodium entry. Results: The inhibitory potencies of BIA 2-093 and CBZ increased as the holding potential was made less negative (−100, −90, −80, and −70 mV) with median inhibitory concentration (IC50) values (in μM) of, respectively, 4,337, 618, 238, and 139 for BIA 2-093, and 1,506, 594, 194, and 101 for CBZ. BIA 2-093 displayed a similar potency in displacing [3H]-BTX (IC50 values, 222 vs. 361 μM; p {\textgreater} 0.05) and inhibiting the uptake of 22Na (IC50 values, 36 vs. 138 μM; p {\textgreater} 0.05). Both drugs failed to displace [3H]-saxitoxin in concentrations up to 300 μM. Conclusions: BIA 2-093, like CBZ, inhibits sodium currents in a voltage-dependent way by an interaction predominantly with the inactivated state of the channel and interacts with neurotoxin receptor site 2, but not with receptor site 1. BIA 2-093 displayed a potency blocking VGSCs similar to that of CBZ.}, - language = {en}, - number = {5}, - urldate = {2021-06-20}, - journal = {Epilepsia}, - author = {Bonifácio, M. J. and Sheridan, R. D. and Parada, A. and Cunha, R. A. and Patmore, L. and Soares-da-Silva, P.}, - year = {2001}, - keywords = {Carbamazepine, Batrachotoxinin, BIA 2-093, Saxitoxin, Voltage-gated sodium channels}, - pages = {600--608}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9FA28M7X\\Bonifácio et al. - 2001 - Interaction of the Novel Anticonvulsant, BIA 2-093.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H2SG5ITY\\j.1528-1157.2001.43600.html:text/html}, -} - -@article{pawlowicz_clinical_2017, - series = {Abstracts of {EPNS} 2017 - 12th {European} {Paediatric} {Neurology} {Society} {Congress}}, - title = {Clinical heterogeneity of {Episodic} {Ataxia} type 1 presentation in family with the c.{677C}{\textgreater}{G} {KCNA1} gene heterozygosity}, - volume = {21}, - issn = {1090-3798}, - url = {https://www.sciencedirect.com/science/article/pii/S1090379817313818}, - doi = {10.1016/j.ejpn.2017.04.1122}, - language = {en}, - urldate = {2021-06-20}, - journal = {European Journal of Paediatric Neurology}, - author = {Pawlowicz, M. and Lemka, M. and Szmuda, M. and Zawadzka, M. and Matheisel, A. and Mazurkiewicz-Beldzinska, M.}, - month = jun, - year = {2017}, - pages = {e216}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\HG5FK3CJ\\S1090379817313818.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\W72ZPLN8\\S1090379817313818.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\KLE434SL\\fulltext.html:text/html}, -} - -@article{klein_episodic_2004, - title = {Episodic {Ataxia} {Type} 1 with {Distal} {Weakness}: {A} {Novel} {Manifestation} of a {Potassium} {Channelopathy}}, - volume = {35}, - copyright = {Georg Thieme Verlag KG Stuttgart · New York}, - issn = {0174-304X, 1439-1899}, - shorttitle = {Episodic {Ataxia} {Type} 1 with {Distal} {Weakness}}, - url = {http://www.thieme-connect.de/DOI/DOI?10.1055/s-2004-817921}, - doi = {10.1055/s-2004-817921}, - abstract = {Thieme E-Books \& E-Journals}, - language = {en}, - number = {02}, - urldate = {2021-06-20}, - journal = {Neuropediatrics}, - author = {Klein, A. and Boltshauser, E. and Jen, J. and Baloh, R. W.}, - month = apr, - year = {2004}, - pages = {147--149}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KIHX3AY3\\Klein et al. - 2004 - Episodic Ataxia Type 1 with Distal Weakness A Nov.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ZV7ZX3T9\\s-2004-817921.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\AIDM7EJ2\\s-2004-817921.html:text/html}, -} - -@article{noauthor_notitle_nodate, -} - -@article{lassche_novel_2014, - title = {A novel {KCNA1} mutation causing episodic ataxia type {I}}, - volume = {50}, - copyright = {Copyright © 2014 Wiley Periodicals, Inc.}, - issn = {1097-4598}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.24242}, - doi = {10.1002/mus.24242}, - abstract = {We describe the clinical phenotype of a novel de novo KNCA1 mutation, and functional characterization of the effects of the mutation on Kv1.1 channel function. HEK293 cells were transfected transiently with either wild-type or mutant channels. Representative currents were evoked after application of a series of square voltage steps from −80 mV to +50 mV in 200-ms intervals from Vh = −80 mV. Extracellular K+ was added to evoke tail currents. Equal amounts of wild-type and Kv1.1I262M mutant DNA were transfected transiently in HEK293 cells to evaluate the influence of the mutation. We found that Kv1.1I262M leads to a defective voltage-gated potassium channel. Coexpression studies revealed a dominant-negative effect. We describe the phenotype of a novel KCNA1 mutation causing episodic ataxia. Patch-clamp studies confirm the pathogenicity of the mutation in vitro and suggest that it is dominant with respect to wild-type. Muscle Nerve 50:289–291, 2014}, - language = {en}, - number = {2}, - urldate = {2021-06-22}, - journal = {Muscle \& Nerve}, - author = {Lassche, Saskia and Lainez, Sergio and Bloem, Bastiaan R. and Warrenburg, Bart P. C. van de and Hofmeijer, Jeannette and Lemmink, Henny H. and Hoenderop, Joost G. J. and Bindels, René J. M. and Drost, Gea}, - year = {2014}, - keywords = {ion channels, potassium channel, episodic ataxia type 1, KCNA1, channelopathy}, - pages = {289--291}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\VZ6K629L\\Lassche et al. - 2014 - A novel KCNA1 mutation causing episodic ataxia typ.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7L4UEZTM\\mus.html:text/html}, -} - -@article{chen_episodic_2016, - title = {The episodic ataxia type 1 mutation {I262T} alters voltage-dependent gating and disrupts protein biosynthesis of human {Kv1}.1 potassium channels}, - volume = {6}, - copyright = {2016 The Author(s)}, - issn = {2045-2322}, - url = {https://www.nature.com/articles/srep19378}, - doi = {10.1038/srep19378}, - abstract = {Voltage-gated potassium (Kv) channels are essential for setting neuronal membrane excitability. Mutations in human Kv1.1 channels are linked to episodic ataxia type 1 (EA1). The EA1-associated mutation I262T was identified from a patient with atypical phenotypes. Although a previous report has characterized its suppression effect, several key questions regarding the impact of the I262T mutation on Kv1.1 as well as other members of the Kv1 subfamily remain unanswered. Herein we show that the dominant-negative effect of I262T on Kv1.1 current expression is not reversed by co-expression with Kvβ1.1 or Kvβ2 subunits. Biochemical examinations indicate that I262T displays enhanced protein degradation and impedes membrane trafficking of Kv1.1 wild-type subunits. I262T appears to be the first EA1 mutation directly associated with impaired protein stability. Further functional analyses demonstrate that I262T changes the voltage-dependent activation and Kvβ1.1-mediated inactivation, uncouples inactivation from activation gating and decelerates the kinetics of cumulative inactivation of Kv1.1 channels. I262T also exerts similar dominant effects on the gating of Kv1.2 and Kv1.4 channels. Together our data suggest that I262T confers altered channel gating and reduced functional expression of Kv1 channels, which may account for some of the phenotypes of the EA1 patient.}, - language = {en}, - number = {1}, - urldate = {2021-06-22}, - journal = {Scientific Reports}, - author = {Chen, Szu-Han and Fu, Ssu-Ju and Huang, Jing-Jia and Tang, Chih-Yung}, - month = jan, - year = {2016}, - pages = {19378}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Y8JT5JZM\\Chen et al. - 2016 - The episodic ataxia type 1 mutation I262T alters v.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5Z5R9FLT\\srep19378.html:text/html}, -} - -@article{imbrici_novel_2017, - title = {A novel {KCNA1} mutation in a patient with paroxysmal ataxia, myokymia, painful contractures and metabolic dysfunctions}, - volume = {83}, - issn = {1044-7431}, - url = {https://www.sciencedirect.com/science/article/pii/S1044743116302755}, - doi = {10.1016/j.mcn.2017.06.006}, - abstract = {Episodic ataxia type 1 (EA1) is a human dominant neurological syndrome characterized by continuous myokymia, episodic attacks of ataxic gait and spastic contractions of skeletal muscles that can be triggered by emotional stress and fatigue. This rare disease is caused by missense mutations in the KCNA1 gene coding for the neuronal voltage gated potassium channel Kv1.1, which contributes to nerve cell excitability in the cerebellum, hippocampus, cortex and peripheral nervous system. We identified a novel KCNA1 mutation, E283K, in an Italian proband presenting with paroxysmal ataxia and myokymia aggravated by painful contractures and metabolic dysfunctions. The E283K mutation is located in the S3–S4 extracellular linker belonging to the voltage sensor domain of Kv channels. In order to test whether the E283K mutation affects Kv1.1 biophysical properties we transfected HEK293 cells with WT or mutant cDNAs alone or in a 1:1 combination, and recorded relative potassium currents in the whole-cell configuration of patch-clamp. Mutant E283K channels display voltage-dependent activation shifted by 10mV toward positive potentials and kinetics of activation slowed by {\textasciitilde}2 fold compared to WT channels. Potassium currents resulting from heteromeric WT/E283K channels show voltage-dependent gating and kinetics of activation intermediate between WT and mutant homomeric channels. Based on homology modeling studies of the mutant E283K, we propose a molecular explanation for the reduced voltage sensitivity and slow channel opening. Overall, our results suggest that the replacement of a negatively charged residue with a positively charged lysine at position 283 in Kv1.1 causes a drop of potassium current that likely accounts for EA-1 symptoms in the heterozygous carrier.}, - language = {en}, - urldate = {2021-06-22}, - journal = {Molecular and Cellular Neuroscience}, - author = {Imbrici, Paola and Altamura, Concetta and Gualandi, Francesca and Mangiatordi, Giuseppe Felice and Neri, Marcella and De Maria, Giovanni and Ferlini, Alessandra and Padovani, Alessandro and D'Adamo, Maria Cristina and Nicolotti, Orazio and Pessia, Mauro and Conte, Diana and Filosto, Massimiliano and Desaphy, Jean-Francois}, - month = sep, - year = {2017}, - keywords = {Patch clamp, Genetics, Episodic ataxia, Homology modeling, Kv1.1 channel}, - pages = {6--12}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YEL9BZ6F\\Imbrici et al. - 2017 - A novel KCNA1 mutation in a patient with paroxysma.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EDGGQNAK\\S1044743116302755.html:text/html}, -} - -@article{karalok_identification_2018, - title = {Identification of a {New} de {Novo} {Mutation} {Underlying} {Regressive} {Episodic} {Ataxia} {Type} {I}}, - volume = {9}, - issn = {1664-2295}, - url = {https://www.frontiersin.org/articles/10.3389/fneur.2018.00587/full}, - doi = {10.3389/fneur.2018.00587}, - abstract = {Episodic ataxia type 1 (EA1), a Shaker-like K+ channelopathy, is a consequence of genetic anomalies in the KCNA1 gene that lead to dysfunctions in the voltage-gated K+ channel Kv1.1. Generally, KCNA1 mutations are inherited in an autosomal dominant manner. Here we report the clinical phenotype of an EA1 patient characterized by ataxia attacks that decrease in frequency with age, and eventually leading to therapy discontinuation. A new de novo mutation (c.932G{\textgreater}A) that changed a highly conserved glycine residue into an aspartate (p.G311D) was identified by using targeted next-generation sequencing. The conserved glycine is located in the S4-S5 linker, a crucial domain controlling Kv1.1 channel gating. In silico analyses predicted the mutation deleterious. Heterologous expression of the mutant (Kv1.1-G311D) channels resulted in remarkably decreased amplitudes of measured current, confirming the identified variant is pathogenic. Collectively, these findings corroborate the notion that EA1 also results from de novo variants and point out that regardless of the mutation-induced deleterious loss of Kv1.1 channel function the ataxia phenotype may improve spontaneously.}, - language = {English}, - urldate = {2021-06-22}, - journal = {Frontiers in Neurology}, - author = {Karalok, Zeynep S. and Megaro, Alfredo and Cenciarini, Marta and Guven, Alev and Hasan, Sonia M. and Taskin, Birce D. and Imbrici, Paola and Ceylaner, Serdar and Pessia, Mauro and D'Adamo, Maria C.}, - year = {2018}, - keywords = {Kcna1, Diplopia, Episodic ataxia type 1(EA1), G311D, Myokymia}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\EVBAVHMF\\Karalok et al. - 2018 - Identification of a New de Novo Mutation Underlyin.pdf:application/pdf}, -} - -@article{dadamo_mutations_1999, - title = {Mutations in the {KCNA1} gene associated with episodic ataxia type-1 syndrome impair heteromeric voltage-gated {K}+ channel function}, - volume = {13}, - copyright = {© FASEB}, - issn = {1530-6860}, - url = {https://faseb.onlinelibrary.wiley.com/doi/abs/10.1096/fasebj.13.11.1335}, - doi = {10.1096/fasebj.13.11.1335}, - abstract = {ABSTRACTEpisodic ataxia type-1 syndrome (EA-1) is an autosomal dominant neurological disorder that manifests itself during infancy and results from point mutations in the voltage-gated potassium channel gene hKv1.1. The hallmark of the disease is continuous myokymia and episodic attacks of spastic contractions of the skeletal muscles, which cause permanent disability. Coexpression of hKv1.1 and hKv1.2 subunits produces heteromeric potassium channels with biophysical and pharmacological properties intermediate between the respective homomers. By using tandemly linked subunits, we demonstrate that hKv1.1 subunits bearing the EA-1 mutations V408A and E325D combine with hKv1.2 to produce channels with altered kinetics of activation, deactivation, C-type inactivation, and voltage dependence. Moreover, hKv1.1V408A single-channel analysis reveals a ∼threefold reduction of the mean open duration of the channel compared with the wild-type, and this mutation alters the open-state stability of both homomeric and heteromeric channels. The results demonstrate that human Kv1.2 and Kv1.1 subunits coassemble to form a novel channel with distinct gating properties that are altered profoundly by EA-1 mutations, thus uncovering novel physiopathogenetic mechanisms of episodic ataxia type-1 myokymia syndrome.—D'Adamo, M. C., Imbrici, P., Sponcichetti, F., Pessia, M. Mutations in the KCNA1 gene associated with episodic ataxia type-1 syndrome impair heteromeric voltage-gated K+ channel function. FASEB J. 13, 1335–1345 (1999)}, - language = {en}, - number = {11}, - urldate = {2021-06-22}, - journal = {The FASEB Journal}, - author = {D'Adamo, Maria Cristina and Imbrici, Paola and Sponcichetti, Fabio and Pessia, Mauro}, - year = {1999}, - keywords = {cerebellum, potassium channel gating, hKv1.2, hKvl.1, myokymia}, - pages = {1335--1345}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3FWZW4IJ\\D'Adamo et al. - 1999 - Mutations in the KCNA1 gene associated with episod.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B3NT4XPJ\\fasebj.13.11.html:text/html}, -} - -@article{upadhyay_potassium_2009, - title = {Potassium channel opening: a subtle two-step}, - volume = {587}, - copyright = {© 2009 The Authors. Journal compilation © 2009 The Physiological Society}, - issn = {1469-7793}, - shorttitle = {Potassium channel opening}, - url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/jphysiol.2009.174730}, - doi = {10.1113/jphysiol.2009.174730}, - abstract = {Voltage-gated K+ channels undergo a voltage-dependent conductance change that plays a key role in modulating cellular excitability. While the Open state is captured in crystal structures of Kv1.2 and a chimeric Kv1.2/Kv2.1 channel, the Close state and the mechanism of this transition are still a subject of debate. Here, we propose a model based on mutagenesis combined with measurements of both ionic and gating currents which is consistent with the idea that the Open state is the default state, the energy of the electric field being used to keep the channel closed. Our model incorporates an ‘Activated state’ where the bulk of sensor movement is completed without channel opening. The model accounts for the well characterized electrophysiology of the ‘V2’ and ‘ILT’ mutations in Shaker, where sensor movement and channel opening occur over distinct voltage ranges. Moreover, the model proposes relatively small protein rearrangements in going from the Activated to the Open state, consistent with the rapid transitions observed in single channel records of Shaker type channels at zero millivolts.}, - language = {en}, - number = {15}, - urldate = {2021-06-22}, - journal = {The Journal of Physiology}, - author = {Upadhyay, Sanjeev K. and Nagarajan, P. and Mathew, M. K.}, - year = {2009}, - pages = {3851--3868}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SMNN7NI2\\Upadhyay et al. - 2009 - Potassium channel opening a subtle two-step.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\DC2MC8UC\\jphysiol.2009.html:text/html}, -} - -@article{imbrici_novel_2008, - title = {A novel {KCNA1} mutation identified in an {Italian} family affected by episodic ataxia type 1}, - volume = {157}, - issn = {0306-4522}, - url = {https://www.sciencedirect.com/science/article/pii/S0306452208013699}, - doi = {10.1016/j.neuroscience.2008.09.022}, - abstract = {Episodic ataxia type 1 (EA1) is a rare human neurological syndrome characterized by continuous myokymia and attacks of generalized ataxia that can be triggered by abrupt movements, emotional stress and fatigue. An Italian family has been identified where related members displayed continuous myokymia, episodes of ataxia, attacks characterized by myokymia only, and neuromyotonia. A novel missense mutation (F414C), in the C-terminal region of the K+ channel Kv1.1, was identified in the affected individuals. The mutant homotetrameric channels were non-functional in Xenopus laevis oocytes. In addition, heteromeric channels resulting from the co-expression of wild-type Kv1.1 and Kv1.1(F414C), or wild-type Kv1.2 and Kv1.1(F414C) subunits displayed reduced current amplitudes and altered gating properties. This indicates that the pathogenic effect of this KCNA1 mutation is likely to be related to the defective functional properties we have identified.}, - language = {en}, - number = {3}, - urldate = {2021-06-22}, - journal = {Neuroscience}, - author = {Imbrici, P. and Gualandi, F. and D'Adamo, M. C. and Masieri, M. Taddei and Cudia, P. and De Grandis, D. and Mannucci, R. and Nicoletti, I. and Tucker, S. J. and Ferlini, A. and Pessia, M.}, - month = dec, - year = {2008}, - keywords = {Kv1.1, episodic ataxia, confocal microscopy, ion channel gene defects, Kv1.2 cerebellum, oocytes}, - pages = {577--587}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DDGN8DMY\\Imbrici et al. - 2008 - A novel KCNA1 mutation identified in an Italian fa.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\384EMEUT\\S0306452208013699.html:text/html}, -} - -@article{mestre_novel_2016, - title = {A novel {KCNA1} mutation in a family with episodic ataxia and malignant hyperthermia}, - volume = {17}, - issn = {1364-6753}, - url = {https://doi.org/10.1007/s10048-016-0486-0}, - doi = {10.1007/s10048-016-0486-0}, - abstract = {Episodic ataxia type 1 (EA1) is an autosomal dominant channelopathy caused by mutations in KCNA1, which encodes the voltage-gated potassium channel, Kv1.1. Eleven members of an EA family were evaluated with molecular and functional studies. A novel c.746T{\textgreater}G (p.Phe249Cys) missense mutation of KCNA1 segregated in the family members with episodic ataxia, myokymia, and malignant hyperthermia susceptibility. No mutations were found in the known malignant hyperthermia genes RYR1 or CACNA1S. The Phe249Cys-Kv1.1 channels did not show any currents upon functional expression, confirming a pathogenic role of the mutation. Malignant hyperthermia may be a presentation of KCNA1 mutations, which has significant implications for the clinical care of these patients and illustrates the phenotypic heterogeneity of KCNA1 mutations.}, - language = {en}, - number = {4}, - urldate = {2021-06-22}, - journal = {neurogenetics}, - author = {Mestre, Tiago A. and Manole, Andreea and MacDonald, Heather and Riazi, Sheila and Kraeva, Natalia and Hanna, Michael G. and Lang, Anthony E. and Männikkö, Roope and Yoon, Grace}, - month = oct, - year = {2016}, - pages = {245--249}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\64ZP2BGX\\Mestre et al. - 2016 - A novel KCNA1 mutation in a family with episodic a.pdf:application/pdf}, -} - -@article{glaudemans_missense_2009, - title = {A missense mutation in the {Kv1}.1 voltage-gated potassium channel–encoding gene \textit{{KCNA1}} is linked to human autosomal dominant hypomagnesemia}, - volume = {119}, - issn = {0021-9738}, - url = {https://www.jci.org/articles/view/36948}, - doi = {10.1172/JCI36948}, - language = {en}, - number = {4}, - urldate = {2021-06-22}, - journal = {The Journal of Clinical Investigation}, - author = {Glaudemans, Bob and Wijst, Jenny van der and Scola, Rosana H. and Lorenzoni, Paulo J. and Heister, Angelien and Kemp, AnneMiete W. van der and Knoers, Nine V. and Hoenderop, Joost G. and Bindels, René J.}, - month = apr, - year = {2009}, - pages = {936--942}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\S6WMWY5E\\Glaudemans et al. - 2009 - A missense mutation in the Kv1.1 voltage-gated pot.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FQRPKT5B\\36948.html:text/html}, -} - -@article{tomlinson_clinical_2013, - title = {Clinical, genetic, neurophysiological and functional study of new mutations in episodic ataxia type 1}, - volume = {84}, - copyright = {Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/}, - issn = {0022-3050, 1468-330X}, - url = {https://jnnp.bmj.com/content/84/10/1107}, - doi = {10.1136/jnnp-2012-304131}, - abstract = {{\textless}h3{\textgreater}Background and objective{\textless}/h3{\textgreater} {\textless}p{\textgreater}Heterozygous mutations in \textit{KCNA1} cause episodic ataxia type 1 (EA1), an ion channel disorder characterised by brief paroxysms of cerebellar dysfunction and persistent neuromyotonia. This paper describes four previously unreported families with EA1, with the aim of understanding the phenotypic spectrum associated with different mutations.{\textless}/p{\textgreater}{\textless}h3{\textgreater}Methods{\textless}/h3{\textgreater} {\textless}p{\textgreater}15 affected individuals from four families underwent clinical, genetic and neurophysiological evaluation. The functional impact of new mutations identified in the \textit{KCNA1} gene was investigated with in vitro electrophysiology and immunocytochemistry.{\textless}/p{\textgreater}{\textless}h3{\textgreater}Results{\textless}/h3{\textgreater} {\textless}p{\textgreater}Detailed clinical documentation, dating back to 1928 in one family, indicates that all patients manifested episodic ataxia of varying severity. Four subjects from three families reported hearing impairment, which has not previously been reported in association with EA1. New mutations (R167M, C185W and I407M) were identified in three out of the four families. When expressed in human embryonic kidney cells, all three new mutations resulted in a loss of K$_{\textrm{v}}$1.1 channel function. The fourth family harboured a previously reported A242P mutation, which has not been previously described in association with ataxia.{\textless}/p{\textgreater}{\textless}h3{\textgreater}Conclusions{\textless}/h3{\textgreater} {\textless}p{\textgreater}The genetic basis of EA1 in four families is established and this report presents the earliest documented case from 1928. All three new mutations caused a loss of K$_{\textrm{v}}$1.1 channel function. The finding of deafness in four individuals raises the possibility of a link between K$_{\textrm{v}}$1.1 dysfunction and hearing impairment. Our findings broaden the phenotypic range associated with mutations in \textit{KCNA1}.{\textless}/p{\textgreater}}, - language = {en}, - number = {10}, - urldate = {2021-06-22}, - journal = {Journal of Neurology, Neurosurgery \& Psychiatry}, - author = {Tomlinson, Susan Elizabeth and Rajakulendran, Sanjeev and Tan, Stella Veronica and Graves, Tracey Dawn and Bamiou, Doris-Eva and Labrum, Robyn W. and Burke, David and Sue, Carolyn M. and Giunti, Paola and Schorge, Stephanie and Kullmann, Dimitri M. and Hanna, Michael G.}, - month = oct, - year = {2013}, - pages = {1107--1112}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\887DGRWU\\Tomlinson et al. - 2013 - Clinical, genetic, neurophysiological and function.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2LGYAQL7\\Tomlinson et al. - 2013 - Clinical, genetic, neurophysiological and function.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\D6XT3X6J\\1107.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\7C76LQVH\\1107.html:text/html}, -} - -@article{dadamo_novel_2015, - title = {Novel phenotype associated with a mutation in the {KCNA1}({Kv1}.1) gene}, - volume = {5}, - issn = {1664-042X}, - url = {https://www.frontiersin.org/articles/10.3389/fphys.2014.00525/full}, - doi = {10.3389/fphys.2014.00525}, - abstract = {Episodic ataxia type 1 (EA1) is an autosomal dominant K+ channelopathy which manifests with short attacks of cerebellar ataxia and dysarthria, and may also show interictal myokymia. Episodes can be triggered by emotional or physical stress, startle response, sudden postural change or fever. Here we describe a 31-year-old man displaying markedly atypical symptoms, including long-lasting attacks of jerking muscle contractions associated with hyperthermia, severe migraine, and a relatively short-sleep phenotype. A single nucleotide change in KCNA1 (c.555C{\textgreater}G) was identified that changes a highly conserved residue (p.C185W) in the first transmembrane segment of the voltage-gated K+ channel Kv1.1. The patient is heterozygous and the mutation was inherited from his asymptomatic mother. Next generation sequencing revealed no variations in the CACNA1A, CACNB4, KCNC3, KCNJ10, PRRT2 or SCN8A genes of either the patient or mother, except for a benign variant in SLC1A3. Functional analysis of the p.C185W mutation in KCNA1 demonstrated a deleterious dominant-negative phenotype where the remaining current displayed slower activation kinetics, subtle changes in voltage-dependence and faster recovery from slow inactivation. Structural modeling also predicts the C185W mutation to be functionally deleterious. This description of novel clinical features, associated with a Kv1.1 mutation highlights a possibly unrecognized relationship between K+ channel dysfunction, hyperthermia and migraine in EA1, and suggests that thorough assessments for these symptoms should be carefully considered for all patients affected by EA1.}, - language = {English}, - urldate = {2021-06-22}, - journal = {Frontiers in Physiology}, - author = {D'Adamo, Maria C. and Gallenmüller, Constanze and Servettini, Ilenio and Hartl, Elisabeth and Tucker, Stephen J. and Arning, Larissa and Biskup, Saskia and Grottesi, Alessandro and Guglielmi, Luca and Imbrici, Paola and Bernasconi, Pia and Di Giovanni, Giuseppe and Franciolini, Fabio and Catacuzzeno, Luigi and Pessia, Mauro and Klopstock, Thomas}, - year = {2015}, - keywords = {Sleep, episodic ataxia type 1, Kcna1, channelopathy, C185W, hyperthermia, Kv1.1 Potassium Channel, Migraine, Shaker potassium channels}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\MMN7B34L\\D'Adamo et al. - 2015 - Novel phenotype associated with a mutation in the .pdf:application/pdf}, -} - -@article{imbrici_functional_2003, - title = {Functional characterization of an episodic ataxia type-1 mutation occurring in the {S1} segment of {hKv1}.1 channels}, - volume = {446}, - issn = {1432-2013}, - url = {https://doi.org/10.1007/s00424-002-0962-2}, - doi = {10.1007/s00424-002-0962-2}, - abstract = {Voltage-gated potassium channels (Kv) play important roles in neurotransmission, nerve cell excitability and disease. Several missense mutations in the Kv1.1 gene have been associated with episodic ataxia type-1 syndrome (EA-1), which is characterized by continuous myokymia, episodic attacks of ataxic gait and spastic contractions of skeletal muscles. In this study we show that I177N, an EA-1 mutation located in S1 segment, alters the expression and gating properties of the channel expressed in Xenopus oocytes. In particular, it reduces {\textasciitilde}17-fold the current amplitude, accelerates {\textasciitilde}4-fold the deactivation kinetics of the channel and shifts the voltage dependence of activation {\textasciitilde}60 mV to more depolarized potentials. Single-channel recordings also showed that the mean open duration of I177N channels was {\textasciitilde}2.6-fold smaller than the wild-type. These results demonstrate that both reduced current levels and specific gating defects are the likely causes of EA-1 symptoms in patients bearing the I177N mutation. Furthermore, the data suggest that the I177N substitution may alter the gating properties of the channel that are specifically defined by the S1 segment.}, - language = {en}, - number = {3}, - urldate = {2021-06-22}, - journal = {Pflügers Archiv}, - author = {Imbrici, Paola and Cusimano, Antonella and D'Adamo, Maria and De Curtis, Amalia and Pessia, Mauro}, - month = jun, - year = {2003}, - pages = {373--379}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6L4M5JRV\\Imbrici et al. - 2003 - Functional characterization of an episodic ataxia .pdf:application/pdf}, -} - -@article{tristan-clavijo_dominant-negative_2016, - title = {Dominant-negative mutation p.{Arg324Thr} in {KCNA1} impairs {Kv1}.1 channel function in episodic ataxia}, - volume = {31}, - copyright = {© 2016 International Parkinson and Movement Disorder Society}, - issn = {1531-8257}, - url = {https://movementdisorders.onlinelibrary.wiley.com/doi/abs/10.1002/mds.26737}, - doi = {10.1002/mds.26737}, - abstract = {Background Episodic ataxia type 1 is a rare autosomal dominant neurological disorder caused by mutations in the KCNA1 gene that encodes the α subunit of voltage-gated potassium channel Kv1.1. The functional consequences of identified mutations on channel function do not fully correlate with the clinical phenotype of patients. Methods A clinical and genetic study was performed in a family with 5 patients with episodic ataxia type 1, with concurrent epilepsy in 1 of them. Protein expression, modeling, and electrophysiological analyses were performed to study Kv1.1 function. Results Whole-genome linkage and candidate gene analyses revealed the novel heterozygous mutation p.Arg324Thr in the KCNA1 gene. The encoded mutant Kv1.1 channel displays reduced currents and altered activation and inactivation. Conclusions Taken together, we provide genetic and functional evidence that mutation p.Arg324Thr in the KCNA1 gene is pathogenic and results in episodic ataxia type 1 through a dominant-negative effect. © 2016 International Parkinson and Movement Disorder Society}, - language = {en}, - number = {11}, - urldate = {2021-06-22}, - journal = {Movement Disorders}, - author = {Tristán-Clavijo, Enriqueta and Scholl, Francisco G. and Macaya, Alfons and Iglesias, Gemma and Rojas, Ana M. and Lucas, Miguel and Castellano, Antonio and Martinez-Mir, Amalia}, - year = {2016}, - keywords = {electrophysiology, Kv1.1, episodic ataxia, KCNA1, mutation}, - pages = {1743--1748}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\HEXQNMKA\\Tristán-Clavijo et al. - 2016 - Dominant-negative mutation p.Arg324Thr in KCNA1 im.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2VYC76SQ\\27477325.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WZ5QSMR6\\mds.html:text/html}, -} - -@article{qiao_properties_2014, - title = {Properties of human brain sodium channel α-subunits expressed in {HEK293} cells and their modulation by carbamazepine, phenytoin and lamotrigine}, - volume = {171}, - issn = {0007-1188}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925043/}, - doi = {10.1111/bph.12534}, - abstract = {Background and purpose -Voltage-activated Na+ channels contain one distinct α-subunit. In the brain NaV1.1, NaV1.2, NaV1.3 and NaV1.6 are the four most abundantly expressed α-subunits. The antiepileptic drugs (AEDs) carbamazepine, phenytoin and lamotrigine have voltage-gated Na+ channels as their primary therapeutic targets. This study provides a systematic comparison of the biophysical properties of these four α-subunits and characterizes their interaction with carbamazepine, phenytoin and lamotrigine. - -Experimental approach -Na+ currents were recorded in voltage-clamp mode in HEK293 cells stably expressing one of the four α-subunits. - -Key results -NaV1.2 and NaV1.3 subunits have a relatively slow recovery from inactivation, compared with the other subunits and NaV1.1 subunits generate the largest window current. Lamotrigine evokes a larger maximal shift of the steady-state inactivation relationship than carbamazepine or phenytoin. Carbamazepine shows the highest binding rate to the α-subunits. Lamotrigine binding to NaV1.1 subunits is faster than to the other α-subunits. Lamotrigine unbinding from the α-subunits is slower than that of carbamazepine and phenytoin. - -Conclusions and implications -The four Na+ channel α-subunits show subtle differences in their biophysical properties, which, in combination with their (sub)cellular expression patterns in the brain, could contribute to differences in neuronal excitability. We also observed differences in the parameters that characterize AED binding to the Na+ channel subunits. Particularly, lamotrigine binding to the four α-subunits suggests a subunit-specific response. Such differences will have consequences for the clinical efficacy of AEDs. Knowledge of the biophysical and binding parameters could be employed to optimize therapeutic strategies and drug development.}, - number = {4}, - urldate = {2021-06-22}, - journal = {British Journal of Pharmacology}, - author = {Qiao, Xin and Sun, Guangchun and Clare, Jeffrey J and Werkman, Taco R and Wadman, Wytse J}, - month = feb, - year = {2014}, - pages = {1054--1067}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\PKHTM6LI\\Qiao et al. - 2014 - Properties of human brain sodium channel α-subunit.pdf:application/pdf}, -} - -@article{schmickl_side_2020, - title = {Side effects of acetazolamide: a systematic review and meta-analysis assessing overall risk and dose dependence}, - volume = {7}, - copyright = {© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.. http://creativecommons.org/licenses/by-nc/4.0/This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.}, - issn = {2052-4439}, - shorttitle = {Side effects of acetazolamide}, - url = {https://bmjopenrespres.bmj.com/content/7/1/e000557}, - doi = {10.1136/bmjresp-2020-000557}, - abstract = {{\textless}h3{\textgreater}Introduction{\textless}/h3{\textgreater} {\textless}p{\textgreater}Acetazolamide (AZM) is used for various conditions (eg, altitude sickness, sleep apnoea, glaucoma), but therapy is often limited by its side effect profile. Our objective was to estimate the risk of commonly reported side effects based on meta-analyses. We hypothesised that these risks are dose-dependent.{\textless}/p{\textgreater}{\textless}h3{\textgreater}Methods{\textless}/h3{\textgreater} {\textless}p{\textgreater}We queried MEDLINE/EMBASE (Medical Literature Analysis and Retrieval System Online/Excerpta Medica dataBASE) up until 04/10/2019, including any randomised placebo-controlled trial in which adults received oral AZM versus placebo reporting side effects. Eligibility assessment was performed by two independent reviewers. Data were abstracted by one reviewer who verified key entries at a second time point. For side effects reported by \>3 studies a pooled effect estimate was calculated, and heterogeneity assessed via I$^{\textrm{2}}$; for outcomes reported by \>5 studies effect modification by total daily dose (EMbyTDD; \<400 mg/d, 400–600 mg/d, \>600 mg/d) was assessed via meta-regression. For pre-specified, primary outcomes (paraesthesias, taste disturbances, polyuria and fatigue) additional subgroup analyses were performed using demographics, intervention details, laboratory changes and risk of bias.{\textless}/p{\textgreater}{\textless}h3{\textgreater}Results{\textless}/h3{\textgreater} {\textless}p{\textgreater}We included 42 studies in the meta-analyses (N$_{\textrm{subjects}}$=1274/1211 in AZM/placebo groups). AZM increased the risk of all primary outcomes (p\<0.01, I$^{\textrm{2}}$ ≤16\% and low-to-moderate quality of evidence for all)—the numbers needed to harm (95\% CI; n$_{\textrm{Studies}}$) for each were: paraesthesias 2.3 (95\% CI 2 to 2.7; n=39), dysgeusia 18 (95\% CI 10 to 38, n=22), polyuria 17 (95\% CI 9 to 49; n=22), fatigue 11 (95\% CI 6 to 24; n=14). The risk for paraesthesias (beta=1.8 (95\% CI 1.1 to 2.9); P$_{\textrm{EMbyTDD}}$=0.01) and dysgeusia (beta=3.1 (95\% CI 1.2 to 8.2); P$_{\textrm{EMbyTDD}}$=0.02) increased with higher AZM doses; the risk of fatigue also increased with higher dose but non-significantly (beta=2.6 (95\% CI 0.7 to 9.4); P$_{\textrm{EMbyTDD}}$=0.14).{\textless}/p{\textgreater}{\textless}h3{\textgreater}Discussion{\textless}/h3{\textgreater} {\textless}p{\textgreater}This comprehensive meta-analysis of low-to-moderate quality evidence defines risk of common AZM side effects and corroborates dose dependence of some side effects. These results may inform clinical decision making and support efforts to establish the lowest effective dose of AZM for various conditions.{\textless}/p{\textgreater}}, - language = {en}, - number = {1}, - urldate = {2021-06-24}, - journal = {BMJ Open Respiratory Research}, - author = {Schmickl, Christopher N. and Owens, Robert L. and Orr, Jeremy E. and Edwards, Bradley A. and Malhotra, Atul}, - month = apr, - year = {2020}, - pages = {e000557}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UK3X68BX\\Schmickl et al. - 2020 - Side effects of acetazolamide a systematic review.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\RNCP8ZUT\\e000557.html:text/html}, -} - -@article{dreifuss_treatment_1983, - title = {Treatment of the {Nonconvulsive} {Epilepsies}}, - volume = {24}, - issn = {1528-1167}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1528-1157.1983.tb04642.x}, - doi = {10.1111/j.1528-1157.1983.tb04642.x}, - abstract = {Summary: Eliminating seizures should be the first goal of therapy for non-convulsive epilepsies, but preventing seizures, i.e., guarding against head injuries and immunizing against agents that attack the nervous system, is the second goal. An accurate diagnosis of seizure type helps ensure that the appropriate medication for that particular form of epilepsy will be prescribed. Drug decisions should also be based on the risk:benefit ratio to the individual patient, and drug interactions should be considered when more than one drug is required. Frequent monitoring of drug serum levels is necessary in the case of multiple drug therapy or until seizures are controlled. Ethosuximide is considered the drug of choice in absence seizures, but valproic acid is equally effective. Although effective in controlling absence seizures, clonazepam is not favored in this indication because of a high incidence of side effects and the development of tolerance. Atonic seizures are generally refractory to treatment, but valproate, clonazepam, and occasionally carbamazepine represent the drugs of choice in management. Phenytoin continues to be a very popular drug for most types of seizures, but carbamazepine, used adjunctively until recently, is effective as monotherapy for the control of partial seizures, particularly those of the complex partial variety.}, - language = {en}, - number = {s1}, - urldate = {2021-06-28}, - journal = {Epilepsia}, - author = {Dreifuss, F. E.}, - year = {1983}, - keywords = {Bromides, Phenobarbital, Phenytoin, Valproic acid}, - pages = {S45--S54}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\DNMS27J3\\j.1528-1157.1983.tb04642.html:text/html}, -} - -@article{mantegazza_voltage-gated_2010, - title = {Voltage-gated sodium channels as therapeutic targets in epilepsy and other neurological disorders}, - volume = {9}, - issn = {1474-4422}, - url = {https://www.sciencedirect.com/science/article/pii/S1474442210700594}, - doi = {10.1016/S1474-4422(10)70059-4}, - abstract = {Voltage-gated sodium channels (VGSCs) are key mediators of intrinsic neuronal and muscle excitability. Abnormal VGSC activity is central to the pathophysiology of epileptic seizures, and many of the most widely used antiepileptic drugs, including phenytoin, carbamazepine, and lamotrigine, are inhibitors of VGSC function. These antiepileptic drugs might also be efficacious in the treatment of other nervous system disorders, such as migraine, multiple sclerosis, neurodegenerative diseases, and neuropathic pain. In this Review, we summarise the structure and function of VGSCs and their involvement in the pathophysiology of several neurological disorders. We also describe the biophysical and molecular bases for the mechanisms of action of antiepileptic VGSC blockers and discuss the efficacy of these drugs in the treatment of epileptic and non-epileptic disorders. Overall, clinical and experimental data indicate that these drugs are efficacious for a range of diseases, and that the development of drugs with enhanced selectivity for specific VGSC isoforms might be an effective and novel approach for the treatment of several neurological diseases.}, - language = {en}, - number = {4}, - urldate = {2021-06-28}, - journal = {The Lancet Neurology}, - author = {Mantegazza, Massimo and Curia, Giulia and Biagini, Giuseppe and Ragsdale, David S and Avoli, Massimo}, - month = apr, - year = {2010}, - pages = {413--424}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\N7M65CI7\\Mantegazza et al. - 2010 - Voltage-gated sodium channels as therapeutic targe.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MC337XAI\\S1474442210700594.html:text/html}, -} - -@article{wolff_amitriptyline_2016, - title = {Amitriptyline and carbamazepine utilize voltage-gated ion channel suppression to impair excitability of sensory dorsal horn neurons in thin tissue slice: {An} in vitro study}, - volume = {109}, - issn = {0168-0102}, - shorttitle = {Amitriptyline and carbamazepine utilize voltage-gated ion channel suppression to impair excitability of sensory dorsal horn neurons in thin tissue slice}, - url = {https://www.sciencedirect.com/science/article/pii/S0168010216000481}, - doi = {10.1016/j.neures.2016.02.006}, - abstract = {Amitriptyline, carbamazepine and gabapentin are often used for the treatment of neuropathic pain. However, their analgesic action on central sensory neurons is still not fully understood. Moreover, the expression pattern of their target ion channels is poorly elucidated in the dorsal horn of the spinal cord. Thus, we performed patch-clamp investigations in visualized neurons of lamina I–III of the spinal cord. The expression of the different voltage-gated ion channels, as the targets of these drugs, was detected by RT-PCR and immunohistochemistry. Neurons of the lamina I–III express the TTX-sensitive voltage-gated Na+ as well as voltage-gated K+ subunits assembling the fast inactivating (A-type) currents and the delayed rectifier K+ currents. Our pharmacological studies show that tonically-firing, adapting-firing and single spike neurons responded dose-dependently to amitriptyline and carbamazepine. The ion channel inhibition consecutively reduced the firing rate of tonically-firing and adapting-firing neurons. This study provides evidence for the distribution of voltage-gated Na+ and K+ subunits in lamina I–III of the spinal cord and for the action of drugs used for the treatment of neuropathic pain. Our work confirms that modulation of voltage-gated ion channels in the central nervous system contributes to the antinociceptive effects of these drugs.}, - language = {en}, - urldate = {2021-06-28}, - journal = {Neuroscience Research}, - author = {Wolff, Matthias and Czorlich, Patrick and Nagaraj, Chandran and Schnöbel-Ehehalt, Rose and Li, Yingji and Kwapiszewska, Grazyna and Olschewski, Horst and Heschl, Stefan and Olschewski, Andrea}, - month = aug, - year = {2016}, - keywords = {Spinal cord, Antidepressants, Action potential, Firing pattern, Lamina I–III, Sensory neurons}, - pages = {16--27}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8NWQY3PX\\Wolff et al. - 2016 - Amitriptyline and carbamazepine utilize voltage-ga.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FIDCFZ4I\\S0168010216000481.html:text/html}, -} - -@article{mclean_carbamazepine_1986, - title = {Carbamazepine and 10,11-epoxycarbamazepine produce use- and voltage-dependent limitation of rapidly firing action potentials of mouse central neurons in cell culture.}, - volume = {238}, - number = {2}, - journal = {Journal of Pharmacology and Experimental Therapeutics}, - author = {McLean, M. J. and Macdonald, R. L.}, - month = aug, - year = {1986}, - pages = {727--738}, - file = {Carbamazepine and 10,11-epoxycarbamazepine produce use- and voltage-dependent limitation of rapidly firing action potentials of mouse central neurons in cell culture. | Journal of Pharmacology and Experimental Therapeutics:C\:\\Users\\nilsk\\Zotero\\storage\\DHFFHZN3\\727.html:text/html}, -} - -@article{hood_analysis_1983, - title = {Analysis of carbamazepine actions in hippocampal slices of the rat}, - volume = {3}, - issn = {1573-6830}, - url = {https://doi.org/10.1007/BF00710948}, - doi = {10.1007/BF00710948}, - abstract = {1.Carbamazepine at therapeutic concentrations has a strong inhibitory effect on the spontaneous field bursts of the CA 1 region of rat hippocampal slices in low-Ca2+, high-Mg2+ solution.2.A reduction of excitability and synaptic transmission as well as no effect on posttetanic potentiation in the rat hippocampal slice by carbamazepine agrees with previous studies on spinal cord and peripheral nerve.3.Carbamazepine left synaptic inhibition and hyperpolarizing afterpotentials unaltered while these inhibitory processes were markedly enhanced by pentobarbital and adenosine, respectively.4.The spontaneous field bursts are, at least in part, synchronized by ephaptic transmission and may serve as a model of epilepsy and trigeminal neuralgia. The clinical effectiveness of carbamazepine in these two ailments may be explained by a suppression of this pathological synchronization.}, - language = {en}, - number = {3}, - urldate = {2021-06-28}, - journal = {Cellular and Molecular Neurobiology}, - author = {Hood, T. W. and Siegfried, J. and Haas, H. L.}, - month = sep, - year = {1983}, - pages = {213--222}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4BFJQVYH\\Hood et al. - 1983 - Analysis of carbamazepine actions in hippocampal s.pdf:application/pdf}, -} - -@article{gavrilovici_electrophysiological_2014, - title = {Electrophysiological properties and carbamazepine sensitivity of epileptic human cortical neurons}, - volume = {1}, - copyright = {Copyright (c)}, - issn = {2330-3891}, - url = {https://smartscitech.com/index.php/MCE/article/view/936}, - abstract = {There are between 20 and 30 drugs available for the treatment of seizures but despite this {\textasciitilde}30\% of the epilepsy population remains unresponsive to treatment. The underlying mechanisms behind drug resistance in temporal lobe epilepsy (TLE) have not been completely identified. The purpose of this study was to determine if distinct types of neuronal firing patterns occurring in human epileptic cortex are altered by carbamazepine (CBZ). We used whole-cell patch-clamp techniques combined with intracellular labeling to electrophysiologically and morphologically characterize neuronal populations in resected cortical tissue from patients with drug resistant epilepsy. We then determined if cells were uniformly resistant to carbamazepine or whether only a subset did not respond. Cortical spiking patterns were segregated in six main clusters: adapting high frequency cluster 1 and 2 (AHF1 and AHF2), adapting low frequency cluster 1 and 2 (ALF1 and ALF2), strongly adapting low frequency group (sALF) and one spike cluster (OS). A morphological analysis showed that some spiking patterns tend to be associated with specific neuronal morphology. OS group included only pyramidal cells while adapting high frequency groups (AHF1 \&AHF2) displayed typical interneuron phenotype. Finally, we found that CBZ does not uniformly suppress neuronal activity as only {\textasciitilde}27\% of interneurons and {\textasciitilde}40\% of pyramidal cells were carbamazepine insensitive. These data indicate that in humans with DRE there is a heterogeneous CBZ insensitivity in all sub-populations of neurons.}, - language = {en}, - urldate = {2021-06-28}, - journal = {Molecular \& Cellular Epilepsy}, - author = {Gavrilovici, Cezar and McLachlan, Richard and Poulter, Michael Owen}, - year = {2014}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SAFJVX7S\\Gavrilovici et al. - 2014 - Electrophysiological properties and carbamazepine .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\M8LQ37YV\\936.html:text/html}, -} - -@article{watts_effects_1993, - title = {Effects of carbamazepine and baclofen on 4-aminopyridine-induced epileptic activity in rat hippocampal slices}, - volume = {108}, - copyright = {1993 British Pharmacological Society}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1111/j.1476-5381.1993.tb12884.x}, - doi = {10.1111/j.1476-5381.1993.tb12884.x}, - abstract = {1 Rat transverse hippocampal slices exposed to 100 μm 4-aminopyridine (4-AP) generate spontaneous epileptic discharges ranging in duration from short 50 ms ‘interictal’ bursts to long 0.5–2 s ‘polyspike’ activity. 2 Here we compared the effects of the commonly used anticonvulsant, carbamazepine (40 μm) and the antispastic drug, baclofen (2 μm) on the various types of burst. 3 Carbamazepine completely abolished long bursts whilst leaving shorter bursts intact. This is consistent with its known anticonvulsant properties. 4 Baclofen greatly reduced the frequency of short bursts but did not block the long bursts. Rather, they became significantly more prolonged, indicating that baclofen does not have an anticonvulsant action, and may be proconvulsant. 5 These results conflict with conclusions based on studies using models that exhibited only interictal bursts, and emphasize the need to use experimental epilepsies which generate several types of epileptic discharge to evaluate the effects of putative anticonvulsant drugs. 6 The present findings suggest that GABAB receptors play a role in the transition of benign interictal bursts to longer polyspike activity which could develop into seizures in the whole animal.}, - language = {en}, - number = {3}, - urldate = {2021-06-28}, - journal = {British Journal of Pharmacology}, - author = {Watts, A. E. and Jefferys, J. G. R.}, - year = {1993}, - keywords = {epilepsy, 4-Aminopyridine, carbamazepine, anticonvulsant drugs, baclofen, CA3 pyramidal cell, GABAB receptors, hippocampal slice}, - pages = {819--823}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GJHNJB4D\\Watts and Jefferys - 1993 - Effects of carbamazepine and baclofen on 4-aminopy.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ITEL4SX4\\j.1476-5381.1993.tb12884.html:text/html}, -} - -@article{otoom_action_2000, - title = {Action of carbamazepine on epileptiform activity of the verartidine model in {CA1} neurons}, - volume = {885}, - issn = {0006-8993}, - url = {https://www.sciencedirect.com/science/article/pii/S0006899300029772}, - doi = {10.1016/S0006-8993(00)02977-2}, - abstract = {The veratridine epileptiform model was utilized to assess the antiepileptic effect of Carbamazepine (CBZ) in rat hippocampal CA1 pyramidal neurons using conventional intracellular recording techniques. In the veratridine model, where brain slices are treated with veratridine (0.3 μM), a single intracellular stimulus evokes epileptiform bursting. Additionally, spontaneous epileptiform activity commonly appears on prolonged exposure to veratridine in this model. In this model, therapeutic (7–15 μM) and high (50 μM) concentrations of CBZ inhibited the evoked and spontaneous epileptiform bursting in a concentration- and voltage-dependent manner. At all concentrations tested, CBZ produced inhibition of epileptiform activity without affecting the membrane resting potential or input resistance. However, at 50 μM, the drug increased the firing threshold of neurons. These results confirm the suitability of this model for testing sodium channel-dependent antiepileptic agents.}, - language = {en}, - number = {2}, - urldate = {2021-06-28}, - journal = {Brain Research}, - author = {Otoom, Sameer A. and Alkadhi, Karim A.}, - month = dec, - year = {2000}, - keywords = {Brain slice, Hippocampus, Carbamazepine, Evoked bursting, Spontaneous bursting, Therapeutic, Veratridine}, - pages = {289--294}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2MP2UCF7\\Otoom and Alkadhi - 2000 - Action of carbamazepine on epileptiform activity o.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WG8CT876\\S0006899300029772.html:text/html}, -} - -@article{hebeisen_eslicarbazepine_2015, - title = {Eslicarbazepine and the enhancement of slow inactivation of voltage-gated sodium channels: {A} comparison with carbamazepine, oxcarbazepine and lacosamide}, - volume = {89}, - issn = {0028-3908}, - shorttitle = {Eslicarbazepine and the enhancement of slow inactivation of voltage-gated sodium channels}, - url = {https://www.sciencedirect.com/science/article/pii/S0028390814003153}, - doi = {10.1016/j.neuropharm.2014.09.008}, - abstract = {This study aimed at evaluating the effects of eslicarbazepine, carbamazepine (CBZ), oxcarbazepine (OXC) and lacosamide (LCM) on the fast and slow inactivated states of voltage-gated sodium channels (VGSC). The anti-epileptiform activity was evaluated in mouse isolated hippocampal slices. The anticonvulsant effects were evaluated in MES and the 6-Hz psychomotor tests. The whole-cell patch-clamp technique was used to investigate the effects of eslicarbazepine, CBZ, OXC and LCM on sodium channels endogenously expressed in N1E-115 mouse neuroblastoma cells. CBZ and eslicarbazepine exhibit similar concentration dependent suppression of epileptiform activity in hippocampal slices. In N1E-115 mouse neuroblastoma cells, at a concentration of 250 μM, the voltage dependence of the fast inactivation was not influenced by eslicarbazepine, whereas LCM, CBZ and OXC shifted the V0.5 value (mV) by −4.8, −12.0 and −16.6, respectively. Eslicarbazepine- and LCM-treated fast-inactivated channels recovered similarly to control conditions, whereas CBZ- and OXC-treated channels required longer pulses to recover. CBZ, eslicarbazepine and LCM shifted the voltage dependence of the slow inactivation (V0.5, mV) by −4.6, −31.2 and −53.3, respectively. For eslicarbazepine, LCM, CBZ and OXC, the affinity to the slow inactivated state was 5.9, 10.4, 1.7 and 1.8 times higher than to the channels in the resting state, respectively. In conclusion, eslicarbazepine did not share with CBZ and OXC the ability to alter fast inactivation of VGSC. Both eslicarbazepine and LCM reduce VGSC availability through enhancement of slow inactivation, but LCM demonstrated higher interaction with VGSC in the resting state and with fast inactivation gating.}, - language = {en}, - urldate = {2021-06-28}, - journal = {Neuropharmacology}, - author = {Hebeisen, Simon and Pires, Nuno and Loureiro, Ana I. and Bonifácio, Maria João and Palma, Nuno and Whyment, Andrew and Spanswick, David and Soares-da-Silva, Patrício}, - month = feb, - year = {2015}, - keywords = {Carbamazepine, Oxcarbazepine, Voltage-gated sodium channel, Eslicarbazepine, Fast inactivation, Lacosamide, Slow inactivation}, - pages = {122--135}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3HU974K9\\Hebeisen et al. - 2015 - Eslicarbazepine and the enhancement of slow inacti.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\C6CKHKK7\\S0028390814003153.html:text/html}, -} - -@article{perucca_pharmacological_2011, - title = {The pharmacological treatment of epilepsy in adults}, - volume = {10}, - issn = {1474-4422}, - url = {https://www.sciencedirect.com/science/article/pii/S1474442211700473}, - doi = {10.1016/S1474-4422(11)70047-3}, - abstract = {Treatment decisions in epilepsy need to be individualised on the basis of careful analysis of the risk-benefit ratio of each available option. Key decision steps include the time at which antiepileptic drug treatment should be started, which drug should be chosen for first-line therapy, and which strategy is most appropriate for people who did not respond to the initially prescribed drug. With more than 20 antiepileptic drugs currently available to treat epilepsy in adults, opportunities to tailor drug therapy have never been greater, but optimum use of such a complex armamentarium is a challenge even for the epilepsy specialist. Antiepileptic drug choice is primarily based on evidence of efficacy and effectiveness for the individual's seizure type, but other patient-specific factors need to be considered, including age, sex, childbearing potential, comorbidities, and concomitant medications.}, - language = {en}, - number = {5}, - urldate = {2021-06-28}, - journal = {The Lancet Neurology}, - author = {Perucca, Emilio and Tomson, Torbjörn}, - month = may, - year = {2011}, - pages = {446--456}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\K2XIPHSX\\Perucca and Tomson - 2011 - The pharmacological treatment of epilepsy in adult.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\L9UZVVLE\\S1474442211700473.html:text/html}, -} - -@article{ay_investigation_2020, - title = {An investigation on the effects of carbamazepine and sodium valproate on neuromuscular transmission}, - volume = {120}, - issn = {2240-2993}, - url = {https://doi.org/10.1007/s13760-017-0839-y}, - doi = {10.1007/s13760-017-0839-y}, - abstract = {The aim of this study was to investigate the effects of sodium valproate (SV) and carbamazepine (CBZ) on neuromuscular transmission using single-fibre electromyography (SFEMG) in patients with epilepsy. We performed SFEMG during the voluntary contraction of extensor digitorum communis muscle. 30 epileptic patients taking SV, 25 epileptic patients taking CBZ, and 25 age-matched healthy volunteers were included in the study. Mean jitter values (MCD) of subjects taking SV and CBZ were compared with normal controls. MCD values of subjects taking SV and CBZ were statistically significantly higher than those of control group. Review of the correlation between disease duration and MCD values of patients showed that MCD values were increased with the prolonged use of drugs, and thus, indicated a positive relationship between these two parameters. These results suggest that both SV and CBZ reduce neuromuscular transmission in patients without a neuromuscular junction disease.}, - language = {en}, - number = {3}, - urldate = {2021-06-28}, - journal = {Acta Neurologica Belgica}, - author = {Ay, Halil and Ethemoğlu, Özlem}, - month = jun, - year = {2020}, - pages = {545--548}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\J3WLL27B\\Ay and Ethemoğlu - 2020 - An investigation on the effects of carbamazepine a.pdf:application/pdf}, -} - -@article{li_cell-specific_2013, - title = {Cell-{Specific} {mRNA} {Alterations} in {Na}+, {K}+-{ATPase} α and β {Isoforms} and {FXYD} in {Mice} {Treated} {Chronically} with {Carbamazepine}, an {Anti}-{Bipolar} {Drug}}, - volume = {38}, - issn = {1573-6903}, - url = {https://doi.org/10.1007/s11064-013-0986-3}, - doi = {10.1007/s11064-013-0986-3}, - abstract = {Evidence accumulating during almost 50 years suggests Na+, K+-ATPase dysfunction in bipolar disorder, a disease treatable with chronic administration of lithium salts, carbamazepine or valproic acid. Three Na+, K+-ATPase α subunits (α1–3) and two β subunits (β1 and β2) are expressed in brain together with the auxiliary protein FXYD7. FXYD7 decreases K+ affinity, and thus contributes to stimulation of the enzyme at elevated extracellular K+ concentrations. Na+, K+-ATPase subtype and FXYD7 genes were determined by RT-PCR in mice co-expressing one fluorescent signal with an astrocytic marker or a different fluorescent signal with a neuronal marker and treated for 14 days with carbamazepine. Following fluorescence-activated cell sorting of neurons and astrocytes it was shown that α2 Expression was upregulated in astrocytes and neurons and α1 selectively in neurons, but α3 was unchanged. β1 was upregulated in astrocytes, but not in neurons. β2 was unaffected in astrocytes and absent in neurons. FXYD7 was downregulated specifically in neurons. According to cited literature data these changes should facilitate K+ uptake in neurons, without compromising preferential uptake in astrocytes at increased extracellular K+ concentrations. This process seems to be important for K+ homeostasis of the cellular level of the brain (Xu et al. Neurochem Res E-pub Dec. 12, 2012).}, - language = {en}, - number = {4}, - urldate = {2021-06-28}, - journal = {Neurochemical Research}, - author = {Li, Baoman and Hertz, Leif and Peng, Liang}, - month = apr, - year = {2013}, - pages = {834--841}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\PBXD6JQK\\Li et al. - 2013 - Cell-Specific mRNA Alterations in Na+, K+-ATPase α.pdf:application/pdf}, -} - -@article{ding_carbamazepine_2020, - title = {Carbamazepine {Restores} {Neuronal} {Signaling}, {Protein} {Synthesis}, and {Cognitive} {Function} in a {Mouse} {Model} of {Fragile} {X} {Syndrome}}, - volume = {21}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - url = {https://www.mdpi.com/1422-0067/21/23/9327}, - doi = {10.3390/ijms21239327}, - abstract = {Fragile X syndrome (FXS) is a leading genetic disorder of intellectual disability caused by the loss of the functional fragile X mental retardation protein (FMRP). To date, there is no efficacious mechanism-based medication for FXS. With regard to potential disease mechanisms in FXS, it is widely accepted that the lack of FMRP causes elevated protein synthesis and deregulation of neuronal signaling. Abnormal enhancement of the ERK\½ (extracellular signal-regulated kinase \½) and PI3K-Akt (Phosphoinositide 3 kinase-protein kinase B) signaling pathways has been identified in both FXS patients and FXS mouse models. In this study, we show that carbamazepine, which is an FDA-approved drug and has been mainly used to treat seizure and neuropathic pain, corrects cognitive deficits including passive avoidance and object location memory in FXS mice. Carbamazepine also rescues hyper locomotion and social deficits. At the cellular level, carbamazepine dampens the elevated level of ERK\½ and Akt signaling as well as protein synthesis in FXS mouse neurons. Together, these results advocate repurposing carbamazepine for FXS treatment.}, - language = {en}, - number = {23}, - urldate = {2021-06-28}, - journal = {International Journal of Molecular Sciences}, - author = {Ding, Qi and Zhang, Fan and Feng, Yue and Wang, Hongbing}, - month = jan, - year = {2020}, - keywords = {carbamazepine, cAMP, drug repurposing, ERK½, fragile X syndrome, intellectual disability, learning and memory, mouse model, phosphodiesterase, PI3 kinase, protein translation, therapeutics, type 1 adenylyl cyclase}, - pages = {9327}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P4K8S5TI\\Ding et al. - 2020 - Carbamazepine Restores Neuronal Signaling, Protein.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\R49M9WNR\\9327.html:text/html}, -} - -@article{mann_inhibition_2009, - title = {Inhibition of specific adenylyl cyclase isoforms by lithium and carbamazepine, but not valproate, may be related to their antidepressant effect}, - volume = {11}, - issn = {1398-5647}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1399-5618.2009.00762.x}, - doi = {10.1111/j.1399-5618.2009.00762.x}, - abstract = {Objectives:? Lithium, valproate, and carbamazepine decrease stimulated brain cyclic-AMP (cAMP) levels. Adenylyl cyclase (AC), of which there are nine membrane-bound isoforms (AC1-AC9), catalyzes the formation of cAMP. We have recently demonstrated preferential inhibition of AC5 by lithium. We now sought to determine whether carbamazepine and valproate also preferentially inhibit specific AC isoforms or decrease cAMP levels via different mechanisms. Methods:? COS7 cells were transfected with one of AC1-AC9, with or without D1-dopamine receptors. Carbamazepine?s and valproate?s effect on forskolin- or D1 agonist-stimulated ACs was studied. The effect of Mg2+ on lithium?s inhibition was studied in membrane-enriched fraction from COS7 cells co-expressing AC5 and D1 receptors. AC5 knockout mice were tested for a behavioral phenotype similar to that of lithium treatment. Results:? Carbamazepine preferentially inhibited forskolin-stimulated AC5 and AC1 and all D1 agonist-stimulated ACs, with AC5 and AC7 being the most sensitive. When compared to 1 or 3?mM Mg2+, 10?mM Mg2+ reduced lithium-induced AC5 inhibition by 70\%. In silico modeling suggests that among AC isoforms carbamazepine preferentially affects AC1 and AC5 by interacting with the catechol-estrogen site. Valproate did not affect any forskolin- or D1 receptor-stimulated AC. AC5 knockout mice responded similarly to antidepressant- or lithium-treated wild-types in the forced-swim test but not in the amphetamine-induced hyperactivity mania model. Conclusions:? Lithium and carbamazepine preferentially inhibit AC5, albeit via different mechanisms. Lithium competes with Mg2+, which is essential for AC activity; carbamazepine competes for AC?s catechol-estrogen site. Antidepressant-like behavior of AC5 knockout mice in the forced-swim test supports the notion that AC5 inhibition is involved in the antidepressant effect of lithium and carbamazepine. The effect of lithium and carbamazepine to lower cAMP formation in AC5-rich dopaminergic brain regions suggests that D1-dopamine receptors in these regions are involved in the antidepressant effect of mood stabilizers.}, - number = {8}, - urldate = {2021-06-28}, - journal = {Bipolar Disorders}, - author = {Mann, Liad and Heldman, Eliahu and Bersudsky, Yuly and Vatner, Stephen F and Ishikawa, Yoshihiro and Almog, Orna and Belmaker, Robert H and Agam, Galila}, - month = dec, - year = {2009}, - keywords = {carbamazepine, adenylyl cyclase, lithium, mood stabilization, valproate}, - pages = {885--896}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H7B7F6P4\\j.1399-5618.2009.00762.html:text/html}, -} - -@article{lampe_carbamazepine_1990, - title = {Carbamazepine blocks {NMDA}-activated currents in cultured spinal cord neurons}, - volume = {1}, - issn = {0959-4965}, - url = {https://journals.lww.com/neuroreport/Abstract/1990/09000/Carbamazepine_blocks_NMDA_activated_currents_in.8.aspx}, - abstract = {THE antiepileptic agents, carbamazepine and phenytoin, suppress seizures in man and convulsant-induced hyper-activity in spinal cord nerve cell cultures. In the present study, we have shown by whole cell recording that carbamazepine, in contrast to phenytoin, blocks N-methyl-D-aspartate (NMDA)-activated membrane currents in cultured neurons in a dose-dependent fashion. The NMDA receptor-activated channel, which is blocked at physiological concentrations of Mg2+ at resting membrane potential, can be activated by glutamate in depolarized neurons and thus be involved in epileptogenesis. Therefore, the block of NMDA-evoked membrane currents in cultured neurons may contribute to the clinical effectiveness of carbamazepine.}, - language = {en-US}, - number = {1}, - urldate = {2021-06-28}, - journal = {NeuroReport}, - author = {Lampe, Hansjörg and Bigalke, Hans}, - month = sep, - year = {1990}, - pages = {26--28}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\H5V3RZV9\\Carbamazepine_blocks_NMDA_activated_currents_in.8.html:text/html}, -} - -@article{kramer_cross-site_2020, - title = {Cross-site and cross-platform variability of automated patch clamp assessments of drug effects on human cardiac currents in recombinant cells}, - volume = {10}, - copyright = {2020 The Author(s)}, - issn = {2045-2322}, - url = {https://www.nature.com/articles/s41598-020-62344-w}, - doi = {10.1038/s41598-020-62344-w}, - abstract = {Automated patch clamp (APC) instruments enable efficient evaluation of electrophysiologic effects of drugs on human cardiac currents in heterologous expression systems. Differences in experimental protocols, instruments, and dissimilar site procedures affect the variability of IC50 values characterizing drug block potency. This impacts the utility of APC platforms for assessing a drug’s cardiac safety margin. We determined variability of APC data from multiple sites that measured blocking potency of 12 blinded drugs (with different levels of proarrhythmic risk) against four human cardiac currents (hERG [IKr], hCav1.2 [L-Type ICa], peak hNav1.5, [Peak INa], late hNav1.5 [Late INa]) with recommended protocols (to minimize variance) using five APC platforms across 17 sites. IC50 variability (25/75 percentiles) differed for drugs and currents (e.g., 10.4-fold for dofetilide block of hERG current and 4-fold for mexiletine block of hNav1.5 current). Within-platform variance predominated for 4 of 12 hERG blocking drugs and 4 of 6 hNav1.5 blocking drugs. hERG and hNav1.5 block. Bland-Altman plots depicted varying agreement across APC platforms. A follow-up survey suggested multiple sources of experimental variability that could be further minimized by stricter adherence to standard protocols. Adoption of best practices would ensure less variable APC datasets and improved safety margins and proarrhythmic risk assessments.}, - language = {en}, - number = {1}, - urldate = {2021-06-29}, - journal = {Scientific Reports}, - author = {Kramer, James and Himmel, Herbert M. and Lindqvist, Anders and Stoelzle-Feix, Sonja and Chaudhary, Khuram W. and Li, Dingzhou and Bohme, Georg Andrees and Bridgland-Taylor, Matthew and Hebeisen, Simon and Fan, Jingsong and Renganathan, Muthukrishnan and Imredy, John and Humphries, Edward S. A. and Brinkwirth, Nina and Strassmaier, Tim and Ohtsuki, Atsushi and Danker, Timm and Vanoye, Carlos and Polonchuk, Liudmila and Fermini, Bernard and Pierson, Jennifer Beck and Gintant, Gary}, - month = mar, - year = {2020}, - pages = {5627}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\M2GJ32YZ\\Kramer et al. - 2020 - Cross-site and cross-platform variability of autom.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JYVMT6EY\\s41598-020-62344-w.html:text/html}, -} - -@article{lacomblez_confirmatory_1996, - title = {A confirmatory dose-ranging study of riluzole in {ALS}}, - volume = {47}, - copyright = {Copyright 1996 by Advanstar Communications Inc.}, - issn = {0028-3878, 1526-632X}, - url = {https://n.neurology.org/content/47/6_Suppl_4/242S}, - doi = {10.1212/WNL.47.6_Suppl_4.242S}, - abstract = {{\textless}p{\textgreater}ALS is a progressive motor neuron disease with no effective treatment.The anti-excitotoxic drug riluzole (100 mg/day) has been shown to decrease mortality and muscular deterioration in ALS patients. To confirm and extend the therapeutic effect of riluzole, we performed a double-blind, placebo-controlled, multicenter, international, dose-ranging (50, 100, 200 mg/day), stratified study in 959 ALS outpatients treated for up to 18 months. Primary efficacy criterion was survival and the effect of treatment was analyzed before (Wilcoxon and log rank tests) and after adjustment on prognostic factors (Cox model). Secondary efficacy criterion was disease progression assessed through change in functional measures. Tracheostomy-free survival rates were: 50.4\% (placebo), 55.3\% (50 mg riluzole) (p = 0.23, Wilcoxon test; p = 0.25, log-rank test), 56.8\% (100 mg riluzole) (p = 0.05, Wilcoxon test; p = 0.076, log-rank test), and 57.8\% (200 mg riluzole) (p = 0.061, Wilcoxon test; p = 0.075, log-rank test). At the end of the 18-month study, there was a significant dose-related decrease in risk of death or tracheostomy (p = 0.04). Adjustment for baseline prognostic factors showed a 35\% decreased risk of death with the 100-mg dose compared with placebo (p = 0.002). No significant treatment effects were detected for the functional assessments. The most frequent dose-related adverse events included nausea, asthenia, and elevated liver enzyme levels. This study confirms the therapeutic effect of riluzole in a large representative ALS sample, over an 18-month period. Riluzole is well tolerated and decreases the risk of death or tracheostomy in ALS patients.{\textless}/p{\textgreater}{\textless}p{\textgreater}\textbf{NEUROLOGY 1996;47(Suppl 4): } S242-S250{\textless}/p{\textgreater}}, - language = {en}, - number = {6 Suppl 4}, - urldate = {2021-06-29}, - journal = {Neurology}, - author = {Lacomblez, L. and Bensimon, G. and Leigh, P. N. and Guillet, P. and Powe, L. and Durrleman, S. and Delumeau, J. C. and Meininger, V.}, - month = dec, - year = {1996}, - pages = {242S--250S}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2YKGLLHM\\Lacomblez et al. - 1996 - A confirmatory dose-ranging study of riluzole in A.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2B83ID8X\\242S.html:text/html}, -} - -@article{b_c_riluzole_2010, - title = {Riluzole, {Neuroprotection} and {Amyotrophic} {Lateral} {Sclerosis}}, - volume = {17}, - url = {https://www.eurekaselect.com/70209/article}, - abstract = {Amyotrophic lateral sclerosis (ALS) is a universally fatal neurodegenerative disease of the human motor system. Aetiological mechanisms implicated in the d...}, - language = {en}, - number = {18}, - urldate = {2021-06-29}, - journal = {Current Medicinal Chemistry}, - author = {B. C., Cheah and S., Vucic and A., V. Krishnan and M. C., Kiernan}, - month = may, - year = {2010}, - pages = {1942--1959}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5F464K8N\\article.html:text/html}, -} - -@article{andrews_real-world_2020, - title = {Real-world evidence of riluzole effectiveness in treating amyotrophic lateral sclerosis}, - volume = {21}, - issn = {2167-8421}, - url = {https://doi.org/10.1080/21678421.2020.1771734}, - doi = {10.1080/21678421.2020.1771734}, - abstract = {Objective To compare the effect of riluzole on median survival in population studies of patients with amyotrophic lateral sclerosis (ALS) with that observed in clinical trials. Methods: Two independent PubMed searches were conducted, to identify population studies that reported median survival for ALS patients who were either treated with riluzole or remained riluzole-free. Results: We identified 14 studies that met the inclusion criteria of reporting median survival and an additional study that reported mean survival of both riluzole and riluzole-free patients. Analysis of the 15 studies found that a majority reported increased survival of riluzole vs. riluzole-free patients. In 8 studies, the median survival for patients treated with riluzole was 6–19 months longer compared with patients not treated with riluzole (p {\textless} 0.05). Three additional studies reported a clinically meaningful treatment effect (range 3–5.9 months) but did not meet statistical significance. The remaining 4 studies did not show a meaningful treatment effect between riluzole and riluzole-free groups ({\textless}3 months), and differences among the groups were not significant. Also, 5 of the studies used multivariate regression analysis to investigate the level of association between treatment with riluzole and survival; these analyses supported the positive effect of riluzole on survival. Conclusions: A majority of population studies that compared riluzole vs. riluzole-free ALS patients found significant differences in median survival between the two groups, ranging from 6 to 19 months. This is substantially longer than the 2- to 3-month survival benefit observed in the pivotal clinical trials of riluzole.}, - number = {7-8}, - urldate = {2021-06-29}, - journal = {Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration}, - author = {Andrews, Jinsy A. and Jackson, Carlayne E. and Heiman-Patterson, Terry D. and Bettica, Paolo and Brooks, Benjamin Rix and Pioro, Erik P.}, - month = oct, - year = {2020}, - keywords = {amyotrophic lateral sclerosis, Riluzole, survival, neurodegenerative, real-world}, - pages = {509--518}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DT6NTRAQ\\Andrews et al. - 2020 - Real-world evidence of riluzole effectiveness in t.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2GAUDE5N\\21678421.2020.html:text/html}, -} - -@article{okada_carbamazepine_2019, - title = {Carbamazepine {Attenuates} {Astroglial} {L}-{Glutamate} {Release} {Induced} by {Pro}-{Inflammatory} {Cytokines} via {Chronically} {Activation} of {Adenosine} {A2A} {Receptor}}, - volume = {20}, - copyright = {http://creativecommons.org/licenses/by/3.0/}, - url = {https://www.mdpi.com/1422-0067/20/15/3727}, - doi = {10.3390/ijms20153727}, - abstract = {Carbamazepine (CBZ) binds adenosine receptors, but detailed effects of CBZ on astroglial transmission associated with adenosine receptor still need to be clarified. To clarify adenosinergic action of CBZ on astroglial transmission, primary cultured astrocytes were acutely or chronically treated with CBZ, proinflammatory cytokines (interferon \γ (IFN\γ) and tumor necrosis factor \α (TNF\α)), and adenosine A2A receptor (A2AR) agonist (CGS21680). IFN\γ and TNF\α increased basal, adenophostin-A (AdA)-evoked, and 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)propanoic acid (AMPA)-evoked astroglial L-glutamate releases. In physiological condition, CGS21680 increased basal astroglial L-glutamate release but glutamate transporter inhibition prevented this CGS21680 action. CBZ did not affect basal release, whereas glutamate transporter inhibition generated CBZ-induced glutamate release. Furthermore, AdA-evoked and AMPA-evoked releases were inhibited by CBZ but were unaffected by CGS21680. Contrary to physiological condition, chronic administrations of IFN\γ and TNF\α enhanced basal, AdA-, and AMPA-evoked releases, whereas IFN\γ and TNF\α decreased and increased CGS21680-evoked releases via modulation A2AR expression. Both chronic administration of CGS21680 and CBZ suppressed astroglial L-glutamate release responses induced by chronic cytokine exposer. Especifically, chronic administration of CBZ and CGS21680 prevented the reduction and elevation of A2AR expression by respective IFN\γ and TNF\α. These findings suggest that A2AR agonistic effects of CBZ contribute to chronic prevention of pathomechanisms developments of several neuropsychiatric disorders associated with proinflammatory cytokines.}, - language = {en}, - number = {15}, - urldate = {2021-06-30}, - journal = {International Journal of Molecular Sciences}, - author = {Okada, Motohiro and Fukuyama, Kouji and Shiroyama, Takashi and Ueda, Yuto}, - month = jan, - year = {2019}, - keywords = {carbamazepine, adenosine receptor, astrocyte, L-glutamate, tripartite synaptic transmission}, - pages = {3727}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\LK3PL8ZQ\\Okada et al. - 2019 - Carbamazepine Attenuates Astroglial L-Glutamate Re.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Y5VJJXLZ\\3727.html:text/html}, -} - -@article{yoshida_carbamazepine_2007, - title = {Carbamazepine prevents breakdown of neurotransmitter release induced by hyperactivation of ryanodine receptor}, - volume = {52}, - issn = {0028-3908}, - url = {https://www.sciencedirect.com/science/article/pii/S0028390807000573}, - doi = {10.1016/j.neuropharm.2007.02.009}, - abstract = {To clarify the mechanisms of the pharmacological action of carbamazepine (CBZ), we determined the effect of CBZ on GABA and glutamate release associated with the ryanodine receptor (Ryr)-sensitive Ca2+-induced Ca2+-releasing system (CICR) in the rat hippocampus using microdialysis. The therapeutically relevant concentration of CBZ increased basal GABA release without affecting basal glutamate release; however, K+-evoked releases were concentration-dependently reduced by CBZ. Lower-concentration ryanodine increased basal and K+-evoked releases of GABA and glutamate in a concentration dependent manner, whereas higher-concentration ryanodine reduced them. These inflection points in the concentration-response curves of ryanodine for neurotransmitter release (critical concentrations) were shifted to the left by K+-evoked stimulation. The critical concentration of ryanodine in GABA release was lower than that in glutamate release. During the resting stage, the critical concentrations of ryanodine were unaffected by inhibition of L-type, N-type and P-type voltage-sensitive Ca2+ channels (VSCCs) but were prevented by CBZ; however, during the neuronal hyperexcitable stage, the critical concentration was increased by CBZ, L-type and P-type VSCC inhibitors but not the N-type VSCC inhibitor. Therefore, a therapeutically relevant concentration of CBZ protects against the breakdown of the neurotransmitter release mechanism induced by hyperactivation of Ryr via inhibition of L-type and P-type VSCCs as well as inhibition of Ryr-sensitive CICR. These actions of CBZ appear to be involved, at least partially, in its anti-seizure mechanisms.}, - language = {en}, - number = {7}, - urldate = {2021-06-30}, - journal = {Neuropharmacology}, - author = {Yoshida, Shukuko and Okada, Motohiro and Zhu, Gang and Kaneko, Sunao}, - month = jun, - year = {2007}, - keywords = {Glutamate, GABA, Epilepsy, Carbamazepine, CICR, Ryanodine receptor}, - pages = {1538--1546}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EXBYNS3M\\S0028390807000573.html:text/html}, -} - -@article{okada_interaction_1998, - title = {Interaction between {Ca2}+, {K}+, carbamazepine and zonisamide on hippocampal extracellular glutamate monitored with a microdialysis electrode}, - volume = {124}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1038/sj.bjp.0701941}, - doi = {10.1038/sj.bjp.0701941}, - abstract = {1 Multiple components of hippocampal glutamate release were examined by study of Ca2+- and K+-evoked hippocampal extracellular glutamate release using an in vivo microdialysis glutamate biosensor in urethane-anaesthetized rats. In addition, the effects of the antiepileptic drugs, carbamazepine (CBZ) and zonisamide (ZNS) perfused through the probe on glutamate release were assessed. 2 Basal glutamate levels were below detection limits (∼0.1 μm). An increase in extracellular KCl (from 2.7 to 50 and 100 mm) increased extracellular hippocampal glutamate levels to 9.2±1.4 and 20.0±2.6 μm, respectively, calculated from the area under curve (AUC) for 60 min. 3 This KCl-evoked glutamate release consisted of three components: an initial transient rise, a late gentle rise, and late multiple phasic transient rises. 4 An increase in or removal of extracellular CaCl2 levels respectively enhanced and reduced the 50 mm KCl-evoked hippocampal glutamate release (AUC for 60 min) from 9.2±1.4 to 12.4±2.1 and 5.8±0.9 μm. 5 Perfusion with 100 μm CBZ or 1 mm ZNS inhibited both the 50 mm KCl-evoked hippocampal glutamate release (AUC for 60 min) from 9.2±1.4 to 5.5±1.1 and to 5.8±1.3 μm, respectively, as well as the stimulatory effects of Ca2+ on KCl-evoked hippocampal glutamate release. 6 These results suggest that both CBZ and ZNS may reduce epileptiform events by inhibiting excitatory glutamatergic transmission. British Journal of Pharmacology (1998) 124, 1277–1285; doi:10.1038/sj.bjp.0701941}, - language = {en}, - number = {6}, - urldate = {2021-06-30}, - journal = {British Journal of Pharmacology}, - author = {Okada, Motohiro and Kawata, Yuko and Mizuno, Kazuhisa and Wada, Kazumaru and Kondo, Tuyoshi and Kaneko, Sunao}, - year = {1998}, - keywords = {glutamate, carbamazepine, microdialysis electrode, spreading depression, zonisamide}, - pages = {1277--1285}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SHDTRP5U\\Okada et al. - 1998 - Interaction between Ca2+, K+, carbamazepine and zo.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\REN2PVJ7\\sj.bjp.html:text/html}, -} - -@article{yamamura_topiramate_2009, - title = {Topiramate and zonisamide prevent paradoxical intoxication induced by carbamazepine and phenytoin}, - volume = {84}, - issn = {0920-1211}, - url = {https://www.sciencedirect.com/science/article/pii/S0920121109000333}, - doi = {10.1016/j.eplepsyres.2009.01.015}, - abstract = {The mechanisms of paradoxical aggravation of epileptic seizures induced by selected antiepileptic drugs (AEDs) remain unclear. The present study addressed this issue by determining the seizure-threshold doses of carbamazepine (CBZ) and phenytoin (PHT), as well the dose-dependent effects of CBZ, PHT, and carbonic anhydrase-inhibiting AEDs, acetazolamide (AZM), topiramate (TPM), and zonisamide (ZNS), on neurotransmitter release in rat hippocampus. The dose-dependent effects of AEDs on hippocampal extracellular levels of glutamate (Glu), GABA, norepinephrine (NE), dopamine (DA), and serotonin (5-HT) were determined by microdialysis with high-speed and high-sensitive extreme liquid chromatography. Proconvulsive effects of AEDs were determined by telemetric-electrocorticography. Therapeutically relevant doses of AZM, CBZ, TPM, and ZNS increased hippocampal extracellular levels of GABA, NE, DA, and 5-HT, while PHT had no effect. Supratherapeutic doses of AZM, CBZ, PHT, TPM, and ZNS decreased extracellular levels of GABA, NE, DA, and 5-HT, without affecting Glu levels. Toxic doses of CBZ and PHT produced seizures (paradoxical intoxication), markedly increasing all transmitter levels, but TPM and ZNS even at toxic doses did not produce seizure. Co-administration experiments showed that therapeutically relevant doses of CBZ or PHT reduced the seizure-threshold doses of PHT or CBZ, respectively. In contrast, therapeutically relevant doses of AZM, TPM, and ZNS elevated the seizure-threshold doses of CBZ and PHT. These results suggested that blockade of high percentage of the population of voltage-dependent sodium channels by CBZ and PHT might be important in inducing paradoxical intoxication/reaction, and that inhibition of carbonic anhydrase inhibits this effect. TPM and ZNS are candidate first-choice agents in treatment of epilepsy when first-line AEDs are ineffective.}, - language = {en}, - number = {2}, - urldate = {2021-06-30}, - journal = {Epilepsy Research}, - author = {Yamamura, Satoshi and Hamaguchi, Tatsuya and Ohoyama, Keiko and Sugiura, Yoshihiro and Suzuki, Dai and Kanehara, Shinich and Nakagawa, Masanori and Motomura, Eishi and Matsumoto, Takuya and Tanii, Hisashi and Shiroyama, Takashi and Okada, Motohiro}, - month = apr, - year = {2009}, - keywords = {Carbonic anhydrase, Microdialysis, Neurotransmitter release, Paradoxical intoxication}, - pages = {172--186}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\LWBBJ9JF\\S0920121109000333.html:text/html}, -} - -@article{kawata_pharmacological_2001, - title = {Pharmacological discrimination between effects of carbamazepine on hippocampal basal, {Ca2}+- and {K}+-evoked serotonin release}, - volume = {133}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1038/sj.bjp.0704104}, - doi = {10.1038/sj.bjp.0704104}, - abstract = {To elucidate mechanisms of hippocampal serotonin release and possible mechanisms of clinical action of carbamazepine (CBZ), we determined interaction between antagonists of N-type (ω-conotoxin GVIA:GVIA), P-type (ω-agatoxin IVA:IVA) Ca2+ channels, Na+ channel (tetrodotoxin: TTX) and CBZ on hippocampal basal, Ca2+- and K+-evoked serotonin releases, using microdialysis in freely moving rats. Basal release was reduced by TTX, GVIA and IVA (GVIA{\textgreater}IVA). Ca2+-evoked release was reduced by GVIA but unaffected by TTX and IVA. K+-evoked release was reduced by TTX, GVIA and IVA (GVIA{\textless}IVA). TTX inhibited actions of IVA and GVIA on respective basal and K+-evoked releases, without affecting Ca2+-evoked release. Perfusion with 100 μM CBZ (estimated-concentration in hippocampal tissue: 19±2 μM) enhanced basal and Ca2+-evoked releases, but reduced K+-evoked release, whereas 1000 μM CBZ (estimated-concentration in hippocampal tissue: 188±16 μM) reduced three types of releases. Under condition of pretreatment with 100 and 1000 μM CBZ, TTX unaffected basal and K+-evoked releases. Under condition of pretreatment with 100 μM CBZ, IVA and GVIA unaffected basal and K+-evoked releases, respectively, but GVIA reduced basal, Ca2+-evoked releases and IVA also reduced K+-evoked release. Under condition of pretreatment with 1000 μM CBZ, GVIA unaffected three types of releases, and IVA unaffected basal release but reduced K+-evoked release. These findings contribute towards the possible mechanisms of concentration-dependent antiepileptic action of CBZ, which possibly inhibits Na+ channel related neurotransmitter release mechanisms during K+-evoked stage, and simultaneously enhances N-type Ca2+ channel related basal serotonin release at the resting stage. British Journal of Pharmacology (2001) 133, 557–567; doi:10.1038/sj.bjp.0704104}, - language = {en}, - number = {4}, - urldate = {2021-06-30}, - journal = {British Journal of Pharmacology}, - author = {Kawata, Yuko and Okada, Motohiro and Murakami, Takuya and Kamata, Akihisa and Zhu, Gang and Kaneko, Sunao}, - year = {2001}, - keywords = {serotonin, hippocampus, epilepsy, carbamazepine, Ca2+ channel, Na+ channel}, - pages = {557--567}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JNG25WC8\\Kawata et al. - 2001 - Pharmacological discrimination between effects of .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\PSY2PDHP\\sj.bjp.html:text/html}, -} - -@article{mizuno_effects_2000, - title = {Effects of carbamazepine on acetylcholine release and metabolism}, - volume = {40}, - issn = {0920-1211}, - url = {https://www.sciencedirect.com/science/article/pii/S0920121100001297}, - doi = {10.1016/S0920-1211(00)00129-7}, - abstract = {To clarify the mechanisms of action of carbamazepine (CBZ), we investigated the effects of CBZ on acetylcholine (ACh) release and metabolism in rat striatum and hippocampus. Acute administration of effective dose of CBZ (25 mg/kg) increased both striatal and hippocampal extracellular levels of ACh, whereas a supraeffective dose of CBZ (50 mg/kg) did not affect the levels and a toxic dose of CBZ (100 mg/kg) decreased the extracellular ACh levels in both brain regions. Both acute and chronic administrations of CBZ (25 and 50 mg/kg, mg/kg per day) increased intracellular ACh levels in striatum and hippocampus. The striatal intracellular ACh levels were decreased by both acute and chronic administrations of CBZ (100 mg/kg, mg/kg per day), whereas the hippocampal intracellular ACh levels were not affected. The effective CBZ concentration did not affect cholinesterase activity, whereas supraeffective CBZ concentration reduced it weakly. Effective dose of CBZ enhanced ACh release and synthesis; however, supraeffective doses of CBZ reduced ACh release and synthesis without enhancement of ACh degradation, indicating that CBZ has biphasic effects on ACh release and synthesis. Thus, the present findings, the slight stimulation of ACh function by effective dose of CBZ, are involved, at least partially, in the antiepileptic and mood stabilizing mechanisms of action of CBZ.}, - language = {en}, - number = {2}, - urldate = {2021-06-30}, - journal = {Epilepsy Research}, - author = {Mizuno, Kazuhisa and Okada, Motohiro and Murakami, Takuya and Kamata, Akihisa and Zhu, Gang and Kawata, Yuko and Wada, Kazumaru and Kaneko, Sunao}, - month = jul, - year = {2000}, - keywords = {Acetylcholine, Striatum, Epilepsy, Hippocampus, Carbamazepine, Microdialysis}, - pages = {187--195}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VVPKBH6A\\S0920121100001297.html:text/html}, -} - -@article{murakami_determination_2001, - title = {Determination of effects of antiepileptic drugs on {SNAREs}-mediated hippocampal monoamine release using in vivo microdialysis}, - volume = {134}, - issn = {1476-5381}, - url = {https://bpspubs.onlinelibrary.wiley.com/doi/abs/10.1038/sj.bjp.0704285}, - doi = {10.1038/sj.bjp.0704285}, - abstract = {To elucidate possible mechanisms underlying the effects of carbamazepine (CBZ), valproate (VPA) and zonisamide (ZNS) on neurotransmitter exocytosis, the interaction between these three antiepileptic drugs (AEDs) and botulinum toxins (BoNTs) on basal, Ca2+- and K+-evoked release of dopamine (DA) and serotonin (5-HT) were determined by microdialysis in the hippocampus of freely moving rats. Basal release of monoamine was decreased by pre-microinjection of the syntaxin inhibitor, BoNT/C, but only weakly affected by the synaptobrevin inhibitor, BoNT/B. Ca2+-evoked release was inhibited by BoNT/C selectively. K+-evoked release was reduced by BoNT/B predominantly and BoNT/C weakly. Perfusion with low and high concentrations of CBZ and ZNS increased and decreased basal monoamine release, respectively. Perfusion with VPA increased basal 5-HT release concentration-dependently, whereas basal DA release was affected by VPA biphasic concentration-dependently, similar to CBZ and ZNS. This stimulatory action of AEDs on basal release was inhibited by BoNT/C predominantly. Ca2+-evoked monoamine release was increased by low concentrations of CBZ, ZNS and VPA, but decreased by high concentrations. These effects of the AEDs on Ca2+-evoked release were inhibited by BoNT/C, but not by BoNT/B. K+-evoked monoamine release was reduced by AEDs concentration-dependently. The inhibitory effect of these three AEDs on K+-evoked release was inhibited by BoNT/B, but not by BoNT/C, These findings suggest that the therapeutic-relevant concentration of CBZ, VPA and ZNS affects exocytosis of DA and 5-HT, the enhancement of syntaxin-mediated monoamine release during resting stage, and the inhibition of synaptobrevin-mediated release during depolarizing stage. British Journal of Pharmacology (2001) 134, 507–520; doi:10.1038/sj.bjp.0704285}, - language = {en}, - number = {3}, - urldate = {2021-06-30}, - journal = {British Journal of Pharmacology}, - author = {Murakami, Takuya and Okada, Motohiro and Kawata, Yuko and Zhu, Gan and Kamata, Akihisa and Kaneko, Sunao}, - year = {2001}, - keywords = {serotonin, dopamine, valproate, zonisamide, botulinum toxin, Carbamezepine, exocytosis}, - pages = {507--520}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UM3CMAES\\Murakami et al. - 2001 - Determination of effects of antiepileptic drugs on.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B7Q4CQHU\\sj.bjp.html:text/html}, -} - -@article{zhu_interaction_2002, - title = {Interaction between carbamazepine, zonisamide and voltage-sensitive {Ca2}+ channel on acetylcholine release in rat frontal cortex}, - volume = {49}, - issn = {0920-1211}, - url = {https://www.sciencedirect.com/science/article/pii/S0920121102000153}, - doi = {10.1016/S0920-1211(02)00015-3}, - abstract = {To clarify the mechanisms of action of antiepileptic drugs (AEDs), carbamazepine (CBZ) and zonisamide (ZNS), on exocytosis mechanisms, the present study determined the concentration-dependent action of CBZ and ZNS, as well as the interaction between these AEDs and voltage-sensitive Ca2+ channel (VSCC) activity on basal, Ca2+- and K+-evoked acetylcholine (ACh) release in frontal cortex of freely moving rat using in vivo microdialysis. Perfusion with therapeutic-relevant concentrations of CBZ and ZNS increased basal ACh release, which was regulated by N-type VSCC predominantly and P-type VSCC weakly, whereas supratherapeutic-relevant concentrations of these AEDs reduced this release. The 3.4 mM Ca2+-evoked release, which was regulated by N-type VSCC selectively, but not by P-type VSCC, was increased by therapeutic-relevant concentrations of CBZ and ZNS, whereas this release was reduced by supratherapeutic-relevant concentrations of them. The 50 mM K+-evoked release, which was regulated by P-type VSCC predominantly and N-type VSCC weakly, was decreased by CBZ and ZNS, in a concentration-dependent manner. These findings indicate that the interplay between enhancement of basal ACh release and reduction of depolarization-related ACh release in the frontal cortex are at least partially involved in a common mechanism of antiepileptic action between CBZ and ZNS.}, - language = {en}, - number = {1}, - urldate = {2021-06-30}, - journal = {Epilepsy Research}, - author = {Zhu, Gang and Okada, Motohiro and Murakami, Takuya and Kawata, Yuko and Kamata, Akihisa and Kaneko, Sunao}, - month = mar, - year = {2002}, - keywords = {Acetylcholine, Epilepsy, Carbamazepine, Microdialysis, Frontal cortex, Zonisamide}, - pages = {49--60}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4IEP9NZN\\S0920121102000153.html:text/html}, -} - -@article{tanahashi_effect_2012, - title = {Effect of lamotrigine and carbamazepine on corticotropin-releasing factor-associated serotonergic transmission in rat dorsal raphe nucleus}, - volume = {220}, - issn = {1432-2072}, - url = {https://doi.org/10.1007/s00213-011-2506-y}, - doi = {10.1007/s00213-011-2506-y}, - abstract = {Corticotropin-releasing factor (CRF) and serotonin are important transmitters of the pathophysiology of mood disorder. To clarify the mechanisms of action of lamotrigine (LTG) and carbamazepine (CBZ), we determined their effects on serotonin release associated with CRF in rat dorsal raphe nucleus (DRN) and median prefrontal cortex (mPFC) using dual-probe microdialysis. Neither perfusion with CRF1 nor CRF2 antagonists into DRN-affected serotonin release in DRN and mPFC. Perfusion of 10 μM CRF into DRN increased serotonin release in both regions, whereas 0.1 μM CRF decreased and had no effect on serotonin release in DRN and mPFC, respectively. Pre-perfusion with CRF1 antagonist into DRN inhibited 0.1 μM CRF-induced serotonin reduction, whereas pre-perfusion with CRF2 antagonist in DRN inhibited 10 μM CRF-induced serotonin elevation, without affecting 0.1 μM CRF-induced serotonin reduction. LTG perfusion concentration dependently decreased serotonin releases in DRN and mPFC. Therapeutic and supratherapeutic concentrations of CBZ increased and decreased serotonin releases in both regions, respectively. Pre-perfusion with sub-therapeutic concentration LTG inhibited CRF1-induced serotonin reduction without affecting CRF2-induced serotonin release, whereas pre-perfusion with therapeutic concentration of LTG inhibited both CRF1- and CRF2-actions. In contrast, both therapeutic and supratherapeutic concentrations of CBZ inhibited CRF2-induced serotonin release without affecting CRF1-induced serotonin reduction. Neither LTG nor CBZ affected the CRF-induced cAMP production in cells over-expressing CRF1 and CRF2 receptors. This study demonstrated that inhibition of CRF2-receptor-mediated serotonergic transmission is a mechanism shared by LTG and CBZ, two clinically related compounds, whereas LTG but not CBZ inhibits CRF1-receptor-mediated serotonergic transmission. Therefore, these mechanisms may contribute to the clinical actions of these agents.}, - language = {en}, - number = {3}, - urldate = {2021-06-30}, - journal = {Psychopharmacology}, - author = {Tanahashi, Shunske and Yamamura, Satoshi and Nakagawa, Masanori and Motomura, Eishi and Okada, Motohiro}, - month = apr, - year = {2012}, - pages = {599--610}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ZXRQS5KG\\Tanahashi et al. - 2012 - Effect of lamotrigine and carbamazepine on cortico.pdf:application/pdf}, +@Article{chi_manipulation_2007, + author = {Chi, Xian Xuan and Nicol, G. D.}, + title = {Manipulation of the {Potassium} {Channel} {Kv1}.1 and {Its} {Effect} on {Neuronal} {Excitability} in {Rat} {Sensory} {Neurons}}, + doi = {10.1152/jn.00437.2007}, + issn = {0022-3077}, + number = {5}, + pages = {2683--2692}, + url = {https://journals.physiology.org/doi/full/10.1152/jn.00437.2007}, + urldate = {2021-06-10}, + volume = {98}, + abstract = {Potassium channels play a critical role in regulating many aspects of action potential (AP) firing. To establish the contribution of the voltage-dependent potassium channel Kv1.1 in regulating excitability, we used the selective blocker dendrotoxin-K (DTX-K) and small interfering RNA (siRNA) targeted to Kv1.1 to determine their effects on AP firing in small-diameter capsaicin-sensitive sensory neurons. A 5-min exposure to 10 nM DTX-K suppressed the total potassium current (IK) measured at +40 mV by about 33\%. DTX-K produced a twofold increase in the number of APs evoked by a ramp of depolarizing current. Associated with increased firing was a decrease in firing threshold and rheobase. DTX-K did not alter the resting membrane potential or the AP duration. A 48-h treatment with siRNA targeted to Kv1.1 reduced the expression of this channel protein by about 60\% as measured in Western blots. After treatment with siRNA, IK was no longer sensitive to DTX-K, indicating a loss of functional protein. Similarly, after siRNA treatment exposure to DTX-K had no effect on the number of evoked APs, firing threshold, or rheobase. However, after siRNA treatment, the firing threshold had values similar to those obtained after acute exposure to DTX-K, suggesting that the loss of Kv1.1 plays a critical role in setting this parameter of excitability. These results demonstrate that Kv1.1 plays an important role in limiting AP firing and that siRNA may be a useful approach to establish the role of specific ion channels in the absence of selective antagonists.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4K5J2PLY\\Chi and Nicol - 2007 - Manipulation of the Potassium Channel Kv1.1 and It.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\K6U2R6HN\\jn.00437.html:text/html}, + journal = {Journal of Neurophysiology}, + month = nov, + year = {2007}, +} + +@Article{johannesen_genotype-phenotype_2021, + author = {Johannesen, Katrine M. and Liu, Yuanyuan and Gjerulfsen, Cathrine E. and Koko, Mahmoud and Sonnenberg, Lukas and Schubert, Julian and Fenger, Christina D. and Eltokhi, Ahmed and Rannap, Maert and Koch, Nils A. and Lauxmann, Stephan and Krüger, Johanna and Kegele, Josua and Canafoglia, Laura and Franceschetti, Silvana and Mayer, Thomas and Rebstock, Johannes and Zacher, Pia and Ruf, Susanne and Alber, Michael and Sterbova, Katalin and Lassuthová, Petra and Vlckova, Marketa and Lemke, Johannes R. and Krey, Ilona and Heine, Constanze and Wieczorek, Dagmar and Kroell-Seger, Judith and Lund, Caroline and Klein, Karl Martin and Au, PY Billie and Rho, Jong M. and Ho, Alice W. and Masnada, Silvia and Veggiotti, Pierangelo and Giordano, Lucio and Accorsi, Patrizia and Hoei-Hansen, Christina E. and Striano, Pasquale and Zara, Federico and Verhelst, Helene and S.Verhoeven, Judith and Zwaag, Bert van der and Harder, Aster V. E. and Brilstra, Eva and Pendziwiat, Manuela and Lebon, Sebastian and Vaccarezza, Maria and Le, Ngoc Minh and Christensen, Jakob and Schmidt-Petersen, Mette U. and Grønborg, Sabine and Scherer, Stephen W. and Howe, Jennifer and Fazeli, Walid and Howell, Katherine B. and Leventer, Richard and Stutterd, Chloe and Walsh, Sonja and Gerard, Marion and Gerard, Bénédicte and Matricardi, Sara and Bonardi, Claudia M. and Sartori, Stefano and Berger, Andrea and Hoffman-Zacharska, Dorota and Mastrangelo, Massimo and Darra, Francesca and Vøllo, Arve and Motazacker, M. Mahdi and Lakeman, Phillis and Nizon, Mathilde and Betzler, Cornelia and Altuzarra, Cecilia and Caume, Roseline and Roubertie, Agathe and Gélisse, Philippe and Marini, Carla and Guerrini, Renzo and Bilan, Frederic and Tibussek, Daniel and Koch-Hogrebe, Margarete and Perry, M. Scott and Ichikawa, Shoji and Dadali, Elena and Sharkov, Artem and Mishina, Irina and Abramov, Mikhail and Kanivets, Ilya and Korostelev, Sergey and Kutsev, Sergey and Wain, Karen E. and Eisenhauer, Nancy and Wagner, Monisa and Savatt, Juliann M. and Müller-Schlüter, Karen and Bassan, Haim and Borovikov, Artem and Nassogne, Marie-Cecile and Destrée, Anne and Schoonjans, An-Sofie and Meuwissen, Marije and Buzatu, Marga and Jansen, Anna and Scalais, Emmanuel and Srivastava, Siddharth and Tan, Wen-Hann and Olson, Heather E. and Loddenkemper, Tobias and Poduri, Annapurna and Helbig, Katherine L. and Helbig, Ingo and Fitzgerald, Mark P. and Goldberg, Ethan M. and Roser, Timo and Borggraefe, Ingo and Brünger, Tobias and May, Patrick and Lal, Dennis and Lederer, Damien and Rubboli, Guido and Lesca, Gaetan and Hedrich, Ulrike BS and Benda, Jan and Gardella, Elena and Lerche, Holger and Møller, Rikke S.}, + title = {Genotype-phenotype correlations in {SCN8A}-related disorders reveal prognostic and therapeutic implications}, + doi = {10.1101/2021.03.22.21253711}, + language = {en}, + pages = {2021.03.22.21253711}, + url = {https://www.medrxiv.org/content/10.1101/2021.03.22.21253711v1}, + urldate = {2021-07-29}, + abstract = {{\textless}h3{\textgreater}Abstract{\textless}/h3{\textgreater} {\textless}p{\textgreater}We report detailed functional analyses and genotype-phenotype correlations in 433 individuals carrying disease-causing variants in \textit{SCN8A}, encoding the voltage-gated Na$^{\textrm{+}}$ channel Na$_{\textrm{V}}$1.6. Five different clinical subgroups could be identified: 1) Benign familial infantile epilepsy (BFIE) (n=17, normal cognition, treatable seizures), 2) intermediate epilepsy (n=36, mild ID, partially pharmacoresponsive), 3) developmental and epileptic encephalopathy (DEE, n=191, severe ID, majority pharmacoresistant), 4) generalized epilepsy (n=21, mild to moderate ID, frequently with absence seizures), and 5) affected individuals without epilepsy (n=25, mild to moderate ID). Groups 1-3 presented with early-onset (median: four months) focal or multifocal seizures and epileptic discharges, whereas the onset of seizures in group 4 was later (median: 39 months) with generalized epileptic discharges. The epilepsy was not classifiable in 143 individuals. We performed functional studies expressing missense variants in ND7/23 neuroblastoma cells and primary neuronal cultures using recombinant tetrodotoxin insensitive human Na$_{\textrm{V}}$1.6 channels and whole-cell patch clamping. Two variants causing DEE showed a strong gain-of-function (GOF, hyperpolarising shift of steady-state activation, strongly increased neuronal firing rate), and one variant causing BFIE or intermediate epilepsy showed a mild GOF (defective fast inactivation, less increased firing). In contrast, all three variants causing generalized epilepsy induced a loss-of-function (LOF, reduced current amplitudes, depolarising shift of steady-state activation, reduced neuronal firing). Including previous studies, functional effects were known for 165 individuals. All 133 individuals carrying GOF variants had either focal (76, groups 1-3), or unclassifiable epilepsy (37), whereas 32 with LOF variants had either generalized (14), no (11) or unclassifiable (5) epilepsy; only two had DEE. Computational modeling in the GOF group revealed a significant correlation between the severity of the electrophysiological and clinical phenotypes. GOF variant carriers responded significantly better to sodium channel blockers (SCBs) than to other anti-seizure medications, and the same applied for all individuals of groups 1-3.{\textless}/p{\textgreater}{\textless}p{\textgreater}In conclusion, our data reveal clear genotype-phenotype correlations between age at seizure onset, type of epilepsy and gain- or loss-of-function effects of \textit{SCN8A} variants. Generalized epilepsy with absence seizures is the main epilepsy phenotype of LOF variant carriers and the extent of the electrophysiological dysfunction of the GOF variants is a main determinant of the severity of the clinical phenotype in focal epilepsies. Our pharmacological data indicate that SCBs present a therapeutic treatment option in early onset \textit{SCN8A}-related focal epilepsy.{\textless}/p{\textgreater}}, + copyright = {© 2021, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0, as described at http://creativecommons.org/licenses/by-nd/4.0/}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\473Q4W4Z\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\I4ATHYDV\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5BLXZ69T\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4UWL4V5H\\2021.03.22.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\E7KCJBEZ\\2021.03.22.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FS6JAG82\\2021.03.22.html:text/html}, + journal = {medRxiv}, + month = mar, + year = {2021}, +} + +@Article{smart_deletion_1998, + author = {Smart, Sharon L. and Lopantsev, Valeri and Zhang, C. L. and Robbins, Carol A. and Wang, Hao and Chiu, S. Y. and Schwartzkroin, Philip A. and Messing, Albee and Tempel, Bruce L.}, + title = {Deletion of the {KV1}.1 {Potassium} {Channel} {Causes} {Epilepsy} in {Mice}}, + doi = {10.1016/S0896-6273(00)81018-1}, + issn = {0896-6273}, + language = {en}, + number = {4}, + pages = {809--819}, + url = {https://www.sciencedirect.com/science/article/pii/S0896627300810181}, + urldate = {2021-06-10}, + volume = {20}, + abstract = {Mice lacking the voltage-gated potassium channel α subunit, KV1.1, display frequent spontaneous seizures throughout adult life. In hippocampal slices from homozygous KV1.1 null animals, intrinsic passive properties of CA3 pyramidal cells are normal. However, antidromic action potentials are recruited at lower thresholds in KV1.1 null slices. Furthermore, in a subset of slices, mossy fiber stimulation triggers synaptically mediated long-latency epileptiform burst discharges. These data indicate that loss of KV1.1 from its normal localization in axons and terminals of the CA3 region results in increased excitability in the CA3 recurrent axon collateral system, perhaps contributing to the limbic and tonic–clonic components of the observed epileptic phenotype. Axonal action potential conduction was altered as well in the sciatic nerve—a deficit potentially related to the pathophysiology of episodic ataxia/myokymia, a disease associated with missense mutations of the human KV1.1 gene.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BWWW4ZL8\\Smart et al. - 1998 - Deletion of the KV1.1 Potassium Channel Causes Epi.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\A7QYCC6F\\S0896627300810181.html:text/html}, + journal = {Neuron}, + month = apr, + year = {1998}, +} + +@Article{wang__1999, + author = {Wang, Fan C. and Parcej, David N. and Dolly, J. Oliver}, + title = {α {Subunit} compositions of {Kv1}.1-containing {K}+ channel subtypes fractionated from rat brain using dendrotoxins}, + doi = {https://doi.org/10.1046/j.1432-1327.1999.00493.x}, + issn = {1432-1033}, + language = {en}, + number = {1}, + pages = {230--237}, + url = {https://febs.onlinelibrary.wiley.com/doi/abs/10.1046/j.1432-1327.1999.00493.x}, + urldate = {2021-06-07}, + volume = {263}, + abstract = {K+ channels from the Kv1 subfamily contain four α-subunits and the combinations (from Kv1.1–1.6) determine susceptibility to dendrotoxin (DTX) homologues. The subunit composition of certain subtypes in rat brain was investigated using DTXk which only interacts with Kv1.1-containing channels and αDTX (and its closely related homologue DTXi) that binds preferentially to Kv1.2-possessing homo- or hetero-oligomers. Covalent attachment of [125I]DTXk bound to channels in synaptic membranes unveiled subunits of Mr = 78 000 and 96 000. Immunoprecipitation of these solubilized and dissociated cross-linked proteins with IgG specific for each of the α-subunits identified Kv1.1, 1.2 and 1.4; this led to assemblies of Kv1.1/1.2 and 1.1/1.4 being established. Kv1.2-enriched channels, purified from rat brain by chromatography on immobilized DTXi, contained Kv1.1, 1.2 and 1.6 confirming one of the above-noted pairs and indicating an additional Kv1.1-containing oligomer (Kv1.1/1.2/1.6); the notable lack of Kv1.4 excludes a Kv1.1/1.2/1.4 combination. On the other hand, channels with Kv1.1 as a constituent, isolated using DTXk, possessed Kv1.4 in addition to those found in the DTXi-purified oligomers; this provides convergent support for the occurrence of the three combinations established above but adds a possible fourth (Kv1.1/1.4/1.6), though this was not confirmed. Moreover, sequential purification on DTXi and DTXk resins yielded channels containing only Kv1.1/1.2 but with an apparent predominance of Kv1.1, reaffirming the latter multimer.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\UZDUM8RP\\Wang et al. - 1999 - α Subunit compositions of Kv1.1-containing K+ chan.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\99X9K88C\\j.1432-1327.1999.00493.html:text/html}, + journal = {European Journal of Biochemistry}, + keywords = {K+ channels, dendrotoxins., hetero-oligomers, voltage-gated, α and β subunits}, + year = {1999}, } -@article{gjorgjieva_computational_2016, - series = {Neurobiology of cognitive behavior}, - title = {Computational implications of biophysical diversity and multiple timescales in neurons and synapses for circuit performance}, - volume = {37}, - issn = {0959-4388}, - url = {https://www.sciencedirect.com/science/article/pii/S0959438815001865}, - doi = {10.1016/j.conb.2015.12.008}, - abstract = {Despite advances in experimental and theoretical neuroscience, we are still trying to identify key biophysical details that are important for characterizing the operation of brain circuits. Biological mechanisms at the level of single neurons and synapses can be combined as ‘building blocks’ to generate circuit function. We focus on the importance of capturing multiple timescales when describing these intrinsic and synaptic components. Whether inherent in the ionic currents, the neuron's complex morphology, or the neurotransmitter composition of synapses, these multiple timescales prove crucial for capturing the variability and richness of circuit output and enhancing the information-carrying capacity observed across nervous systems.}, - language = {en}, - urldate = {2021-06-30}, - journal = {Current Opinion in Neurobiology}, - author = {Gjorgjieva, Julijana and Drion, Guillaume and Marder, Eve}, - month = apr, - year = {2016}, - pages = {44--52}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DNIIV7XN\\Gjorgjieva et al. - 2016 - Computational implications of biophysical diversit.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2B5ST6MT\\S0959438815001865.html:text/html}, + +@Article{Smith2018, + author = {Smith, Richard S. and Kenny, Connor J. and Ganesh, Vijay and Jang, Ahram and Borges-Monroy, Rebeca and Partlow, Jennifer N. and Hill, R. Sean and Shin, Taehwan and Chen, Allen Y. and Doan, Ryan N. and Anttonen, Anna-Kaisa and Ignatius, Jaakko and Medne, Livija and Bönnemann, Carsten G. and Hecht, Jonathan L. and Salonen, Oili and Barkovich, A. James and Poduri, Annapurna and Wilke, Martina and de Wit, Marie Claire Y. and Mancini, Grazia M. S. and Sztriha, Laszlo and Im, Kiho and Amrom, Dina and Andermann, Eva and Paetau, Ritva and Lehesjoki, Anna-Elina and Walsh, Christopher A. and Lehtinen, Maria K.}, + title = {Sodium {Channel} {SCN3A} ({NaV1}.3) {Regulation} of {Human} {Cerebral} {Cortical} {Folding} and {Oral} {Motor} {Development}}, + doi = {10.1016/j.neuron.2018.07.052}, + issn = {0896-6273}, + language = {en}, + number = {5}, + pages = {905--913.e7}, + url = {https://www.sciencedirect.com/science/article/pii/S0896627318306500}, + urldate = {2022-04-03}, + volume = {99}, + abstract = {Channelopathies are disorders caused by abnormal ion channel function in differentiated excitable tissues. We discovered a unique neurodevelopmental channelopathy resulting from pathogenic variants in SCN3A, a gene encoding the voltage-gated sodium channel NaV1.3. Pathogenic NaV1.3 channels showed altered biophysical properties including increased persistent current. Remarkably, affected individuals showed disrupted folding (polymicrogyria) of the perisylvian cortex of the brain but did not typically exhibit epilepsy; they presented with prominent speech and oral motor dysfunction, implicating SCN3A in prenatal development of human cortical language areas. The development of this disorder parallels SCN3A expression, which we observed to be highest early in fetal cortical development in progenitor cells of the outer subventricular zone and cortical plate neurons and decreased postnatally, when SCN1A (NaV1.1) expression increased. Disrupted cerebral cortical folding and neuronal migration were recapitulated in ferrets expressing the mutant channel, underscoring the unexpected role of SCN3A in progenitor cells and migrating neurons.}, + file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S0896627318306500/pdfft?md5=d4b6d398954109734090f8df1166b96c&pid=1-s2.0-S0896627318306500-main.pdf&isDTMRedir=Y:application/pdf}, + groups = {Jan}, + journal = {Neuron}, + keywords = {Cortical Development, Polymicrogyria, Oromotor, Speech, Na1.3, Na1.1, Voltage-Gated Sodium Channel (VGSC), Outer Radial Glia}, + month = sep, + year = {2018}, +} + +@Article{golowasch_failure_2002, + author = {Golowasch, Jorge and Goldman, Mark S. and Abbott, L. F. and Marder, Eve}, + title = {Failure of {Averaging} in the {Construction} of a {Conductance}-{Based} {Neuron} {Model}}, + doi = {10.1152/jn.00412.2001}, + issn = {0022-3077}, + number = {2}, + pages = {1129--1131}, + url = {https://journals.physiology.org/doi/full/10.1152/jn.00412.2001}, + urldate = {2021-06-17}, + volume = {87}, + abstract = {Parameters for models of biological systems are often obtained by averaging over experimental results from a number of different preparations. To explore the validity of this procedure, we studied the behavior of a conductance-based model neuron with five voltage-dependent conductances. We randomly varied the maximal conductance of each of the active currents in the model and identified sets of maximal conductances that generate bursting neurons that fire a single action potential at the peak of a slow membrane potential depolarization. A model constructed using the means of the maximal conductances of this population is not itself a one-spike burster, but rather fires three action potentials per burst. Averaging fails because the maximal conductances of the population of one-spike bursters lie in a highly concave region of parameter space that does not contain its mean. This demonstrates that averages over multiple samples can fail to characterize a system whose behavior depends on interactions involving a number of highly variable components.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3XUIS8H6\\Golowasch et al. - 2002 - Failure of Averaging in the Construction of a Cond.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\3PM5WXVV\\jn.00412.html:text/html}, + journal = {Journal of Neurophysiology}, + month = feb, + year = {2002}, +} + +@Article{lamb_correlated_2013, + author = {Lamb, Damon G. and Calabrese, Ronald L.}, + title = {Correlated {Conductance} {Parameters} in {Leech} {Heart} {Motor} {Neurons} {Contribute} to {Motor} {Pattern} {Formation}}, + doi = {10.1371/journal.pone.0079267}, + issn = {1932-6203}, + language = {en}, + number = {11}, + pages = {e79267}, + url = {https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0079267}, + urldate = {2021-07-01}, + volume = {8}, + abstract = {Neurons can have widely differing intrinsic membrane properties, in particular the density of specific conductances, but how these contribute to characteristic neuronal activity or pattern formation is not well understood. To explore the relationship between conductances, and in particular how they influence the activity of motor neurons in the well characterized leech heartbeat system, we developed a new multi-compartmental Hodgkin-Huxley style leech heart motor neuron model. To do so, we evolved a population of model instances, which differed in the density of specific conductances, capable of achieving specific output activity targets given an associated input pattern. We then examined the sensitivity of measures of output activity to conductances and how the model instances responded to hyperpolarizing current injections. We found that the strengths of many conductances, including those with differing dynamics, had strong partial correlations and that these relationships appeared to be linked by their influence on heart motor neuron activity. Conductances that had positive correlations opposed one another and had the opposite effects on activity metrics when perturbed whereas conductances that had negative correlations could compensate for one another and had similar effects on activity metrics.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\L77ATPCI\\Lamb and Calabrese - 2013 - Correlated Conductance Parameters in Leech Heart M.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\V74V8IWQ\\article.html:text/html}, + journal = {PLOS ONE}, + keywords = {Interneurons, Motor neurons, Action potentials, Membrane potential, Axons, Heart, Leeches, Neurites}, + month = nov, + year = {2013}, +} + +@Article{morales-villagran_protection_1996, + author = {Morales-Villagrán, Alberto and Ureña-Guerrero, Mónica E. and Tapia, Ricardo}, + title = {Protection by {NMDA} receptor antagonists against seizures induced by intracerebral administration of 4-aminopyridine}, + doi = {10.1016/0014-2999(96)00157-4}, + issn = {0014-2999}, + language = {en}, + number = {1}, + pages = {87--93}, + url = {https://www.sciencedirect.com/science/article/pii/0014299996001574}, + urldate = {2021-06-12}, + volume = {305}, + abstract = {The effects of NMDA receptor antagonists on the convulsant action of the administration of 4-aminopyridine in the rat lateral cerebral ventricle (i.c.v. injection) and motor cerebral cortex (i.cx. injection) were studied. 4-Aminopyridine administration in both regions induced various preconvulsive symptoms, such as salivation, tremors, chewing and rearing, followed by continuous clonic convulsions and, only after i.c.v. injection, running fits and generalized tonic convulsions. This behavioral pattern appeared 5–9 min after administration of 4-aminopyridine and persisted for 100–150 min. 4-Aminopyridine also generated epileptiform electroencephalographic (EEG) discharges characterized by isolated spikes, poly-spikes and spike-wave complexes, which began some seconds after administration of the drug and were present for more than 2 h. The NMDA receptor antagonists (±)-3-(2-carboxy-piperazin-4-yl)-propyl-1-phosphonic acid (CPP), (±)-2-amino-7-phosphono-heptanoic acid (AP7) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine hydrogen maleate (MK-801) clearly protected against some of the behavioral alterations induced by i.c.v. 4-aminopyridine, particularly the tonic convulsions, but were less effective against those produced by i.cx. 4-aminopyridine. These antagonists also delayed the appearance of EEG epileptiform discharges, reduced its amplitude, frequency and duration, and blocked their propagation to other cortical regions after i.cx. 4-aminopyridine. These results, together with previous data showing that 4-aminopyridine stimulates the release of glutamate in vivo, suggest that an excessive glutamatergic neurotransmission involving NMDA receptors is implicated in 4-aminopyridine-induced seizures.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CIJQBWZV\\Morales-Villagrán et al. - 1996 - Protection by NMDA receptor antagonists against se.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9EDF8NNK\\0014299996001574.html:text/html}, + journal = {European Journal of Pharmacology}, + keywords = {Seizure, 4-Aminopyridine, Excitatory amino acid neurotransmission, NMDA receptor antagonist}, + month = jun, + year = {1996}, +} + +@Article{graves_episodic_2014, + author = {Graves, Tracey D. and Cha, Yoon-Hee and Hahn, Angelika F. and Barohn, Richard and Salajegheh, Mohammed K. and Griggs, Robert C. and Bundy, Brian N. and Jen, Joanna C. and Baloh, Robert W. and Hanna, Michael G. and {on behalf of the CINCH Investigators}}, + title = {Episodic ataxia type 1: clinical characterization, quality of life and genotype–phenotype correlation}, + doi = {10.1093/brain/awu012}, + issn = {0006-8950}, + number = {4}, + pages = {1009--1018}, + url = {https://doi.org/10.1093/brain/awu012}, + urldate = {2021-06-10}, + volume = {137}, + abstract = {Episodic ataxia type 1 is considered a rare neuronal ion channel disorder characterized by brief attacks of unsteadiness and dizziness with persistent myokymia. To characterize the natural history, develop outcome measures for future clinical trials, and correlate genotype with phenotype, we undertook an international, prospective, cross-sectional study. Thirty-nine individuals (51\% male) were enrolled: median age 37 years (range 15–65 years). We identified 10 different pathogenic point mutations in KCNA1 that accounted for the genetic basis of 85\% of the cohort. Participants with KCNA1 mutations were more likely to have a positive family history. Analysis of the total cohort showed that the first episode of ataxia occurred before age 20 in all but one patient, with an average age of onset of 7.9 years. Physical exertion, emotional stress and environmental temperature were the most common triggers for attacks. Attack frequency ranged from daily to monthly, even with the same KCNA1 genotype. Average attack duration was in the order of minutes. Ten participants (26\%) developed permanent cerebellar signs, which were related to disease duration. The average Scale for the Assessment and Rating of Ataxia score (SARA, a standardized measure of cerebellar dysfunction on clinical examination, scores range from 0–40) was an average of 3.15 for all participants (range 0–14), but was only 2 in those with isolated episodic ataxia compared with 7.7 in those with progressive cerebellar ataxia in addition to episodic ataxia. Thirty-seven participants completed the SF-36, a quality of life survey; all eight domain norm-based average scores (mean = 50) were below normal with mental health being the lowest (41.3) in those with mutation positive episodic ataxia type 1. Scores on SF-36 correlated negatively with attack frequency. Of the 39 participants in the study, 33 harboured mutations in KCNA1 whereas the remaining six had no mutation identified. Episodic ataxia type 1 phenocopies have not been described previously and we report their clinical features, which appear to be different to those with a KCNA1 mutation. This large prospective study of both genetically confirmed episodic ataxia type 1 and episodic ataxia type 1 phenocopies provides detailed baseline characteristics of these disorders and their impact on participants. We found that attacks had a significant effect on quality of life. Unlike previous studies, we found that a significant number of individuals with genetically confirmed episodic ataxia type 1 (21\%) had accumulated persistent cerebellar symptoms and signs. These data will enable the development of outcome measures for clinical trials of treatment.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GW4CYP4I\\Graves et al. - 2014 - Episodic ataxia type 1 clinical characterization,.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\962LHS6A\\Graves et al. - 2014 - Episodic ataxia type 1 clinical characterization,.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\G5KRDWAE\\367720.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FAHUQPK8\\367720.html:text/html}, + journal = {Brain}, + month = apr, + shorttitle = {Episodic ataxia type 1}, + year = {2014}, +} + +@Article{dadamo_episodic_1998, + author = {D'Adamo, Maria Cristina and Liu, Zhaoping and Adelman, John P. and Maylie, James and Pessia, Mauro}, + title = {Episodic ataxia type-1 mutations in the {hKv1}.1 cytoplasmic pore region alter the gating properties of the channel}, + doi = {10.1093/emboj/17.5.1200}, + issn = {0261-4189}, + number = {5}, + pages = {1200--1207}, + url = {https://www.embopress.org/doi/full/10.1093/emboj/17.5.1200}, + urldate = {2021-06-12}, + volume = {17}, + abstract = {Episodic ataxia type-1 is a rare human neurological syndrome which occurs during childhood and persists through the whole life of affected patients. Several heterozygous point mutations have been found in the coding sequence of the voltage-gated potassium channel gene hKv1.1 of different affected families. V408A and E325D mutations are located in the cytoplasmic putative pore region of hKv1.1 channels and profoundly alter their gating properties. V408A channels showed increased kinetic rates of activation, deactivation and C-type inactivation. Expression of E325D channels in Xenopus oocytes led to an ?13-fold current amplitude reduction and to a 52.4 mV positive shift in the voltage dependence of activation. Moreover, the E325D mutation altered the kinetics of activation, deactivation, C-type inactivation and channel open probability. Heteromeric channels composed of two wild-type and two mutated subunits, linked as dimers, showed gating properties intermediate between channels formed from four normal or four mutated subunits. The results demonstrate that the highly conserved residues Val408 and Glu325 play a pivotal role in several gating processes of a human potassium channel, and suggest a pathogenetic mechanism by which the impairment of the delayed-rectifier function of affected neurons is related to the type and number of mutated subunits which make up the hKv1.1 channels.}, + file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\65BKUWQM\\D'Adamo et al. - 1998 - Episodic ataxia type-1 mutations in the hKv1.1 cyt.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4ZQ529AL\\17.5.html:text/html}, + journal = {The EMBO Journal}, + keywords = {potassium channel, gating, episodic ataxia type-1, hKv1.1 channels, mutation}, + month = mar, + year = {1998}, } -@article{goaillard_ion_2021, - title = {Ion {Channel} {Degeneracy}, {Variability}, and {Covariation} in {Neuron} and {Circuit} {Resilience}}, - issn = {0147-006X}, - url = {https://www.annualreviews.org/doi/10.1146/annurev-neuro-092920-121538}, - doi = {10.1146/annurev-neuro-092920-121538}, - abstract = {The large number of ion channels found in all nervous systems poses fundamental questions concerning how the characteristic intrinsic properties of single neurons are determined by the specific subsets of channels they express. All neurons display many different ion channels with overlapping voltage- and time-dependent properties. We speculate that these overlapping properties promote resilience in neuronal function. Individual neurons of the same cell type show variability in ion channel conductance densities even though they can generate reliable and similar behavior. This complicates a simple assignment of function to any conductance and is associated with variable responses of neurons of the same cell type to perturbations, deletions, and pharmacological manipulation. Ion channel genes often show strong positively correlated expression, which may result from the molecular and developmental rules that determine which ion channels are expressed in a given cell type. Expected final online publication date for the Annual Review of Neuroscience, Volume 44 is July 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.}, - urldate = {2021-07-01}, - journal = {Annual Review of Neuroscience}, - author = {Goaillard, Jean-Marc and Marder, Eve}, - month = jul, - year = {2021}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CLGI3EBW\\Goaillard and Marder - 2021 - Ion Channel Degeneracy, Variability, and Covariati.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MVGHAFMQ\\annurev-neuro-092920-121538.html:text/html}, + +@Article{Leffler2005, + author = {Leffler, Andreas and Herzog, Raimund I. and Dib-Hajj, Sulayman D. and Waxman, Stephen G. and Cummins, Theodore R.}, + title = {Pharmacological properties of neuronal {TTX}-resistant sodium channels and the role of a critical serine pore residue}, + doi = {10.1007/s00424-005-1463-x}, + issn = {1432-2013}, + language = {en}, + number = {3}, + pages = {454--463}, + url = {https://doi.org/10.1007/s00424-005-1463-x}, + urldate = {2022-04-03}, + volume = {451}, + abstract = {Voltage-gated sodium channels can be characterized by their sensitivity to inhibitors. Nav1.5 is sensitive to block by cadmium and extracellular QX-314, but relatively insensitive to tetrodotoxin and saxitoxin. Nav1.4 is tetrodotoxin- and saxitoxin-sensitive but resistant to cadmium and extracellular QX-314. Nav1.8 and Nav1.9 generate slowly inactivating (ITTXr-Slow) and persistent (ITTXr-Per) currents in sensory neurons that are tetrodotoxin-resistant. Tetrodotoxin sensitivity is largely determined by the identity of a single residue; tyrosine 401 in Nav1.4, cysteine 374 in Nav1.5 and serine 356 and 355 in Nav1.8 and Nav1.9. We asked whether Nav1.8 and Nav1.9 share other pharmacological properties as a result of this serine residue. ITTXr-Slow and ITTXr-Per were saxitoxin-resistant and resistant to internal QX-314. ITTXr-Slow was also resistant to external QX-314 and displayed a approximately fourfold higher sensitivity than ITTXr-Per to cadmium. The impact of the serine residue was investigated by replacing tyrosine 401 in Nav1.4 with serine (Y401S) or cysteine (Y401C). Both mutants were resistant to tetrodotoxin and saxitoxin. Whereas Nav1.4-Y401C displayed an increased sensitivity to cadmium and extracellular QX-314, the serine substitution did not alter the sensitivity of Nav1.4 to cadmium or QX-314. Our data indicates that while the serine residue determines the sensitivity of ITTXr-Slow and ITTXr-Per to tetrodotoxin and saxitoxin, it does not determine their insensitivity to QX-314 or their differential sensitivities to cadmium.}, + file = {:Leffler2005 - Pharmacological Properties of Neuronal TTX Resistant Sodium Channels and the Role of a Critical Serine Pore Residue.pdf:PDF}, + groups = {Jan}, + journal = {Pflügers Archiv}, + month = dec, + year = {2005}, } -@article{puopolo_roles_2007, - title = {Roles of {Subthreshold} {Calcium} {Current} and {Sodium} {Current} in {Spontaneous} {Firing} of {Mouse} {Midbrain} {Dopamine} {Neurons}}, - volume = {27}, - number = {3}, - journal = {Journal of Neuroscience}, - author = {Puopolo, Michelino and Raviola, Elio and Bean, Bruce P.}, - month = jan, - year = {2007}, - pages = {645--656}, - file = {Roles of Subthreshold Calcium Current and Sodium Current in Spontaneous Firing of Mouse Midbrain Dopamine Neurons | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\ICI7GVB3\\645.html:text/html}, +@Article{Ackerman2013, + author = {Ackerman, Michael J. and Marcou, Cherisse A. and Tester, David J.}, + title = {Personalized {Medicine}: {Genetic} {Diagnosis} for {Inherited} {Cardiomyopathies}/{Channelopathies}}, + doi = {10.1016/j.rec.2012.12.010}, + issn = {1885-5857}, + language = {en}, + number = {4}, + pages = {298--307}, + url = {https://www.sciencedirect.com/science/article/pii/S1885585713000376}, + urldate = {2022-03-06}, + volume = {66}, + abstract = {Major advances in the field of molecular genetics have expanded our ability to identify genetic substrates underlying the pathogenesis of various disorders that follow Mendelian inheritance patterns. Included among these disorders are the potentially lethal and heritable channelopathies and cardiomyopathies for which the underlying genetic basis has been identified and is now better understood. Clinical and genetic heterogeneity are hallmark features of these disorders, with thousands of gene mutations being implicated within these divergent cardiovascular diseases. Genetic testing for several of these heritable channelopathies and cardiomyopathies has matured from discovery to research-based genetic testing to clinically/commercially available diagnostic tests. The purpose of this review is to provide the reader with a basic understanding of human medical genetics and genetic testing in the context of cardiovascular diseases of the heart. We review the state of clinical genetic testing for the more common channelopathies and cardiomyopathies, discuss some of the pertinent issues that arise from genetic testing, and discuss the future of personalized medicine in cardiovascular disease. Resumen Se han producido avances importantes en el campo de la genética molecular que han ampliado nuestra capacidad de identificar sustratos genéticos subyacentes a la patogenia de diversos trastornos que siguen patrones de herencia mendeliana. Entre estos trastornos, se encuentran las canalopatías y miocardiopatías hereditarias y potencialmente mortales con base genética subyacente identificada y que ahora se conoce mejor. La heterogeneidad clínica y genética es una característica distintiva de estos trastornos, con miles de mutaciones génicas involucradas en estas enfermedades cardiovasculares divergentes. Las pruebas genéticas en varias de estas canalopatías y miocardiopatías hereditarias han alcanzado ya la fase de madurez, tras evolucionar desde su descubrimiento a las pruebas genéticas para investigación y las pruebas diagnósticas disponibles para uso clínico/comercial. El objetivo de esta revisión es proporcionar al lector un conocimiento básico de la genética médica humana y las pruebas genéticas existentes en el contexto de las enfermedades cardiovasculares que afectan al corazón. Revisamos el estado actual de las pruebas genéticas clínicas para las canalopatías y miocardiopatías más frecuentes, tratamos asuntos pertinentes que surgen de utilizar pruebas genéticas y sobre el futuro de la medicina personalizada en las enfermedades cardiovasculares.}, + file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S1885585713000376/pdfft?md5=c6c96ffe659f2463a28e50b927b90d06&pid=1-s2.0-S1885585713000376-main.pdf&isDTMRedir=Y:application/pdf}, + groups = {Jan}, + journal = {Revista Española de Cardiología (English Edition)}, + keywords = {Genetics, Ion channels, Cardiomyopathy, Channelopathies, Genética, Canales iónicos, Miocardiopatía, Canalopatías}, + month = apr, + shorttitle = {Personalized {Medicine}}, + year = {2013}, } -@article{amendola_ca2_2012, - title = {Ca2 /{cAMP}-{Sensitive} {Covariation} of {IA} and {IH} {Voltage} {Dependences} {Tunes} {Rebound} {Firing} in {Dopaminergic} {Neurons}}, - volume = {32}, - number = {6}, - journal = {Journal of Neuroscience}, - author = {Amendola, Julien and Woodhouse, Adele and Martin-Eauclaire, Marie-France and Goaillard, Jean-Marc}, - month = feb, - year = {2012}, - pages = {2166--2181}, - file = {Ca2+/cAMP-Sensitive Covariation of IA and IH Voltage Dependences Tunes Rebound Firing in Dopaminergic Neurons | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\ZANV2QEM\\2166.html:text/html}, +@Article{campomanes_kv_2002, + author = {Campomanes, Claire R. and Carroll, Karen I. and Manganas, Louis N. and Hershberger, Marcia E. and Gong, Belvin and Antonucci, Dana E. and Rhodes, Kenneth J. and Trimmer, James S.}, + title = {Kvβ {Subunit} {Oxidoreductase} {Activity} and {Kv1} {Potassium} {Channel} {Trafficking}}, + doi = {10.1074/jbc.M110276200}, + issn = {0021-9258}, + language = {en}, + number = {10}, + pages = {8298--8305}, + url = {https://www.sciencedirect.com/science/article/pii/S0021925819364324}, + urldate = {2021-06-12}, + volume = {277}, + abstract = {Voltage-gated Kv1 potassium channels consist of pore-forming α subunits and cytoplasmic Kvβ subunits. The latter play diverse roles in modulating the gating, stability, and trafficking of Kv1 channels. The crystallographic structure of the Kvβ2 subunit revealed surprising structural homology with aldo-keto reductases, including a triosephosphate isomerase barrel structure, conservation of key catalytic residues, and a bound NADP+ cofactor (Gulbis, J. M., Mann, S., and MacKinnon, R. (1999) Cell 90, 943–952). Each Kv1-associated Kvβ subunit (Kvβ1.1, Kvβ1.2, Kvβ2, and Kvβ3) shares striking amino acid conservation in key catalytic and cofactor binding residues. Here, by a combination of structural modeling and biochemical and cell biological analyses of structure-based mutations, we investigate the potential role for putative Kvβ subunit enzymatic activity in the trafficking of Kv1 channels. We found that all Kvβ subunits promote cell surface expression of coexpressed Kv1.2 α subunits in transfected COS-1 cells. Kvβ1.1 and Kvβ2 point mutants lacking a key catalytic tyrosine residue found in the active site of all aldo-keto reductases have wild-type trafficking characteristics. However, mutations in residues within the NADP+ binding pocket eliminated effects on Kv1.2 trafficking. In cultured hippocampal neurons, Kvβ subunit coexpression led to axonal targeting of Kv1.2, recapitulating the Kv1.2 localization observed in many brain neurons. Similar to the trafficking results in COS-1 cells, mutations within the cofactor binding pocket reduced axonal targeting of Kv1.2, whereas those in the catalytic tyrosine did not. Together, these data suggest that NADP+ binding and/or the integrity of the binding pocket structure, but not catalytic activity, of Kvβ subunits is required for intracellular trafficking of Kv1 channel complexes in mammalian cells and for axonal targeting in neurons.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DQE5VCME\\Campomanes et al. - 2002 - Kvβ Subunit Oxidoreductase Activity and Kv1 Potass.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8SLAS8NP\\S0021925819364324.html:text/html}, + journal = {Journal of Biological Chemistry}, + month = mar, + year = {2002}, } -@article{alonso_temperature_2020, - title = {Temperature compensation in a small rhythmic circuit}, - volume = {9}, - issn = {2050-084X}, - url = {https://doi.org/10.7554/eLife.55470}, - doi = {10.7554/eLife.55470}, - abstract = {Temperature affects the conductances and kinetics of the ionic channels that underlie neuronal activity. Each membrane conductance has a different characteristic temperature sensitivity, which raises the question of how neurons and neuronal circuits can operate robustly over wide temperature ranges. To address this, we employed computational models of the pyloric network of crabs and lobsters. We produced multiple different models that exhibit a triphasic pyloric rhythm over a range of temperatures and explored the dynamics of their currents and how they change with temperature. Temperature can produce smooth changes in the relative contributions of the currents to neural activity so that neurons and networks undergo graceful transitions in the mechanisms that give rise to their activity patterns. Moreover, responses of the models to deletions of a current can be different at high and low temperatures, indicating that even a well-defined genetic or pharmacological manipulation may produce qualitatively distinct effects depending on the temperature.}, - urldate = {2021-07-01}, - journal = {eLife}, - author = {Alonso, Leandro M and Marder, Eve}, - editor = {Skinner, Frances K and Westbrook, Gary L and Nadim, Farzan and Guet-McCreight, Alexandre}, - month = jun, - year = {2020}, - keywords = {ion channels, neuronal oscillators, Q10, temperature}, - pages = {e55470}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GSRZKTKY\\Alonso and Marder - 2020 - Temperature compensation in a small rhythmic circu.pdf:application/pdf}, + +@Article{Helbig2020, + author = {Helbig, Ingo and Ellis, Colin A.}, + title = {Personalized medicine in genetic epilepsies – possibilities, challenges, and new frontiers}, + doi = {10.1016/j.neuropharm.2020.107970}, + issn = {0028-3908}, + language = {en}, + pages = {107970}, + url = {https://www.sciencedirect.com/science/article/pii/S0028390820300368}, + urldate = {2022-03-06}, + volume = {172}, + abstract = {Identifying the optimal treatment based on specific characteristics of each patient is the main promise of precision medicine. In the field of epilepsy, the identification of more than 100 causative genes provides the enticing possibility of treatments targeted to specific disease etiologies. These conditions include classical examples, such as the use of vitamin B6 in antiquitin deficiency or the ketogenic diet in GLUT1 deficiency, where the disease mechanism can be directly addressed by the selection of a specific therapeutic compound. For epilepsies caused by channelopathies there have been advances in understanding how the selection of existing medications can be targeted to the functional consequences of genetic alterations. We discuss the examples of the use of sodium channel blockers such as phenytoin and oxcarbazepine in the sodium channelopathies, quinidine in KCNT1-related epilepsies, and strategies in GRIN-related epilepsies as examples of epilepsy precision medicine. Assessing the clinical response to targeted treatments of these conditions has been complicated by genetic and phenotypic heterogeneity, as well as by various neurological and non-neurological comorbidities. Moving forward, the development of standardized outcome measures will be critical to successful precision medicine trials in complex and heterogeneous disorders like the epilepsies. Finally, we address new frontiers in epilepsy precision medicine, including the need to match the growing volume of genetic data with high-throughput functional assays to assess the functional consequences of genetic variants and the ability to extract clinical data at large scale from electronic medical records and apply quantitative methods based on standardized phenotyping language.}, + file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S0028390820300368/pdfft?md5=dcf89311714033043a9f22309af19b83&pid=1-s2.0-S0028390820300368-main.pdf&isDTMRedir=Y:application/pdf}, + groups = {Jan}, + journal = {Neuropharmacology}, + keywords = {Epilepsy, Neurogenetics, Precision medicine, Electronic medical records, Human phenotype ontology}, + month = aug, + year = {2020}, } -@article{taylor_how_2009, - title = {How {Multiple} {Conductances} {Determine} {Electrophysiological} {Properties} in a {Multicompartment} {Model}}, - volume = {29}, - number = {17}, - journal = {Journal of Neuroscience}, - author = {Taylor, Adam L. and Goaillard, Jean-Marc and Marder, Eve}, - month = apr, - year = {2009}, - pages = {5573--5586}, - file = {How Multiple Conductances Determine Electrophysiological Properties in a Multicompartment Model | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\46GADMUG\\5573.html:text/html}, +@Article{marder_multiple_2011, + author = {Marder, Eve and Taylor, Adam L.}, + title = {Multiple models to capture the variability in biological neurons and networks}, + doi = {10.1038/nn.2735}, + issn = {1546-1726}, + language = {en}, + number = {2}, + pages = {133--138}, + url = {https://www.nature.com/articles/nn.2735}, + urldate = {2021-06-17}, + volume = {14}, + abstract = {Experimental work suggests that synaptic and intrinsic neuronal properties vary considerably across identified neurons in different animals. The authors propose that instead of building a single model that captures the average behavior of a neuron or circuit, one could construct a population of models with different underlying structure and similar behaviors, as a way of investigating compensatory mechanisms that contribute to neuron and network function.}, + copyright = {2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P6AXF7KA\\Marder and Taylor - 2011 - Multiple models to capture the variability in biol.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8VI7UGLZ\\nn.html:text/html}, + journal = {Nature Neuroscience}, + month = feb, + year = {2011}, +} + +@Article{puopolo_roles_2007, + author = {Puopolo, Michelino and Raviola, Elio and Bean, Bruce P.}, + title = {Roles of {Subthreshold} {Calcium} {Current} and {Sodium} {Current} in {Spontaneous} {Firing} of {Mouse} {Midbrain} {Dopamine} {Neurons}}, + number = {3}, + pages = {645--656}, + volume = {27}, + file = {Roles of Subthreshold Calcium Current and Sodium Current in Spontaneous Firing of Mouse Midbrain Dopamine Neurons | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\ICI7GVB3\\645.html:text/html}, + journal = {Journal of Neuroscience}, + month = jan, + year = {2007}, +} + +@Article{ruppersberg_heteromultimeric_1990, + author = {Ruppersberg, J. Peter and Schröter, Klaus H. and Sakmann, Bert and Stocker, Martin and Sewing, Sabine and Pongs, Olaf}, + title = {Heteromultimeric channels formed by rat brain potassium-channel proteins}, + doi = {10.1038/345535a0}, + issn = {1476-4687}, + language = {en}, + number = {6275}, + pages = {535--537}, + url = {https://www.nature.com/articles/345535a0}, + urldate = {2021-06-12}, + volume = {345}, + abstract = {AN important step towards understanding the molecular basis of the functional diversity of voltage-gated K+ channels in the mammalian brain has been the discovery of a family of genes encoding rat brain K+ channel-forming (RCK) proteins1–6. All species of these RCK proteins form homomultimeric voltage-gated K+ channels with distinct functional characteristics in Xenopus laevis oocytes following injection of the respective cRNAs2. RCK-specific mRNAs are coexpressed in several regions of the brain7, suggesting that RCK proteins also assemble into heteromultimeric K+ channels. In addition expression experiments with fractionated poly(A)+ mRNA have suggested that heteromultimeric K+ channels may occur in mammalian brain8. We report here that heteromultimeric K+ channels composed of two different RCK proteins (RCK1 and RCK4) assemble after cotransfection of HeLa cells with the corresponding cDNAs and after coinjection of the corresponding cRNAs into Xenopus oocytes. The heteromultimeric RCK1, 4 channel mediates a transient potassium outward current, similar to the RCK4 channel but inactivates more slowly, has a larger conductance and is more sensitive to block by dendrotoxin and tetraethylammonium chloride.}, + copyright = {1990 Nature Publishing Group}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9MTQJWHB\\Ruppersberg et al. - 1990 - Heteromultimeric channels formed by rat brain pota.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8TLMQMQM\\345535a0.html:text/html}, + journal = {Nature}, + month = jun, + year = {1990}, +} + +@Article{barreiro_-current_2012, + author = {Barreiro, Andrea K. and Thilo, Evan L. and Shea-Brown, Eric}, + title = {A-current and type {I}/type {II} transition determine collective spiking from common input}, + doi = {10.1152/jn.00928.2011}, + issn = {0022-3077}, + number = {6}, + pages = {1631--1645}, + url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3544951/}, + urldate = {2020-10-27}, + volume = {108}, + abstract = {The mechanisms and impact of correlated, or synchronous, firing among pairs and groups of neurons are under intense investigation throughout the nervous system. A ubiquitous circuit feature that can give rise to such correlations consists of overlapping, or common, inputs to pairs and populations of cells, leading to common spike train responses. Here, we use computational tools to study how the transfer of common input currents into common spike outputs is modulated by the physiology of the recipient cells. We focus on a key conductance, gA, for the A-type potassium current, which drives neurons between “type II” excitability (low gA), and “type I” excitability (high gA). Regardless of gA, cells transform common input fluctuations into a tendency to spike nearly simultaneously. However, this process is more pronounced at low gA values. Thus, for a given level of common input, type II neurons produce spikes that are relatively more correlated over short time scales. Over long time scales, the trend reverses, with type II neurons producing relatively less correlated spike trains. This is because these cells' increased tendency for simultaneous spiking is balanced by an anticorrelation of spikes at larger time lags. These findings extend and interpret prior findings for phase oscillators to conductance-based neuron models that cover both oscillatory (superthreshold) and subthreshold firing regimes. We demonstrate a novel implication for neural signal processing: downstream cells with long time constants are selectively driven by type I cell populations upstream and those with short time constants by type II cell populations. Our results are established via high-throughput numerical simulations and explained via the cells' filtering properties and nonlinear dynamics.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4CWLP49S\\Barreiro et al. - 2012 - A-current and type Itype II transition determine .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\B37GK9MB\\jn.00928.html:text/html;Submitted Version:C\:\\Users\\nilsk\\Zotero\\storage\\GRCRXMAN\\Barreiro et al. - 2012 - A-current and type Itype II transition determine .pdf:application/pdf}, + journal = {Journal of Neurophysiology}, + month = sep, + year = {2012}, +} + +@Article{lauxmann_therapeutic_2021, + author = {Lauxmann, Stephan and Sonnenberg, Lukas and Koch, Nils A. and Boßelmann, Christian Malte and Winter, Natalie and Schwarz, Niklas and Wuttke, Thomas Volkmar and Hedrich, Ulrike B. S. and Liu, Yuanyuan and Lerche, Holger and Benda, Jan and Kegele, Josua}, + title = {Therapeutic potential of sodium channel blockers as targeted therapy approach in {KCNA1}-associated episodic ataxia ({EA1}) and a comprehensive review of the literature}, + doi = {10.3389/fneur.2021.703970}, + issn = {1664-2295}, + language = {English}, + url = {https://www.frontiersin.org/articles/10.3389/fneur.2021.703970/abstract}, + urldate = {2021-07-28}, + volume = {In Press}, + abstract = {Among genetic paroxysmal movement disorders, variants in ion channel coding genes constitute a major subgroup. Loss-of-function (LOF) variants in KCNA1, the coding gene for KV1.1 channels, are associated with episodic ataxia type 1 (EA1), characterized by seconds to minutes-lasting attacks including gait incoordination, limb ataxia, truncal instability, dysarthria, nystagmus, tremor, occasionally seizures, but also persistent neuromuscular symptoms like myokymia or neuromyotonia. Standard treatment has not been developed yet and different treatment efforts need to be systematically evaluated. Personalized therapeutic regimens tailored to disease-causing pathophysiological mechanisms may offer the specificity required to overcome limitations in therapy. Toward this aim, we (i) reviewed all available clinical reports on treatment response and functional consequences of KCNA1 variants causing EA1, (ii) examined the potential effects on neuronal excitability of all variants using a predictive scoring system for ion channel variants based on single compartment conductance-based models, (iii) set out to assess a variety of SCBs (Phenytoin, lamotrigine, carbamazepine, and riluzole) regarding their potential to restore the identified underlying pathophysiological mechanisms of KV1.1 channels and (iv) provide a comprehensive review of the literature considering all types of episodic ataxia. Reviewing the treatment efforts of EA1 patients revealed moderate response to acetazolamide and exhibited the strength of sodium channel blockers (SCBs) in the treatment of EA1 patients. Biophysical dysfunction of Kv1.1 channels is typically based on depolarizing shifts of steady-state activation, leading to a loss-of-function of KCNA1 variant channels. Our model predicts a broadening of the action potentials, a lowered rheobase to more hyperpolarized potentials and an increase of the firing rate. Predicted effects of phenytoin, carbamazepine and riluzole could partially restore the altered gating properties of dysfunctional variant channels. These data strengthen the great potential of SCBs by contributing to functional compensation of dysfunctional Kv1.1 channels, propose riluzole as a new drug repurposing candidate and highlight the role of personalized approaches to develop standard care for EA1 patients. These results could have implications for clinical practice in future and highlight the need for the development of individualized and targeted therapies for episodic ataxia and genetic paroxysmal disorders in general.}, + journal = {Frontiers in Neurology}, + keywords = {conduction-based model, episodic ataxia, Kcna1, KV1.1, Paroxysmal movement disorders, precision medicine, Riluzole, Sodium Channel Blockers, Voltage-gated potassium channels}, + year = {2021}, } -@article{ratte_criticality_2014, - title = {Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain}, - volume = {3}, - issn = {2050-084X}, - url = {https://doi.org/10.7554/eLife.02370}, - doi = {10.7554/eLife.02370}, - abstract = {Neuropathic pain remains notoriously difficult to treat despite numerous drug targets. Here, we offer a novel explanation for this intractability. Computer simulations predicted that qualitative changes in primary afferent excitability linked to neuropathic pain arise through a switch in spike initiation dynamics when molecular pathologies reach a tipping point (criticality), and that this tipping point can be reached via several different molecular pathologies (degeneracy). We experimentally tested these predictions by pharmacologically blocking native conductances and/or electrophysiologically inserting virtual conductances. Multiple different manipulations successfully reproduced or reversed neuropathic changes in primary afferents from naïve or nerve-injured rats, respectively, thus confirming the predicted criticality and its degenerate basis. Degeneracy means that several different molecular pathologies are individually sufficient to cause hyperexcitability, and because several such pathologies co-occur after nerve injury, that no single pathology is uniquely necessary. Consequently, single-target-drugs can be circumvented by maladaptive plasticity in any one of several ion channels.}, - urldate = {2021-07-01}, - journal = {eLife}, - author = {Ratté, Stéphanie and Zhu, Yi and Lee, Kwan Yeop and Prescott, Steven A}, - editor = {Calabrese, Ronald L}, - month = apr, - year = {2014}, - keywords = {excitability, bursting, neuropathic pain, dynamic clamp, degeneracy, membrane potential oscillation}, - pages = {e02370}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\37AUH3VK\\Ratté et al. - 2014 - Criticality and degeneracy in injury-induced chang.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5VAWRBGT\\Ratté et al. - 2014 - Criticality and degeneracy in injury-induced chang.pdf:application/pdf}, -} -@article{goaillard_pros_2014, - title = {The pros and cons of degeneracy}, - volume = {3}, - issn = {2050-084X}, - url = {https://doi.org/10.7554/eLife.02615}, - doi = {10.7554/eLife.02615}, - abstract = {Drugs could treat neuropathic pain more effectively if they simultaneously targeted two or more types of ion channel.}, - urldate = {2021-07-01}, - journal = {eLife}, - author = {Goaillard, Jean-Marc and Dufour, Martial A}, - month = apr, - year = {2014}, - keywords = {excitability, bursting, neuropathic pain, dynamic clamp, degeneracy, membrane potential oscillation}, - pages = {e02615}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3J3HSQF4\\Goaillard and Dufour - 2014 - The pros and cons of degeneracy.pdf:application/pdf}, +@Article{Kispersky2012, + author = {Kispersky, Tilman J. and Caplan, Jonathan S. and Marder, Eve}, + title = {Increase in {Sodium} {Conductance} {Decreases} {Firing} {Rate} and {Gain} in {Model} {Neurons}}, + doi = {10.1523/JNEUROSCI.2045-12.2012}, + issn = {0270-6474, 1529-2401}, + language = {en}, + number = {32}, + pages = {10995--11004}, + url = {https://www.jneurosci.org/content/32/32/10995}, + urldate = {2022-03-05}, + volume = {32}, + abstract = {We studied the effects of increased sodium conductance on firing rate and gain in two populations of conductance-based, single-compartment model neurons. The first population consisted of 1000 model neurons with differing values of seven voltage-dependent conductances. In many of these models, increasing the sodium conductance threefold unexpectedly reduced the firing rate and divisively scaled the gain at high input current. In the second population, consisting of 1000 simplified model neurons, we found that enhanced sodium conductance changed the frequency–current (FI) curve in two computationally distinct ways, depending on the firing rate. In these models, increased sodium conductance produced a subtractive shift in the FI curve at low firing rates because the additional sodium conductance allowed the neuron to respond more strongly to equivalent input current. In contrast, at high input current, the increase in sodium conductance resulted in a divisive change in the gain because the increased conductance produced a proportionally larger activation of the delayed rectifier potassium conductance. The control and sodium-enhanced FI curves intersect at a point that delimits two regions in which the same biophysical manipulation produces two fundamentally different changes to the model neuron's computational properties. This suggests a potentially difficult problem for homeostatic regulation of intrinsic excitability.}, + chapter = {Articles}, + copyright = {Copyright © 2012 the authors 0270-6474/12/3210995-10\$15.00/0}, + file = {Full Text PDF:https\://www.jneurosci.org/content/jneuro/32/32/10995.full.pdf:application/pdf;PubMed entry:http\://www.ncbi.nlm.nih.gov/pubmed/22875933:text/html}, + groups = {Jan}, + journal = {Journal of Neuroscience}, + month = aug, + pmid = {22875933}, + publisher = {Society for Neuroscience}, + year = {2012}, } -@article{sarkar_quantification_2011, - title = {Quantification of repolarization reserve to understand interpatient variability in the response to proarrhythmic drugs: {A} computational analysis}, - volume = {8}, - issn = {1547-5271}, - shorttitle = {Quantification of repolarization reserve to understand interpatient variability in the response to proarrhythmic drugs}, - url = {https://www.sciencedirect.com/science/article/pii/S1547527111006758}, - doi = {10.1016/j.hrthm.2011.05.023}, - abstract = {Background -“Repolarization reserve” is frequently invoked to explain why potentially proarrhythmic drugs cause, across a population, a range of changes to cardiac action potentials (APs). However, the mechanisms underlying this interindividual variability are not understood quantitatively. -Objective -The purpose of this study was to perform a novel analysis of mathematical models of ventricular myocytes to quantify repolarization reserve and gain insight into the factors responsible for variability in the response to proarrhythmic drugs. -Methods/Results -In several models of human or canine ventricular myocytes, variability was simulated by randomizing model parameters and running repeated simulations. With each randomly generated set of parameters, APs before and after simulated 75\% block of the rapid delayed rectifier current (IKr) were calculated. Multivariable regression was performed to determine how much each model parameter attenuated or exacerbated the AP prolongation caused by the IKr-blocking drug. Simulations with a human ventricular myocyte model suggest that drug response is influenced most strongly by (1) the density of IKr, (2) the density of slow delayed rectifier current IKs, (3) the voltage dependence of IKr inactivation, (4) the density of L-type Ca2+ current, and (5) the kinetics of IKs activation. The analysis also identified mechanisms underlying nonintuitive behavior, such as ionic currents that prolong baseline APs but decrease drug-induced AP prolongation. Finally, the simulations provided quantitative insight into conditions that aggravate the drug response, such as silent ion channel mutations and heart failure. -Conclusion -These modeling results provide the first thorough quantification of repolarization reserve and improve our understanding of interindividual variability in adverse drug reactions.}, - language = {en}, - number = {11}, - urldate = {2021-07-01}, - journal = {Heart Rhythm}, - author = {Sarkar, Amrita X. and Sobie, Eric A.}, - month = nov, - year = {2011}, - keywords = {Arrhythmia, Long QT syndrome, Modeling, Systems biology, Ventricular tachycardia}, - pages = {1749--1755}, - file = {Accepted Version:C\:\\Users\\nilsk\\Zotero\\storage\\P462Z7HT\\Sarkar and Sobie - 2011 - Quantification of repolarization reserve to unders.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\G3AI36NE\\S1547527111006758.html:text/html}, +@Article{alexander_cerebellar_2019, + author = {Alexander, Ryan P. D. and Mitry, John and Sareen, Vasu and Khadra, Anmar and Bowie, Derek}, + title = {Cerebellar {Stellate} {Cell} {Excitability} {Is} {Coordinated} by {Shifts} in the {Gating} {Behavior} of {Voltage}-{Gated} {Na}+ and {A}-{Type} {K}+ {Channels}}, + doi = {10.1523/ENEURO.0126-19.2019}, + issn = {2373-2822}, + language = {en}, + number = {3}, + url = {https://www.eneuro.org/content/6/3/ENEURO.0126-19.2019}, + urldate = {2021-04-13}, + volume = {6}, + abstract = {Neuronal excitability in the vertebrate brain is governed by the coordinated activity of both ligand- and voltage-gated ion channels. In the cerebellum, spontaneous action potential (AP) firing of inhibitory stellate cells (SCs) is variable, typically operating within the 5- to 30-Hz frequency range. AP frequency is shaped by the activity of somatodendritic A-type K+ channels and the inhibitory effect of GABAergic transmission. An added complication, however, is that whole-cell recording from SCs induces a time-dependent and sustained increase in membrane excitability making it difficult to define the full range of firing rates. Here, we show that whole-cell recording in cerebellar SCs of both male and female mice augments firing rates by reducing the membrane potential at which APs are initiated. AP threshold is lowered due to a hyperpolarizing shift in the gating behavior of voltage-gated Na+ channels. Whole-cell recording also elicits a hyperpolarizing shift in the gating behavior of A-type K+ channels which contributes to increased firing rates. Hodgkin–Huxley modeling and pharmacological experiments reveal that gating shifts in A-type K+ channel activity do not impact AP threshold, but rather promote channel inactivation which removes restraint on the upper limit of firing rates. Taken together, our work reveals an unappreciated impact of voltage-gated Na+ channels that work in coordination with A-type K+ channels to regulate the firing frequency of cerebellar SCs.}, + copyright = {Copyright © 2019 Alexander et al.. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FJT2PTDH\\Alexander et al. - 2019 - Cerebellar Stellate Cell Excitability Is Coordinat.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GQVXJ8F2\\ENEURO.0126-19.html:text/html}, + journal = {eNeuro}, + keywords = {cerebellum, action potential, A-type potassium channel, computational modeling, sodium channel, stellate cell}, + month = may, + year = {2019}, } -@article{glasscock_masking_2007, - title = {Masking epilepsy by combining two epilepsy genes}, - volume = {10}, - copyright = {2007 Nature Publishing Group}, - issn = {1546-1726}, - url = {https://www.nature.com/articles/nn1999}, - doi = {10.1038/nn1999}, - abstract = {Inherited errors in ion channel genes comprise the largest subset of monogenic causes of idiopathic epilepsy, and pathogenic variants contribute to genetic risk in the complex inheritance of this common disorder. We generated a digenic mouse model of human idiopathic epilepsy by combining two epilepsy-associated ion channel mutations with mutually opposing excitability defects and overlapping subcellular localization. We found that increasing membrane excitability by removing Shaker-like K+ channels, which are encoded by the Kcna1 gene, masked the absence epilepsy caused by a P/Q-type Ca2+ channelopathy due to a missense mutation in the Cacna1a gene. Conversely, decreasing network excitability by impairing Cacna1a Ca2+-channel function attenuated limbic seizures and sudden death in Kcna1-null mice. We also identified intermediate excitability phenotypes at the network and axonal levels. Protective interactions between pathogenic ion channel variants may markedly alter the clinical expression of epilepsy, highlighting the need for comprehensive profiling of this candidate gene set to improve the accuracy of genetic risk assessment of this complex disease.}, - language = {en}, - number = {12}, - urldate = {2021-07-01}, - journal = {Nature Neuroscience}, - author = {Glasscock, Edward and Qian, Jing and Yoo, Jong W. and Noebels, Jeffrey L.}, - month = dec, - year = {2007}, - pages = {1554--1558}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\W6TEIWQN\\Glasscock et al. - 2007 - Masking epilepsy by combining two epilepsy genes.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\GZS35ZTV\\nn1999.html:text/html}, +@Article{jonas_regulation_1996, + author = {Jonas, Elizabeth A and Kaczmarek, Leonard K}, + title = {Regulation of potassium channels by protein kinases}, + doi = {10.1016/S0959-4388(96)80114-0}, + issn = {0959-4388}, + language = {en}, + number = {3}, + pages = {318--323}, + url = {https://www.sciencedirect.com/science/article/pii/S0959438896801140}, + urldate = {2021-06-12}, + volume = {6}, + abstract = {Studies of the role of protein phosphorylation in the modulation of neuronal excitability are beginning to identify specific sites on ion channels that are substrates for serine/threonine kinases and that contribute to short-term and long-term regulation of current amplitude and kinetics. In addition, it is becoming apparent that phosphorylation of tyrosine residues may produce acute changes in the characteristics of ion channels. These recent findings are best illustrated by examining the Shaker superfamily of potassium channels.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3GZJ4IP9\\Jonas and Kaczmarek - 1996 - Regulation of potassium channels by protein kinase.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\M3UBSIZQ\\S0959438896801140.html:text/html}, + journal = {Current Opinion in Neurobiology}, + month = jun, + year = {1996}, +} + +@Article{hafez_altered_2020, + author = {Hafez, Omar A. and Gottschalk, Allan}, + title = {Altered neuronal excitability in a {Hodgkin}-{Huxley} model incorporating channelopathies of the delayed rectifier potassium channel}, + doi = {10.1007/s10827-020-00766-1}, + issn = {1573-6873}, + language = {en}, + number = {4}, + pages = {377--386}, + url = {https://doi.org/10.1007/s10827-020-00766-1}, + urldate = {2021-07-26}, + volume = {48}, + abstract = {Channelopathies involving acquired or genetic modifications of the delayed rectifier K+ channel Kv1.1 include phenotypes characterized by enhanced neuronal excitability. Affected Kv1.1 channels exhibit combinations of altered expression, voltage sensitivity, and rates of activation and deactivation. Computational modeling and analysis can reveal the potential of particular channelopathies to alter neuronal excitability. A dynamical systems approach was taken to study the excitability and underlying dynamical structure of the Hodgkin-Huxley (HH) model of neural excitation as properties of the delayed rectifier K+ channel were altered. Bifurcation patterns of the HH model were determined as the amplitude of steady injection current was varied simultaneously with single parameters describing the delayed rectifier rates of activation and deactivation, maximal conductance, and voltage sensitivity. Relatively modest changes in the properties of the delayed rectifier K+ channel analogous to what is described for its channelopathies alter the bifurcation structure of the HH model and profoundly modify excitability of the HH model. Channelopathies associated with Kv1.1 can reduce the threshold for onset of neural activity. These studies also demonstrate how pathological delayed rectifier K+ channels could lead to the observation of the generalized Hopf bifurcation and, perhaps, other variants of the Hopf bifurcation. The observed bifurcation patterns collectively demonstrate that properties of the nominal delayed rectifier in the HH model appear optimized to permit activation of the HH model over the broadest possible range of input currents.}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4CCGDHXQ\\Hafez and Gottschalk - 2020 - Altered neuronal excitability in a Hodgkin-Huxley .pdf:application/pdf}, + journal = {Journal of Computational Neuroscience}, + month = nov, + year = {2020}, } -@article{ransdell_neurons_2013, - title = {Neurons within the {Same} {Network} {Independently} {Achieve} {Conserved} {Output} by {Differentially} {Balancing} {Variable} {Conductance} {Magnitudes}}, - volume = {33}, - number = {24}, - journal = {Journal of Neuroscience}, - author = {Ransdell, Joseph L. and Nair, Satish S. and Schulz, David J.}, - month = jun, - year = {2013}, - pages = {9950--9956}, - file = {Neurons within the Same Network Independently Achieve Conserved Output by Differentially Balancing Variable Conductance Magnitudes | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\YM4JHXV4\\9950.html:text/html}, +@Article{rettig_inactivation_1994, + author = {Rettig, Jens and Heinemann, Stefan H. and Wunder, Frank and Lorra, Christoph and Parcej, David N. and Oliver Dolly, J. and Pongs, Olaf}, + title = {Inactivation properties of voltage-gated {K} + channels altered by presence of β-subunit}, + doi = {10.1038/369289a0}, + issn = {1476-4687}, + language = {en}, + number = {6478}, + pages = {289--294}, + url = {https://www.nature.com/articles/369289a0}, + urldate = {2021-06-07}, + volume = {369}, + abstract = {Structural and functional diversity of voltage-gated Kv1-type potassium channels in rat brain is enhanced by the association of two different types of subunits, the membrane-bound, pore-forming α-subunits and a peripheral β-subunit. We have cloned a β-subunit (Kvβ1) that is specifically expressed in the rat nervous system. Association of Kvβ1 with α-subunits confers rapid A-type inactivation on non-inactivating Kv1 channels (delayed rectifiers) in expression systems in vitro. This effect is mediated by an inactivating ball domain in the Kvβ1 amino terminus.}, + copyright = {1994 Nature Publishing Group}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RCEYBSD2\\Rettig et al. - 1994 - Inactivation properties of voltage-gated K + chann.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9X7D2PY4\\Rettig et al. - 1994 - Inactivation properties of voltage-gated K + chann.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WYSLLXAL\\369289a0.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WCK725TD\\369289a0.html:text/html}, + journal = {Nature}, + month = may, + year = {1994}, } -@article{khaliq_relative_2006, - title = {Relative {Contributions} of {Axonal} and {Somatic} {Na} {Channels} to {Action} {Potential} {Initiation} in {Cerebellar} {Purkinje} {Neurons}}, - volume = {26}, - number = {7}, - journal = {Journal of Neuroscience}, - author = {Khaliq, Zayd M. and Raman, Indira M.}, - month = feb, - year = {2006}, - pages = {1935--1944}, - file = {Relative Contributions of Axonal and Somatic Na Channels to Action Potential Initiation in Cerebellar Purkinje Neurons | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\A2ZU9LSD\\1935.html:text/html}, +@Article{saltelli_how_2010, + author = {Saltelli, Andrea and Annoni, Paola}, + title = {How to avoid a perfunctory sensitivity analysis}, + doi = {10.1016/j.envsoft.2010.04.012}, + issn = {1364-8152}, + language = {en}, + number = {12}, + pages = {1508--1517}, + url = {https://www.sciencedirect.com/science/article/pii/S1364815210001180}, + urldate = {2021-06-02}, + volume = {25}, + abstract = {Mathematical modelers from different disciplines and regulatory agencies worldwide agree on the importance of a careful sensitivity analysis (SA) of model-based inference. The most popular SA practice seen in the literature is that of ’one-factor-at-a-time’ (OAT). This consists of analyzing the effect of varying one model input factor at a time while keeping all other fixed. While the shortcomings of OAT are known from the statistical literature, its widespread use among modelers raises concern on the quality of the associated sensitivity analyses. The present paper introduces a novel geometric proof of the inefficiency of OAT, with the purpose of providing the modeling community with a convincing and possibly definitive argument against OAT. Alternatives to OAT are indicated which are based on statistical theory, drawing from experimental design, regression analysis and sensitivity analysis proper.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SWBUI32R\\Saltelli and Annoni - 2010 - How to avoid a perfunctory sensitivity analysis.pdf:application/pdf;ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\P9EGLCTE\\Saltelli and Annoni - 2010 - How to avoid a perfunctory sensitivity analysis.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\JLYYH3WR\\S1364815210001180.html:text/html}, + journal = {Environmental Modelling \& Software}, + keywords = {Mathematical modeling, One-at-a-time, Robustness, Sensitivity analysis, Uncertainty analysis}, + month = dec, + year = {2010}, +} + + +@Article{Hedrich14874, + author = {Hedrich, Ulrike B.S. and Liautard, Camille and Kirschenbaum, Daniel and Pofahl, Martin and Lavigne, Jennifer and Liu, Yuanyuan and Theiss, Stephan and Slotta, Johannes and Escayg, Andrew and Dihn{\'e}, Marcel and Beck, Heinz and Mantegazza, Massimo and Lerche, Holger}, + title = {Impaired Action Potential Initiation in GABAergic Interneurons Causes Hyperexcitable Networks in an Epileptic Mouse Model Carrying a Human NaV1.1 Mutation}, + doi = {10.1523/JNEUROSCI.0721-14.2014}, + eprint = {https://www.jneurosci.org/content/34/45/14874.full.pdf}, + issn = {0270-6474}, + number = {45}, + pages = {14874--14889}, + url = {https://www.jneurosci.org/content/34/45/14874}, + volume = {34}, + abstract = {Mutations in SCN1A and other ion channel genes can cause different epileptic phenotypes, but the precise mechanisms underlying the development of hyperexcitable networks are largely unknown. Here, we present a multisystem analysis of an SCN1A mouse model carrying the NaV1.1-R1648H mutation, which causes febrile seizures and epilepsy in humans. We found a ubiquitous hypoexcitability of interneurons in thalamus, cortex, and hippocampus, without detectable changes in excitatory neurons. Interestingly, somatic Na+ channels in interneurons and persistent Na+ currents were not significantly changed. Instead, the key mechanism of interneuron dysfunction was a deficit of action potential initiation at the axon initial segment that was identified by analyzing action potential firing. This deficit increased with the duration of firing periods, suggesting that increased slow inactivation, as recorded for recombinant mutated channels, could play an important role. The deficit in interneuron firing caused reduced action potential-driven inhibition of excitatory neurons as revealed by less frequent spontaneous but not miniature IPSCs. Multiple approaches indicated increased spontaneous thalamocortical and hippocampal network activity in mutant mice, as follows: (1) more synchronous and higher-frequency firing was recorded in primary neuronal cultures plated on multielectrode arrays; (2) thalamocortical slices examined by field potential recordings revealed spontaneous activities and pathological high-frequency oscillations; and (3) multineuron Ca2+ imaging in hippocampal slices showed increased spontaneous neuronal activity. Thus, an interneuron-specific generalized defect in action potential initiation causes multisystem disinhibition and network hyperexcitability, which can well explain the occurrence of seizures in the studied mouse model and in patients carrying this mutation.}, + journal = {Journal of Neuroscience}, + publisher = {Society for Neuroscience}, + year = {2014}, } -@article{soofi_co-variation_2012, - title = {Co-variation of ionic conductances supports phase maintenance in stomatogastric neurons}, - volume = {33}, - issn = {1573-6873}, - url = {https://doi.org/10.1007/s10827-011-0375-3}, - doi = {10.1007/s10827-011-0375-3}, - abstract = {Neuronal networks produce reliable functional output throughout the lifespan of an animal despite ceaseless molecular turnover and a constantly changing environment. Central pattern generators, such as those of the crustacean stomatogastric ganglion (STG), are able to robustly maintain their functionality over a wide range of burst periods. Previous experimental work involving extracellular recordings of the pyloric pattern of the STG has demonstrated that as the burst period varies, the inter-neuronal delays are altered proportionally, resulting in burst phases that are roughly invariant. The question whether spike delays within bursts are also proportional to pyloric period has not been explored in detail. The mechanism by which the pyloric neurons accomplish phase maintenance is currently not obvious. Previous studies suggest that the co-regulation of certain ion channel properties may play a role in governing neuronal activity. Here, we observed in long-term recordings of the pyloric rhythm that spike delays can vary proportionally with burst period, so that spike phase is maintained. We then used a conductance-based model neuron to determine whether co-varying ionic membrane conductances results in neural output that emulates the experimentally observed phenomenon of spike phase maintenance. Next, we utilized a model neuron database to determine whether conductance correlations exist in model neuron populations with highly maintained spike phases. We found that co-varying certain conductances, including the sodium and transient calcium conductance pair, causes the model neuron to maintain a specific spike phase pattern. Results indicate a possible relationship between conductance co-regulation and phase maintenance in STG neurons.}, - language = {en}, - number = {1}, - urldate = {2021-07-01}, - journal = {Journal of Computational Neuroscience}, - author = {Soofi, Wafa and Archila, Santiago and Prinz, Astrid A.}, - month = aug, - year = {2012}, - pages = {77--95}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6Q9T34AC\\Soofi et al. - 2012 - Co-variation of ionic conductances supports phase .pdf:application/pdf}, + + + +@Article{makinson_scn1a_2016, + author = {Makinson, Christopher D. and Dutt, Karoni and Lin, Frank and Papale, Ligia A. and Shankar, Anupama and Barela, Arthur J. and Liu, Robert and Goldin, Alan L. and Escayg, Andrew}, + title = {An {Scn1a} epilepsy mutation in {Scn8a} alters seizure susceptibility and behavior}, + doi = {https://doi.org/10.1016/j.expneurol.2015.09.008}, + issn = {0014-4886}, + pages = {46--58}, + url = {https://www.sciencedirect.com/science/article/pii/S001448861530090X}, + volume = {275}, + abstract = {Understanding the role of SCN8A in epilepsy and behavior is critical in light of recently identified human SCN8A epilepsy mutations. We have previously demonstrated that Scn8amed and Scn8amed-jo mice carrying mutations in the Scn8a gene display increased resistance to flurothyl and kainic acid-induced seizures; however, they also exhibit spontaneous absence seizures. To further investigate the relationship between altered SCN8A function and epilepsy, we introduced the SCN1A-R1648H mutation, identified in a family with generalized epilepsy with febrile seizures plus (GEFS+), into the corresponding position (R1627H) of the mouse Scn8a gene. Heterozygous R1627H mice exhibited increased resistance to some forms of pharmacologically and electrically induced seizures and the mutant Scn8a allele ameliorated the phenotype of Scn1a-R1648H mutants. Hippocampal slices from heterozygous R1627H mice displayed decreased bursting behavior compared to wild-type littermates. Paradoxically, at the homozygous level, R1627H mice did not display increased seizure resistance and were susceptible to audiogenic seizures. We furthermore observed increased hippocampal pyramidal cell excitability in heterozygous and homozygous Scn8a-R1627H mutants, and decreased interneuron excitability in heterozygous Scn8a-R1627H mutants. These results expand the phenotypes associated with disruption of the Scn8a gene and demonstrate that an Scn8a mutation can both confer seizure protection and increase seizure susceptibility.}, + journal = {Experimental Neurology}, + keywords = {Audiogenic seizure, Dravet syndrome, GEFS+, Interneuron, Na1.1, Na1.6, Sodium channel, Voltage sensor}, + year = {2016}, +} + +@Article{parker_periodic_1946, + author = {Parker, H. L.}, + title = {Periodic ataxia}, + issn = {0095-9677}, + language = {eng}, + pages = {642--645}, + volume = {38}, + journal = {Collected Papers of the Mayo Clinic and the Mayo Foundation. Mayo Clinic}, + keywords = {Humans, Ataxia, ATAXIA, Spinocerebellar Degenerations}, + year = {1946}, } -@article{lamb_correlated_2013, - title = {Correlated {Conductance} {Parameters} in {Leech} {Heart} {Motor} {Neurons} {Contribute} to {Motor} {Pattern} {Formation}}, - volume = {8}, - issn = {1932-6203}, - url = {https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0079267}, - doi = {10.1371/journal.pone.0079267}, - abstract = {Neurons can have widely differing intrinsic membrane properties, in particular the density of specific conductances, but how these contribute to characteristic neuronal activity or pattern formation is not well understood. To explore the relationship between conductances, and in particular how they influence the activity of motor neurons in the well characterized leech heartbeat system, we developed a new multi-compartmental Hodgkin-Huxley style leech heart motor neuron model. To do so, we evolved a population of model instances, which differed in the density of specific conductances, capable of achieving specific output activity targets given an associated input pattern. We then examined the sensitivity of measures of output activity to conductances and how the model instances responded to hyperpolarizing current injections. We found that the strengths of many conductances, including those with differing dynamics, had strong partial correlations and that these relationships appeared to be linked by their influence on heart motor neuron activity. Conductances that had positive correlations opposed one another and had the opposite effects on activity metrics when perturbed whereas conductances that had negative correlations could compensate for one another and had similar effects on activity metrics.}, - language = {en}, - number = {11}, - urldate = {2021-07-01}, - journal = {PLOS ONE}, - author = {Lamb, Damon G. and Calabrese, Ronald L.}, - month = nov, - year = {2013}, - keywords = {Interneurons, Motor neurons, Action potentials, Membrane potential, Axons, Heart, Leeches, Neurites}, - pages = {e79267}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\L77ATPCI\\Lamb and Calabrese - 2013 - Correlated Conductance Parameters in Leech Heart M.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\V74V8IWQ\\article.html:text/html}, + + +@Article{Waxman2007, + author = {Waxman, Stephen G.}, + title = {Channel, neuronal and clinical function in sodium channelopathies: from genotype to phenotype}, + doi = {10.1038/nn1857}, + issn = {1546-1726}, + language = {en}, + number = {4}, + pages = {405--409}, + url = {https://www.nature.com/articles/nn1857}, + urldate = {2022-03-03}, + volume = {10}, + abstract = {What is the relationship between sodium channel function, neuronal function and clinical status in channelopathies of the nervous system? Given the central role of sodium channels in the generation of neuronal activity, channelopathies involving sodium channels might be expected to cause either enhanced sodium channel function and neuronal hyperexcitability associated with positive clinical manifestations such as seizures, or attenuated channel function and neuronal hypoexcitability associated with negative clinical manifestations such as paralysis. In this article, I review observations showing that changes in neuronal function and clinical status associated with channelopathies are not necessarily predictable solely from the altered physiological properties of the mutated channel itself. I discuss evidence showing that cell background acts as a filter that can strongly influence the effects of ion channel mutations.}, + copyright = {2007 Nature Publishing Group}, + file = {Full Text PDF:https\://www.nature.com/articles/nn1857.pdf:application/pdf}, + groups = {Jan}, + journal = {Nature Neuroscience}, + keywords = {Biomedicine, general, Neurosciences, Behavioral Sciences, Biological Techniques, Neurobiology, Animal Genetics and Genomics}, + month = apr, + publisher = {Nature Publishing Group}, + shorttitle = {Channel, neuronal and clinical function in sodium channelopathies}, + year = {2007}, } -@article{klassen_exome_2011, - title = {Exome sequencing of ion channel genes reveals complex variant profiles confounding personal risk assessment in epilepsy}, - volume = {145}, - issn = {0092-8674}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131217/}, - doi = {10.1016/j.cell.2011.05.025}, - abstract = {Ion channel mutations are an important cause of rare Mendelian disorders affecting brain, heart, and other tissues. We performed parallel exome sequencing of 237 channel genes in a well characterized human sample, comparing variant profiles of unaffected individuals to those with the most common neuronal excitability disorder, sporadic idiopathic epilepsy. Rare missense variation in known Mendelian disease genes is prevalent in both groups at similar complexity, revealing that even deleterious ion channel mutations confer uncertain risk to an individual depending on the other variants with which they are combined. Our findings indicate that variant discovery via large scale sequencing efforts is only a first step in illuminating the complex allelic architecture underlying personal disease risk. We propose that in silico modeling of channel variation in realistic cell and network models will be crucial to future strategies assessing mutation profile pathogenicity and drug response in individuals with a broad spectrum of excitability disorders.}, - number = {7}, - urldate = {2021-07-01}, - journal = {Cell}, - author = {Klassen, Tara and Davis, Caleb and Goldman, Alica and Burgess, Dan and Chen, Tim and Wheeler, David and McPherson, John and Bourquin, Traci and Lewis, Lora and Villasana, Donna and Morgan, Margaret and Muzny, Donna and Gibbs, Richard and Noebels, Jeffrey}, - month = jun, - year = {2011}, - pages = {1036--1048}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\DZKQ42HL\\Klassen et al. - 2011 - Exome sequencing of ion channel genes reveals comp.pdf:application/pdf}, + +@Article{Brunklaus2022, + author = {Brunklaus, Andreas and Feng, Tony and Brünger, Tobias and Perez-Palma, Eduardo and Heyne, Henrike and Matthews, Emma and Semsarian, Christopher and Symonds, Joseph D. and Zuberi, Sameer M. and Lal, Dennis and Schorge, Stephanie}, + title = {Gene variant effects across sodium channelopathies predict function and guide precision therapy}, + doi = {10.1093/brain/awac006}, + issn = {0006-8950}, + pages = {awac006}, + url = {https://doi.org/10.1093/brain/awac006}, + urldate = {2022-03-06}, + abstract = {Pathogenic variants in the voltage-gated sodium channel gene family (SCNs) lead to early onset epilepsies, neurodevelopmental disorders, skeletal muscle channelopathies, peripheral neuropathies and cardiac arrhythmias. Disease-associated variants have diverse functional effects ranging from complete loss-of-function to marked gain-of-function. Therapeutic strategy is likely to depend on functional effect. Experimental studies offer important insights into channel function, but are resource intensive and only performed in a minority of cases. Given the evolutionarily conserved nature of the sodium channel genes we investigated whether similarities in biophysical properties between different voltage-gated sodium channels can predict function and inform precision treatment across sodium channelopathies. We performed a systematic literature search identifying functionally assessed variants in any of the nine voltage-gated sodium channel genes until 28 April 2021. We included missense variants that had been electrophysiologically characterised in mammalian cells in whole-cell patch-clamp recordings. We performed an alignment of linear protein sequences of all sodium channel genes and correlated variants by their overall functional effect on biophysical properties. Of 951 identified records, 437 sodium channel-variants met our inclusion criteria and were reviewed for functional properties. Of these, 141 variants were epilepsy-associated (SCN1/2/3/8A), 79 had a neuromuscular phenotype (SCN4/9/10/11A), 149 were associated with a cardiac phenotype (SCN5/10A) and 68 (16\%) were considered benign. We detected 38 missense variant pairs with an identical disease-associated variant in a different sodium channel gene. 35 out of 38 of those pairs resulted in similar functional consequences indicating up to 92\% biophysical agreement between corresponding sodium channel variants (odds ratio = 11.3; 95\% CI = 2.8 to 66.9; P \< 0.001). Pathogenic missense variants were clustered in specific functional domains, whereas population variants were significantly more frequent across non conserved domains (odds ratio = 18.6; 95\% CI = 10.9 to 34.4; P \< 0.001). Pore-loop regions were frequently associated with loss-of-function (LoF) variants, whereas inactivation sites were associated with gain-of-function (GoF; odds ratio = 42.1, 95\% CI = 14.5 to 122.4; P \< 0.001), whilst variants occurring in voltage-sensing regions comprised a range of gain- and loss-of-function effects. Our findings suggest that biophysical characterisation of variants in one SCN-gene can predict channel function across different SCN-genes where experimental data are not available. The collected data represent the first GoF versus LoF topological map of SCN proteins indicating shared patterns of biophysical effects aiding variant analysis and guiding precision therapy. We integrated our findings into a free online webtool to facilitate functional sodium channel gene variant interpretation (http://SCN-viewer.broadinstitute.org).}, + file = {:Brunklaus2022 - Gene Variant Effects across Sodium Channelopathies Predict Function and Guide Precision Therapy.pdf:PDF}, + groups = {Jan}, + journal = {Brain}, + month = jan, + year = {2022}, } -@article{thomas_prediction_2009, - title = {Prediction by {Modeling} {That} {Epilepsy} {May} {Be} {Caused} by {Very} {Small} {Functional} {Changes} in {Ion} {Channels}}, - volume = {66}, - issn = {0003-9942}, - url = {https://doi.org/10.1001/archneurol.2009.219}, - doi = {10.1001/archneurol.2009.219}, - abstract = {To use computer simulation to perform a “genetic sensitivity” analysis to predict which genes are best positioned to increase risk as well as to predict functionally how variants in these genes might increase network excitability.A previously published, biophysically realistic model of the dentate gyrus that included mossy fiber sprouting between granule cells was used to model putative environmental changes associated with temporal lobe epilepsy. Properties of voltage-gated ion channels, either 1 at a time or in combinations, were varied systematically to determine their effect on network excitability.We found that the network is most sensitive to changes in steady-state voltage dependence of activation and relatively insensitive to changes in inactivation. Changes in sodium channels had the greatest effect on excitability, followed by changes in fast-delayed rectifier potassium channels and then N-type calcium channels. We also investigated the effects of simultaneous small changes in several ion channels, modeling a complex genetic background expected for common epilepsies. A combination of 2 or 3 simultaneous voltage shifts in steady-state activation as small as 2 mV could produce large changes in network excitability.Statistical power calculations indicate that changes this small are effectively undetectable with current experimental practices, thus posing new challenges for the functional analysis and validation of epilepsy genes.Arch Neurol. 2009;66(10):1225-1232--{\textgreater}}, - number = {10}, - urldate = {2021-07-02}, - journal = {Archives of Neurology}, - author = {Thomas, Evan A. and Reid, Christopher A. and Berkovic, Samuel F. and Petrou, Steven}, - month = oct, - year = {2009}, - pages = {1225--1232}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\KVY7Y2ZE\\Thomas et al. - 2009 - Prediction by Modeling That Epilepsy May Be Caused.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\ASQH7SHJ\\798244.html:text/html}, +@Article{goaillard_ion_2021, + author = {Goaillard, Jean-Marc and Marder, Eve}, + title = {Ion {Channel} {Degeneracy}, {Variability}, and {Covariation} in {Neuron} and {Circuit} {Resilience}}, + doi = {10.1146/annurev-neuro-092920-121538}, + issn = {0147-006X}, + url = {https://www.annualreviews.org/doi/10.1146/annurev-neuro-092920-121538}, + urldate = {2021-07-01}, + abstract = {The large number of ion channels found in all nervous systems poses fundamental questions concerning how the characteristic intrinsic properties of single neurons are determined by the specific subsets of channels they express. All neurons display many different ion channels with overlapping voltage- and time-dependent properties. We speculate that these overlapping properties promote resilience in neuronal function. Individual neurons of the same cell type show variability in ion channel conductance densities even though they can generate reliable and similar behavior. This complicates a simple assignment of function to any conductance and is associated with variable responses of neurons of the same cell type to perturbations, deletions, and pharmacological manipulation. Ion channel genes often show strong positively correlated expression, which may result from the molecular and developmental rules that determine which ion channels are expressed in a given cell type. Expected final online publication date for the Annual Review of Neuroscience, Volume 44 is July 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CLGI3EBW\\Goaillard and Marder - 2021 - Ion Channel Degeneracy, Variability, and Covariati.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\MVGHAFMQ\\annurev-neuro-092920-121538.html:text/html}, + journal = {Annual Review of Neuroscience}, + month = jul, + year = {2021}, } -@article{saltelli_sensitivity_2002, - title = {Sensitivity {Analysis} for {Importance} {Assessment}}, - volume = {22}, - issn = {1539-6924}, - url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/0272-4332.00040}, - doi = {10.1111/0272-4332.00040}, - abstract = {We review briefly some examples that would support an extended role for quantitative sensitivity analysis in the context of model-based analysis (Section 1). We then review what features a quantitative sensitivity analysis needs to have to play such a role (Section 2). The methods that meet these requirements are described in Section 3; an example is provided in Section 4. Some pointers to further research are set out in Section 5.}, - language = {en}, - number = {3}, - urldate = {2021-07-20}, - journal = {Risk Analysis}, - author = {Saltelli, Andrea}, - year = {2002}, - keywords = {Uncertainty analysis, assessment of importance, computational models, quantitative sensitivity analysis, risk analysis}, - pages = {579--590}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GGILMCED\\Saltelli - 2002 - Sensitivity Analysis for Importance Assessment.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WMUKUUT5\\0272-4332.html:text/html}, +@Article{Weber2017, + author = {Weber, Yvonne G. and Biskup, Saskia and Helbig, Katherine L. and Von Spiczak, Sarah and Lerche, Holger}, + title = {The role of genetic testing in epilepsy diagnosis and management}, + doi = {10.1080/14737159.2017.1335598}, + issn = {1473-7159}, + number = {8}, + pages = {739--750}, + url = {https://doi.org/10.1080/14737159.2017.1335598}, + urldate = {2022-03-06}, + volume = {17}, + abstract = {Introduction: Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures. More than 500 epilepsy-associated genes have been described in the literature. Most of these genes play an important role in neuronal excitability, cortical development or synaptic transmission. A growing number of genetic variations have implications on diagnosis and prognostic or therapeutic advice in terms of a personalized medicine.Area covered: The review presents the different forms of genetic epilepsies with respect to their underlying genetic and functional pathophysiology and aims to give advice for recommended genetic testing. Moreover, it discusses ethical and legal guidelines, costs and technical limitations which should be considered.Expert commentary: Genetic testing is an important component in the diagnosis and treatment of many forms of epilepsy.}, + file = {Full Text PDF:https\://www.tandfonline.com/doi/pdf/10.1080/14737159.2017.1335598:application/pdf}, + groups = {Jan}, + journal = {Expert Review of Molecular Diagnostics}, + keywords = {Genetic counseling, next generation sequencing, microarray analysis, exome, genome, idiopathic, personalized medicine, precision medicine, metabolic epilepsies, genetic epilepsies}, + month = aug, + pmid = {28548558}, + publisher = {Taylor \& Francis}, + year = {2017}, } -@article{hafez_altered_2020, - title = {Altered neuronal excitability in a {Hodgkin}-{Huxley} model incorporating channelopathies of the delayed rectifier potassium channel}, - volume = {48}, - issn = {1573-6873}, - url = {https://doi.org/10.1007/s10827-020-00766-1}, - doi = {10.1007/s10827-020-00766-1}, - abstract = {Channelopathies involving acquired or genetic modifications of the delayed rectifier K+ channel Kv1.1 include phenotypes characterized by enhanced neuronal excitability. Affected Kv1.1 channels exhibit combinations of altered expression, voltage sensitivity, and rates of activation and deactivation. Computational modeling and analysis can reveal the potential of particular channelopathies to alter neuronal excitability. A dynamical systems approach was taken to study the excitability and underlying dynamical structure of the Hodgkin-Huxley (HH) model of neural excitation as properties of the delayed rectifier K+ channel were altered. Bifurcation patterns of the HH model were determined as the amplitude of steady injection current was varied simultaneously with single parameters describing the delayed rectifier rates of activation and deactivation, maximal conductance, and voltage sensitivity. Relatively modest changes in the properties of the delayed rectifier K+ channel analogous to what is described for its channelopathies alter the bifurcation structure of the HH model and profoundly modify excitability of the HH model. Channelopathies associated with Kv1.1 can reduce the threshold for onset of neural activity. These studies also demonstrate how pathological delayed rectifier K+ channels could lead to the observation of the generalized Hopf bifurcation and, perhaps, other variants of the Hopf bifurcation. The observed bifurcation patterns collectively demonstrate that properties of the nominal delayed rectifier in the HH model appear optimized to permit activation of the HH model over the broadest possible range of input currents.}, - language = {en}, - number = {4}, - urldate = {2021-07-26}, - journal = {Journal of Computational Neuroscience}, - author = {Hafez, Omar A. and Gottschalk, Allan}, - month = nov, - year = {2020}, - pages = {377--386}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\4CCGDHXQ\\Hafez and Gottschalk - 2020 - Altered neuronal excitability in a Hodgkin-Huxley .pdf:application/pdf}, +@Article{glasscock_kv11_2019, + author = {Glasscock, Edward}, + title = {Kv1.1 channel subunits in the control of neurocardiac function}, + doi = {10.1080/19336950.2019.1635864}, + issn = {1933-6950}, + number = {1}, + pages = {299--307}, + url = {https://doi.org/10.1080/19336950.2019.1635864}, + urldate = {2021-06-10}, + volume = {13}, + abstract = {Voltage-gated Kv1.1 potassium channel α-subunits are broadly expressed in the nervous system where they act as critical regulators of neuronal excitability. Mutations in the KCNA1 gene, which encodes Kv1.1, are associated with the neurological diseases episodic ataxia and epilepsy. Studies in mouse models have shown that Kv1.1 is important for neural control of the heart and that Kcna1 deletion leads to cardiac dysfunction that appears to be brain-driven. Traditionally, KCNA1 was not believed to be expressed in the heart. However, recent studies have revealed that Kv1.1 subunits are not only present in cardiomyocytes, but that they also make an important heart-intrinsic functional contribution to outward K+ currents and action potential repolarization. This review recounts the winding history of discovery of KCNA1 gene expression and neurocardiac function from fruit flies to mammals and from brain to heart and looks at some of the salient questions that remain to be answered regarding emerging cardiac roles of Kv1.1.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9HL7ES5Y\\Glasscock - 2019 - Kv1.1 channel subunits in the control of neurocard.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\QZIHSRYT\\19336950.2019.html:text/html}, + journal = {Channels}, + keywords = {epilepsy, action potential, Kv1.1, SUDEP, heart, Kcna1}, + month = jan, + year = {2019}, } -@article{bernard_channelopathies_2008, - title = {Channelopathies: {A} {Review}}, - volume = {38}, - issn = {0887-8994}, - shorttitle = {Channelopathies}, - url = {https://www.sciencedirect.com/science/article/pii/S0887899407004584}, - doi = {10.1016/j.pediatrneurol.2007.09.007}, - abstract = {Channelopathies are a recently delineated, emerging group of neurologic disorders united by genetically determined defects in ion-channel function. These disorders are characterized by a prominent genetic and phenotypic heterogeneity that can make them challenging and bewildering to understand. This systematic review attempts to categorize these disorders according to their predominant clinical manifestations (i.e., myotonia, weakness, migraine, ataxia, epilepsy, and movement disorders) within the context of what is presently known about the molecular basis of recognized clinical syndromes. Areas of both genetic and phenotypic overlap are highlighted. The review is intended to assist clinicians in enhancing their diagnostic acumen and in targeting specific genetic tests.}, - language = {en}, - number = {2}, - urldate = {2021-07-27}, - journal = {Pediatric Neurology}, - author = {Bernard, Genevieve and Shevell, Michael I.}, - month = feb, - year = {2008}, - pages = {73--85}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\MH4R3N5F\\Bernard and Shevell - 2008 - Channelopathies A Review.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VED5EHSZ\\S0887899407004584.html:text/html}, +@Article{brunt_familial_1990, + author = {Brunt, Ewout R. P. and van Weerden, Tiemen W.}, + title = {Familial {Paroxysmal} {Kinesigenic} {Ataxia} and {Continuous} {Myokymia}}, + doi = {10.1093/brain/113.5.1361}, + issn = {0006-8950}, + number = {5}, + pages = {1361--1382}, + url = {https://doi.org/10.1093/brain/113.5.1361}, + urldate = {2021-06-10}, + volume = {113}, + abstract = {A large family with paroxysmal ataxia and continuous myokymic discharges is described. The disorder is of autosomal dominant inheritance. During attacks coordination of movements and balance are disturbed; often a postural tremor of the head and the hands and fine twitching in some of the facial and hand muscles are present. The attacks usually last a few minutes and may occur several times per day. They first appear in childhood and tend to abate after early adulthood. The attacks are frequently precipitated by kinesigenic stimuli similar to those in paroxysmal kinesigenic choreoathetosis. Their occurrence can be reduced or prevented by carbonic anhydrase inhibitors. Between attacks a slight postural tremor and ataxia was found in a few of the elderly affected members. Fine rippling myokymia was obvious in a few and could be detected on close inspection in about half of the adults. Electromyography (EMG) showed myokymic discharges in all affected members. The characteristics and reactivity of this myokymic activity suggest multiple impulse generation in the peripheral nerves.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\558YAH37\\BRUNT and VAN WEERDEN - 1990 - FAMILIAL PAROXYSMAL KINESIGENIC ATAXIA AND CONTINU.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2PIA368R\\267626.html:text/html}, + journal = {Brain}, + month = oct, + year = {1990}, +} + +@Article{taylor_how_2009, + author = {Taylor, Adam L. and Goaillard, Jean-Marc and Marder, Eve}, + title = {How {Multiple} {Conductances} {Determine} {Electrophysiological} {Properties} in a {Multicompartment} {Model}}, + number = {17}, + pages = {5573--5586}, + volume = {29}, + file = {How Multiple Conductances Determine Electrophysiological Properties in a Multicompartment Model | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\46GADMUG\\5573.html:text/html}, + journal = {Journal of Neuroscience}, + month = apr, + year = {2009}, +} + +@Article{ranjan_kinetic_2019, + author = {Ranjan, Rajnish and Logette, Emmanuelle and Marani, Michela and Herzog, Mirjia and Tâche, Valérie and Scantamburlo, Enrico and Buchillier, Valérie and Markram, Henry}, + title = {A {Kinetic} {Map} of the {Homomeric} {Voltage}-{Gated} {Potassium} {Channel} ({Kv}) {Family}}, + doi = {10.3389/fncel.2019.00358}, + issn = {1662-5102}, + language = {English}, + url = {https://www.frontiersin.org/articles/10.3389/fncel.2019.00358/full}, + urldate = {2021-02-16}, + volume = {13}, + abstract = {The voltage-gated potassium (Kv) channels, encoded by 40 genes, repolarize all electrically excitable cells, including plant, cardiac and neuronal cells. Although these genes were fully sequenced decades ago, a comprehensive kinetic characterization of all Kv channels is still missing, especially near physiological temperature. Here, we present a standardized kinetic map of the 40 homomeric Kv channels systematically characterized at 15°C, 25°C and 35°C. Importantly, the Kv kinetics at 35°C differ significantly from commonly reported kinetics, usually performed at room temperature. We observed voltage-dependent Q10 for all active Kv channels and inherent heterogeneity in kinetics for some of them. Kinetic properties are consistent across different host cell lines and conserved across mouse, rat and human. All electrophysiology data from all Kv channels are made available through public website (Channelpedia). This dataset provides a solid foundation for exploring kinetics of heteromeric channels, roles of auxiliary subunits, kinetic modulation, and for building accurate Kv models.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\JP3ET4D5\\Ranjan et al. - 2019 - A Kinetic Map of the Homomeric Voltage-Gated Potas.pdf:application/pdf}, + journal = {Frontiers in Cellular Neuroscience}, + keywords = {Kinetics, automated patch clamp electrophysiology, CHO - Chinese hamster ovary, ion channel, Kv}, + year = {2019}, +} + +@Article{pospischil_minimal_2008, + author = {Pospischil, Martin and Toledo-Rodriguez, Maria and Monier, Cyril and Piwkowska, Zuzanna and Bal, Thierry and Frégnac, Yves and Markram, Henry and Destexhe, Alain}, + title = {Minimal {Hodgkin}–{Huxley} type models for different classes of cortical and thalamic neurons}, + doi = {10.1007/s00422-008-0263-8}, + issn = {1432-0770}, + language = {en}, + number = {4}, + pages = {427--441}, + url = {https://doi.org/10.1007/s00422-008-0263-8}, + urldate = {2020-09-23}, + volume = {99}, + abstract = {We review here the development of Hodgkin–Huxley (HH) type models of cerebral cortex and thalamic neurons for network simulations. The intrinsic electrophysiological properties of cortical neurons were analyzed from several preparations, and we selected the four most prominent electrophysiological classes of neurons. These four classes are “fast spiking” “regular spiking” “intrinsically bursting” and “low-threshold spike” cells. For each class, we fit “minimal” HH type models to experimental data. The models contain the minimal set of voltage-dependent currents to account for the data. To obtain models as generic as possible, we used data from different preparations in vivo and in vitro, such as rat somatosensory cortex and thalamus, guinea-pig visual and frontal cortex, ferret visual cortex, cat visual cortex and cat association cortex. For two cell classes, we used automatic fitting procedures applied to several cells, which revealed substantial cell-to-cell variability within each class. The selection of such cellular models constitutes a necessary step towards building network simulations of the thalamocortical system with realistic cellular dynamical properties.}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SGVJJSXF\\Pospischil et al. - 2008 - Minimal Hodgkin–Huxley type models for different c.pdf:application/pdf}, + journal = {Biological Cybernetics}, + month = nov, + year = {2008}, +} + +@Article{wang_localization_1994, + author = {Wang, H. and Kunkel, D. D. and Schwartzkroin, P. A. and Tempel, B. L.}, + title = {Localization of {Kv1}.1 and {Kv1}.2, two {K} channel proteins, to synaptic terminals, somata, and dendrites in the mouse brain}, + doi = {10.1523/JNEUROSCI.14-08-04588.1994}, + issn = {0270-6474, 1529-2401}, + language = {en}, + number = {8}, + pages = {4588--4599}, + url = {https://www.jneurosci.org/content/14/8/4588}, + urldate = {2021-06-10}, + volume = {14}, + abstract = {Multiple voltage-gated potassium (K) channel gene products are likely to be involved in regulating neuronal excitability of any single neuron in the mammalian brain. Here we show that two closely related voltage- gated K channel proteins, mKv1.1 and mKv1.2, are present in multiple subcellular locations including cell somata, juxta-paranodal regions of myelinated axons, synaptic terminals, unmyelinated axons, specialized junctions among axons, and proximal dendrites. Staining patterns of the two channel polypeptides overlap in some areas of the brain, yet each has a unique pattern of expression. For example, in the hippocampus, both mKv1.1 and mKv1.2 proteins are present in axons, often near or at synaptic terminals in the middle molecular layer of the dentate gyrus, while only mKv1.1 is detected in axons and synaptic terminals in the hilar/CA3 region. In the cerebellum, both channel proteins are localized to axon terminals and specialized junctions among axons in the plexus region of basket cells. Strong differential staining is observed in the olfactory bulb, where mKv1.2 is localized to cell somata and axons, as well as to proximal dendrites of the mitral cells. This overlapping yet differential pattern of expression and specific subcellular localization may contribute to the unique profile of excitability displayed by a particular neuron.}, + copyright = {© 1994 by Society for Neuroscience}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8W3QSPJ8\\Wang et al. - 1994 - Localization of Kv1.1 and Kv1.2, two K channel pro.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XW29S3YF\\4588.html:text/html}, + journal = {Journal of Neuroscience}, + month = aug, + year = {1994}, } -@article{carbone_ion_2020, - title = {Ion channelopathies to bridge molecular lesions, channel function, and clinical therapies}, - volume = {472}, - issn = {1432-2013}, - url = {https://doi.org/10.1007/s00424-020-02424-y}, - doi = {10.1007/s00424-020-02424-y}, - language = {en}, - number = {7}, - urldate = {2021-07-27}, - journal = {Pflügers Archiv - European Journal of Physiology}, - author = {Carbone, Emilio and Mori, Yasuo}, - month = jul, - year = {2020}, - pages = {733--738}, - file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Z33W8XFN\\Carbone and Mori - 2020 - Ion channelopathies to bridge molecular lesions, c.pdf:application/pdf}, +@Article{carbone_ion_2020, + author = {Carbone, Emilio and Mori, Yasuo}, + title = {Ion channelopathies to bridge molecular lesions, channel function, and clinical therapies}, + doi = {10.1007/s00424-020-02424-y}, + issn = {1432-2013}, + language = {en}, + number = {7}, + pages = {733--738}, + url = {https://doi.org/10.1007/s00424-020-02424-y}, + urldate = {2021-07-27}, + volume = {472}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Z33W8XFN\\Carbone and Mori - 2020 - Ion channelopathies to bridge molecular lesions, c.pdf:application/pdf}, + journal = {Pflügers Archiv - European Journal of Physiology}, + month = jul, + year = {2020}, } -@article{rutecki_neuronal_1992, - title = {Neuronal excitability: voltage-dependent currents and synaptic transmission}, - volume = {9}, - issn = {0736-0258}, - shorttitle = {Neuronal excitability}, - abstract = {Neuronal membrane excitability and the synaptic connections among neurons produce behavior and cognition. The intracellular compartment of neurons is negatively charged relative to the extracellular space, and this charge, as well as current flow, is produced by ions. From the perspective of charged ions, the lipid bilayer of the neuronal membrane acts as a capacitor, and transmembrane glycoprotein pores or channels act as resistors. The open and closed states of ionic channels determine the membrane potential. At equilibrium, the lowest resistance or greatest permeability is for potassium, and the resting membrane potential is close to the equilibrium potential for potassium. When a channel is opened, permeable ions diffuse down their electrochemical gradients and the membrane potential is changed. Channels are gated (opened or closed) by voltage, neurotransmitters, and second messengers. The neuron integrates synaptic potentials produced by transmitter-gated channel activity and either generates a subthreshold potential, or a suprathreshold depolarization that generates an action potential or a burst of action potentials. Action potential generation is mediated by a large, brief sodium influx that is followed by activation of a voltage-dependent potassium eflux. The pattern of action potential firing is dependent on the interaction of a repertoire of voltage-dependent ion conductances. The action potential is the main signaling mechanism to activate synaptic transmission at axon terminals. Synaptic transmission is graded depending on the amount of calcium entering the presynaptic terminal. The number of action potentials, or the shape of the action potential, will determine the amount of calcium entering the terminal and the efficacy of synaptic transmission. Presynaptic ion channels may also be controlled by neurotransmitters or modulators and affect synaptic transmission by altering the amount of calcium influx.}, - language = {eng}, - number = {2}, - journal = {Journal of Clinical Neurophysiology: Official Publication of the American Electroencephalographic Society}, - author = {Rutecki, P. A.}, - month = apr, - year = {1992}, - keywords = {Animals, Synapses, Membrane Potentials, Synaptic Transmission, Humans, Axons, Central Nervous System, Dendrites, Ion Channels, Neuromuscular Junction, Neurotransmitter Agents, Synaptic Membranes}, - pages = {195--211}, + + +@Article{Scalmani2006, + author = {Scalmani, Paolo and Rusconi, Raffaella and Armatura, Elena and Zara, Federico and Avanzini, Giuliano and Franceschetti, Silvana and Mantegazza, Massimo}, + title = {Effects in {Neocortical} {Neurons} of {Mutations} of the {Nav1}.2 {Na}+ {Channel} causing {Benign} {Familial} {Neonatal}-{Infantile} {Seizures}}, + doi = {10.1523/JNEUROSCI.2476-06.2006}, + issn = {0270-6474}, + number = {40}, + pages = {10100--10109}, + url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6674637/}, + urldate = {2022-04-03}, + volume = {26}, + abstract = {Mutations of voltage-gated Na+ channels are the most common cause of familial epilepsy. Benign familial neonatal-infantile seizures (BFNIS) is an epileptic trait of the early infancy, and it is the only well characterized epileptic syndrome caused exclusively by mutations of Nav1.2 Na+ channels, but no functional studies of BFNIS mutations have been done. The comparative study of the functional effects and the elucidation of the pathogenic mechanisms of epileptogenic mutations is essential for designing targeted and effective therapies. However, the functional properties of Na+ channels and the effects of their mutations are very sensitive to the cell background and thus to the expression system used. We investigated the functional effects of four of the six BFNIS mutations identified (L1330F, L1563V, R223Q, and R1319Q) using as expression system transfected pyramidal and bipolar neocortical neurons in short primary cultures, which have small endogenous Na+ current and thus permit the selective study of transfected channels. The mutation L1330F caused a positive shift of the inactivation curve, and the mutation L1563V caused a negative shift of the activation curve, effects that are consistent with neuronal hyperexcitability. The mutations R223Q and R1319Q mainly caused positive shifts of both activation and inactivation curves, effects that cannot be directly associated with a specific modification of excitability. Using physiological stimuli in voltage-clamp experiments, we showed that these mutations increase both subthreshold and action Na+ currents, consistently with hyperexcitability. Thus, the pathogenic mechanism of BFNIS mutations is neuronal hyperexcitability caused by increased Na+ current.}, + file = {PubMed Central Link:https\://www.ncbi.nlm.nih.gov/pmc/articles/PMC6674637/:text/html}, + groups = {Jan}, + journal = {The Journal of Neuroscience}, + month = oct, + pmcid = {PMC6674637}, + pmid = {17021166}, + year = {2006}, +} + +@Article{shi_efficacy_2016, + author = {Shi, Xiu-Yu and Tomonoh, Yuko and Wang, Wen-Ze and Ishii, Atsushi and Higurashi, Norimichi and Kurahashi, Hirokazu and Kaneko, Sunao and Hirose, Shinichi and {Epilepsy Genetic Study Group, Japan}}, + title = {Efficacy of antiepileptic drugs for the treatment of {Dravet} syndrome with different genotypes}, + doi = {10.1016/j.braindev.2015.06.008}, + issn = {1872-7131}, + language = {eng}, + number = {1}, + pages = {40--46}, + volume = {38}, + abstract = {OBJECTIVE: Evaluation of the efficacy of antiepileptic drugs (AEDs) used in the treatment of Dravet syndrome (DS) with different genotypes. +METHODS: Patients with DS were recruited from different tertiary hospitals. Using a direct sequencing method and Multiplex Ligation-Dependent Probe Amplification (MLPA), genetic abnormalities were assessed within the exons and flanking introns of SCN1A gene, which encodes the α1 subunit of neuronal sodium channels. Patients were divided into SCN1A-positive and SCN1A-negative groups according to the results of genetic tests. Medical records, including detailed treatment information, were surveyed to compare the effect of different AEDs on clonic or tonic-clonic seizures (GTCS). Efficacy variable was responder rate with regard to seizure reduction. +RESULTS: One hundred and sixty of 276 (57.97\%) patients had mutation in SCN1A gene (only 128 of them had provided detailed medical records). Among the 116 patients without SCN1A mutations, 87 had provided detailed medical records. Both older AEDs (valproate, phenobarbital, bromide, carbamazepine, clonazepam, and clobazam) and newer AEDs such as zonisamide were used in these patients. Valproate was the most frequently used AED (86.72\% in the SCN1A-positive group, 78.16\% in the SCN1A-negative group), with 52.25\% and 41.18\% responder rates in SCN1A-positive and SCN1A-negative patients, respectively (P=0.15). Bromide was used in 40.63\% of the SCN1A-positive patients and 20.69\% of the SCN1A-negative patients, and its responder rates were 71.15\% and 94.44\% in SCN1A-positive and SCN1A-negative patients, respectively (P=0.05). Efficacy rates of clonazepam, clobazam, phenobarbital, and zonisamide ranged from 30\% to 50\%, and these rates were not correlated with different genotypes (P{\textgreater}0.05). Carbamazepine had either no effect or aggravated seizures in all SCN1A-positive patients. +SIGNIFICANCE: Bromide is most effective and is a well-tolerated drug among DS patients, especially among SCN1A-negative patients. Carbamazepine should be avoided in patients with SCN1A mutations.}, + journal = {Brain \& Development}, + keywords = {Seizures, Male, Humans, Female, Adult, Young Adult, Adolescent, Child, Preschool, Infant, Treatment Outcome, Carbamazepine, Anticonvulsants, Mutation, Retrospective Studies, Antiepileptic drug therapy, Bromides, Dravet syndrome, Efficacy, Epilepsies, Myoclonic, Genetic tests, Genotype, Genotyping Techniques, NAV1.1 Voltage-Gated Sodium Channel}, + month = jan, + year = {2016}, } -@article{dunlop_high-throughput_2008, - title = {High-throughput electrophysiology: an emerging paradigm for ion-channel screening and physiology}, - volume = {7}, - copyright = {2008 Nature Publishing Group}, - issn = {1474-1784}, - shorttitle = {High-throughput electrophysiology}, - url = {https://www.nature.com/articles/nrd2552}, - doi = {10.1038/nrd2552}, - abstract = {Ion channels represent an important class of druggable targets; however, it is generally appreciated in the field that ion-channel targeted drug discovery has been hampered by the unavailability of high-throughput platforms that use electrophysiological techniques for the characterization of compound activity. To address this bottleneck, in the past 5 years, several companies have developed and introduced automated platforms for performing electrophysiological studies.This recent explosion includes different approaches taken to carry out multi-channel planar-array based patch-clamp recordings of mammalian cells, resulting in the commercialization of four systems — IonWorks, PatchXpress, Patchliner and CytoPatch. Complementary to these technologies has been the development of lower capacity systems that fully automate conventional manual patch-clamp recordings including the Flyscreen, AutoPatch and RoboPatch for mammalian cells, and the Robocyte and OpusXpress 6000A for Xenopus oocytes.Despite the sophisticated technologies that are now available, automating patch-clamp electrophysiology often presents underestimated challenges regarding reproducibility with the cells being used; this needs to be fully appreciated when embarking on the implementation of any of these approaches.The need to assess the potential of drug candidates to inhibit cardiac ion-channels, particularly hERG, has greatly contributed to the development of these technologies. Although higher throughput non-electrophysiological assays have a reasonable predictive potential, they have several limitations that might be technically or chemically limiting. Consequently, the desire to use electrophysiological assays early on to assess ion-channel liabilities has been one of the key drivers for implementation of automated electrophysiology.Compound screening against molecularly isolated, heterologously expressed ion channels, will often identify drug candidates whose higher-order impact on networked neuronal systems are not necessarily inferable from their effects on individual conductances. Raising the throughput of pharmacological evaluation in such higher-order systems presents a distinct set of challenges. However, recent progress has been made in the development of automated systems for performing electrophysiogical studies in brain slices and other intact biological preparations.The availability of these technologies has re-energized ion-channel targeted drug discovery by allowing the development of screening paradigms that were not feasible in the pre-automation era. In our opinion this holds much promise for the discovery and development of innovative new ion-channel targeted drugs. Tractability of ion channels as drug targets coupled with future advances in technology platforms and decreased cost of consumables are expected to support an even wider implementation of these automated systems.}, - language = {en}, - number = {4}, - urldate = {2021-07-28}, - journal = {Nature Reviews Drug Discovery}, - author = {Dunlop, John and Bowlby, Mark and Peri, Ravikumar and Vasilyev, Dmytro and Arias, Robert}, - month = apr, - year = {2008}, - pages = {358--368}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\U2CUSEMS\\Dunlop et al. - 2008 - High-throughput electrophysiology an emerging par.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\UUCS8RN7\\nrd2552.html:text/html}, +@Article{soofi_co-variation_2012, + author = {Soofi, Wafa and Archila, Santiago and Prinz, Astrid A.}, + title = {Co-variation of ionic conductances supports phase maintenance in stomatogastric neurons}, + doi = {10.1007/s10827-011-0375-3}, + issn = {1573-6873}, + language = {en}, + number = {1}, + pages = {77--95}, + url = {https://doi.org/10.1007/s10827-011-0375-3}, + urldate = {2021-07-01}, + volume = {33}, + abstract = {Neuronal networks produce reliable functional output throughout the lifespan of an animal despite ceaseless molecular turnover and a constantly changing environment. Central pattern generators, such as those of the crustacean stomatogastric ganglion (STG), are able to robustly maintain their functionality over a wide range of burst periods. Previous experimental work involving extracellular recordings of the pyloric pattern of the STG has demonstrated that as the burst period varies, the inter-neuronal delays are altered proportionally, resulting in burst phases that are roughly invariant. The question whether spike delays within bursts are also proportional to pyloric period has not been explored in detail. The mechanism by which the pyloric neurons accomplish phase maintenance is currently not obvious. Previous studies suggest that the co-regulation of certain ion channel properties may play a role in governing neuronal activity. Here, we observed in long-term recordings of the pyloric rhythm that spike delays can vary proportionally with burst period, so that spike phase is maintained. We then used a conductance-based model neuron to determine whether co-varying ionic membrane conductances results in neural output that emulates the experimentally observed phenomenon of spike phase maintenance. Next, we utilized a model neuron database to determine whether conductance correlations exist in model neuron populations with highly maintained spike phases. We found that co-varying certain conductances, including the sodium and transient calcium conductance pair, causes the model neuron to maintain a specific spike phase pattern. Results indicate a possible relationship between conductance co-regulation and phase maintenance in STG neurons.}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\6Q9T34AC\\Soofi et al. - 2012 - Co-variation of ionic conductances supports phase .pdf:application/pdf}, + journal = {Journal of Computational Neuroscience}, + month = aug, + year = {2012}, } -@article{soe_neuroscience_2012, - title = {Neuroscience goes on a chip}, - volume = {35}, - issn = {0956-5663}, - url = {https://www.sciencedirect.com/science/article/pii/S0956566312000723}, - doi = {10.1016/j.bios.2012.02.012}, - abstract = {Advances in microelectronics, microfluidics, polymers and microfabrication have enabled the creation of disposable lab-on-a-chips (LOCs) as the new tools for neuroscience research. The LOCs have been applied for a wide range of neurobiology studies, including cellular and molecular biochemical experimentations, morphological observations and electrophysiological investigations. The integration of miniaturised components leads to analytical instrumentations with unprecedented automation, speed of analysis, and flexibility. These features make LOCs capable enough to replace their bulky and expensive bench-top counterparts. LOCs can be useful for genomic, proteomic, epigenomic, peptidomic, connectomic and electrophysiological studies and also as effective tools for reductionist neuroscientists. Moreover, they can be applied at higher level studies such as developmental neurobiology and behavioural investigations. This work provides an in-depth review of LOC platforms for neuroscience research. First, we review the essential bench-top neuroscience instrumentation as per their functions and features. Next, we present LOC counterparts for those bench-top instrumentations. Finally, we offer perspectives on persistent challenges and our perception of opportunities based on LOC instrumentations in neuroscience research.}, - language = {en}, - number = {1}, - urldate = {2021-07-28}, - journal = {Biosensors and Bioelectronics}, - author = {Soe, Aung K. and Nahavandi, Saeid and Khoshmanesh, Khashayar}, - month = may, - year = {2012}, - keywords = {Lab-on-a-chip, Microfluidics, Molecular biochemistry, Neurobiology}, - pages = {1--13}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5GSIMSZA\\Soe et al. - 2012 - Neuroscience goes on a chip.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\A9PEFFZ2\\S0956566312000723.html:text/html}, + +@Article{Liu2019, + author = {Liu, Yuanyuan and Schubert, Julian and Sonnenberg, Lukas and Helbig, Katherine L and Hoei-Hansen, Christina E and Koko, Mahmoud and Rannap, Maert and Lauxmann, Stephan and Huq, Mahbubul and Schneider, Michael C and Johannesen, Katrine M and Kurlemann, Gerhard and Gardella, Elena and Becker, Felicitas and Weber, Yvonne G and Benda, Jan and Møller, Rikke S and Lerche, Holger}, + title = {Neuronal mechanisms of mutations in {SCN8A} causing epilepsy or intellectual disability}, + doi = {10.1093/brain/awy326}, + issn = {0006-8950}, + number = {2}, + pages = {376--390}, + url = {https://doi.org/10.1093/brain/awy326}, + urldate = {2022-04-03}, + volume = {142}, + abstract = {Ion channel mutations can cause distinct neuropsychiatric diseases. We first studied the biophysical and neurophysiological consequences of four mutations in the human Na+ channel gene SCN8A causing either mild (E1483K) or severe epilepsy (R1872W), or intellectual disability and autism without epilepsy (R1620L, A1622D). Only combined electrophysiological recordings of transfected wild-type or mutant channels in both neuroblastoma cells and primary cultured neurons revealed clear genotype–phenotype correlations. The E1483K mutation causing mild epilepsy showed no significant biophysical changes, whereas the R1872W mutation causing severe epilepsy induced clear gain-of-function biophysical changes in neuroblastoma cells. However, both mutations increased neuronal firing in primary neuronal cultures. In contrast, the R1620L mutation associated with intellectual disability and autism—but not epilepsy—reduced Na+ current density in neuroblastoma cells and expectedly decreased neuronal firing. Interestingly, for the fourth mutation, A1622D, causing severe intellectual disability and autism without epilepsy, we observed a dramatic slowing of fast inactivation in neuroblastoma cells, which induced a depolarization block in neurons with a reduction of neuronal firing. This latter finding was corroborated by computational modelling. In a second series of experiments, we recorded three more mutations (G1475R, M1760I, G964R, causing intermediate or severe epilepsy, or intellectual disability without epilepsy, respectively) that revealed similar results confirming clear genotype–phenotype relationships. We found intermediate or severe gain-of-function biophysical changes and increases in neuronal firing for the two epilepsy-causing mutations and decreased firing for the loss-of-function mutation causing intellectual disability. We conclude that studies in neurons are crucial to understand disease mechanisms, which here indicate that increased or decreased neuronal firing is responsible for distinct clinical phenotypes.}, + file = {:Liu2019 - Neuronal Mechanisms of Mutations in SCN8A Causing Epilepsy or Intellectual Disability.pdf:PDF}, + groups = {Jan}, + journal = {Brain}, + month = feb, + year = {2019}, } -@article{passaro_electrophysiological_2021, - title = {Electrophysiological {Analysis} of {Brain} {Organoids}: {Current} {Approaches} and {Advancements}}, - volume = {0}, - issn = {1662-453X}, - shorttitle = {Electrophysiological {Analysis} of {Brain} {Organoids}}, - url = {https://www.frontiersin.org/articles/10.3389/fnins.2020.622137/full}, - doi = {10.3389/fnins.2020.622137}, - abstract = {Brain organoids, or cerebral organoids, have become widely used to study the human brain in vitro. As pluripotent stem cell-derived structures capable of self-organization and recapitulation of physiological cell types and architecture, brain organoids bridge the gap between relatively simple two-dimensional human cell cultures and non-human animal models. This allows for high complexity and physiological relevance in a controlled in vitro setting, opening the door for a variety of applications including development and disease modeling and high-throughput screening. While technologies such as single cell sequencing have led to significant advances in brain organoid characterization and understanding, improved functional analysis (especially electrophysiology) is needed to realize the full potential of brain organoids. In this review, we highlight key technologies for brain organoid development and characterization, then discuss current electrophysiological methods for brain organoid analysis. While electrophysiological approaches have improved rapidly for two-dimensional cultures, only in the past several years have advances been made to overcome limitations posed by the three-dimensionality of brain organoids. Here, we review major advances in electrophysiological technologies and analytical methods with a focus on advances with applicability for brain organoid analysis.}, - language = {English}, - urldate = {2021-07-28}, - journal = {Frontiers in Neuroscience}, - author = {Passaro, Austin P. and Stice, Steven L.}, - year = {2021}, - keywords = {Electrophysiology, optogenetics, brain organoids, Electrophysiological analysis, multi-electrode array (MEA), neurological disease modeling}, - file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\XESZW56A\\Passaro and Stice - 2021 - Electrophysiological Analysis of Brain Organoids .pdf:application/pdf}, +@Article{bernard_channelopathies_2008, + author = {Bernard, Genevieve and Shevell, Michael I.}, + title = {Channelopathies: {A} {Review}}, + doi = {10.1016/j.pediatrneurol.2007.09.007}, + issn = {0887-8994}, + language = {en}, + number = {2}, + pages = {73--85}, + url = {https://www.sciencedirect.com/science/article/pii/S0887899407004584}, + urldate = {2021-07-27}, + volume = {38}, + abstract = {Channelopathies are a recently delineated, emerging group of neurologic disorders united by genetically determined defects in ion-channel function. These disorders are characterized by a prominent genetic and phenotypic heterogeneity that can make them challenging and bewildering to understand. This systematic review attempts to categorize these disorders according to their predominant clinical manifestations (i.e., myotonia, weakness, migraine, ataxia, epilepsy, and movement disorders) within the context of what is presently known about the molecular basis of recognized clinical syndromes. Areas of both genetic and phenotypic overlap are highlighted. The review is intended to assist clinicians in enhancing their diagnostic acumen and in targeting specific genetic tests.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\MH4R3N5F\\Bernard and Shevell - 2008 - Channelopathies A Review.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\VED5EHSZ\\S0887899407004584.html:text/html}, + journal = {Pediatric Neurology}, + month = feb, + shorttitle = {Channelopathies}, + year = {2008}, +} + +@Article{stuhmer_molecular_1989, + author = {Stühmer, W. and Ruppersberg, J.p. and Schröter, K.h. and Sakmann, B. and Stocker, M. and Giese, K.p. and Perschke, A. and Baumann, A. and Pongs, O.}, + title = {Molecular basis of functional diversity of voltage-gated potassium channels in mammalian brain.}, + doi = {10.1002/j.1460-2075.1989.tb08483.x}, + issn = {0261-4189}, + number = {11}, + pages = {3235--3244}, + url = {https://www.embopress.org/doi/abs/10.1002/j.1460-2075.1989.tb08483.x}, + urldate = {2021-06-07}, + volume = {8}, + abstract = {Cloning and sequencing of cDNAs isolated from a rat cortex cDNA library reveals that a gene family encodes several highly homologous K+ channel forming (RCK) proteins. Functional characterization of the channels expressed in Xenopus laevis oocytes following microinjection of in vitro transcribed RCK-specific RNAs shows that each of the RCK proteins forms K+ channels that differ greatly in both their functional and pharmacological properties. This suggests that the molecular basis for the diversity of voltage-gated K+ channels in mammalian brain is based, at least partly, on the expression of several RCK proteins by a family of genes and their assembly to homooligomeric K+ channels with different functional properties.}, + file = {Full Text:C\:\\Users\\nilsk\\Zotero\\storage\\T4DRXSVK\\Stühmer et al. - 1989 - Molecular basis of functional diversity of voltage.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\T22LZI5H\\j.1460-2075.1989.tb08483.html:text/html}, + journal = {The EMBO Journal}, + month = nov, + year = {1989}, +} + +@Article{jen_primary_2007, + author = {Jen, J.C. and Graves, T.D. and Hess, E.J. and Hanna, M.G. and Griggs, R.C. and Baloh, R.W. and {the CINCH investigators}}, + title = {Primary episodic ataxias: diagnosis, pathogenesis and treatment}, + doi = {10.1093/brain/awm126}, + issn = {0006-8950}, + number = {10}, + pages = {2484--2493}, + url = {https://doi.org/10.1093/brain/awm126}, + urldate = {2021-06-10}, + volume = {130}, + abstract = {Primary episodic ataxias are autosomal dominant channelopathies that manifest as attacks of imbalance and incoordination. Mutations in two genes, KCNA1 and CACNA1A, cause the best characterized and account for the majority of identified cases of episodic ataxia. We summarize current knowledge of clinical and genetic diagnosis, genotype–phenotype correlations, pathophysiology and treatment of episodic ataxia syndromes. We focus on unresolved issues including phenotypic and genetic heterogeneity, lessons from animal models and technological advancement, rationale and feasibility of various treatment strategies, and shared mechanisms underlying episodic ataxia and other far more prevalent paroxysmal conditions such as epilepsy and migraine.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7VS52FIB\\Jen et al. - 2007 - Primary episodic ataxias diagnosis, pathogenesis .pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\STLLRYY4\\Jen et al. - 2007 - Primary episodic ataxias diagnosis, pathogenesis .pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WWTFDAFS\\372064.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\G7MY4DE3\\372064.html:text/html}, + journal = {Brain}, + month = oct, + shorttitle = {Primary episodic ataxias}, + year = {2007}, } -@article{frega_network_2014, - title = {Network dynamics of {3D} engineered neuronal cultures: a new experimental model for in-vitro electrophysiology}, - volume = {4}, - copyright = {2014 The Author(s)}, - issn = {2045-2322}, - shorttitle = {Network dynamics of {3D} engineered neuronal cultures}, - url = {https://www.nature.com/articles/srep05489}, - doi = {10.1038/srep05489}, - abstract = {Despite the extensive use of in-vitro models for neuroscientific investigations and notwithstanding the growing field of network electrophysiology, all studies on cultured cells devoted to elucidate neurophysiological mechanisms and computational properties, are based on 2D neuronal networks. These networks are usually grown onto specific rigid substrates (also with embedded electrodes) and lack of most of the constituents of the in-vivo like environment: cell morphology, cell-to-cell interaction and neuritic outgrowth in all directions. Cells in a brain region develop in a 3D space and interact with a complex multi-cellular environment and extracellular matrix. Under this perspective, 3D networks coupled to micro-transducer arrays, represent a new and powerful in-vitro model capable of better emulating in-vivo physiology. In this work, we present a new experimental paradigm constituted by 3D hippocampal networks coupled to Micro-Electrode-Arrays (MEAs) and we show how the features of the recorded network dynamics differ from the corresponding 2D network model. Further development of the proposed 3D in-vitro model by adding embedded functionalized scaffolds might open new prospects for manipulating, stimulating and recording the neuronal activity to elucidate neurophysiological mechanisms and to design bio-hybrid microsystems.}, - language = {en}, - number = {1}, - urldate = {2021-07-28}, - journal = {Scientific Reports}, - author = {Frega, Monica and Tedesco, Mariateresa and Massobrio, Paolo and Pesce, Mattia and Martinoia, Sergio}, - month = jun, - year = {2014}, - pages = {5489}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\V3EX3LHY\\Frega et al. - 2014 - Network dynamics of 3D engineered neuronal culture.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\WRPHUNXL\\srep05489.html:text/html}, +@Article{coleman_subunit_1999, + author = {Coleman, Sarah K. and Newcombe, Jia and Pryke, Jonathan and Dolly, J. Oliver}, + title = {Subunit {Composition} of {Kv1} {Channels} in {Human} {CNS}}, + doi = {10.1046/j.1471-4159.1999.0730849.x}, + issn = {1471-4159}, + language = {en}, + number = {2}, + pages = {849--858}, + url = {https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1471-4159.1999.0730849.x}, + urldate = {2021-06-12}, + volume = {73}, + abstract = {: The α subunits of Shaker-related K+ channels (Kv1.X) show characteristic distributions in mammalian brain and restricted coassembly. Despite the functional importance of these voltage-sensitive K+ channels and involvement in a number of diseases, little progress has been achieved in deciphering the subunit composition of the (α)4(β)4 oligomers occurring in human CNS. Thus, the association of α and β subunits was investigated in cerebral grey and white matter and spinal cord from autopsy samples. Immunoblotting established the presence of Kv1.1, 1.2, and 1.4 in all the tissues, with varying abundance. Sequential immunoprecipitations identified the subunits coassembled. A putative tetramer of Kv1.3/1.4/1.1/1.2 was found in grey matter. Both cerebral white matter and spinal cord contained the heterooligomers Kv1.1/1.4 and Kv1.1/1.2, similar to grey matter, but both lacked Kv1.3 and the Kv1.4/1.2 combination. An apparent Kv1.4 homooligomer was detected in all the samples, whereas only the brain tissue possessed a putative Kv1.2 homomer. In grey matter, Kvβ2.1 was coassociated with the Kv1.1/1.2 combination and Kv1.2 homooligomer. In white matter, Kvβ2.1 was associated with Kv1.2 only, whereas Kvβ1.1 coprecipitated with all the α subunits present. This represents the first description of Kv1 subunit complexes in the human CNS and demonstrates regional variations, indicative of functional specialisation.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\9N6K9G2L\\Coleman et al. - 1999 - Subunit Composition of Kv1 Channels in Human CNS.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\54GLRDQU\\j.1471-4159.1999.0730849.html:text/html}, + journal = {Journal of Neurochemistry}, + keywords = {Human, Potassium channel, Axolemma, CNS, Delayed rectifier, Immunoprecipitation.}, + year = {1999}, } -@article{jakel_using_2004, - title = {Using human neural stem cells to model neurological disease}, - volume = {5}, - copyright = {2004 Nature Publishing Group}, - issn = {1471-0064}, - url = {https://www.nature.com/articles/nrg1268}, - doi = {10.1038/nrg1268}, - abstract = {Many common neurological diseases have an underlying genetic basis that can be modelled in transgenic animals. However, animal models do not always faithfully reproduce the human syndrome. The urgent need for therapeutics that are aimed at neuroprotection underscores the necessity for alternative model systems.The study of the diseased human brain is crucial for understanding how mutant proteins lead to neuronal cell death. Unfortunately, this tissue is scarce and difficult to manipulate in vitro.Human stem cells represent a renewable source of human neural tissue that is naturally mitotic without transformation or immortalization. Stem cells can be generated from embryonic, fetal brain and adult brain tissue. Cells that are derived from the different sources have different characteristics that make them more or less useful for modelling neurological disease.Isolation of stem cells from diseased tissues might help to uncover mechanisms of cell death that have been seen in non-human models. Furthermore, mutations can be introduced into both mitotic and non-mitotic neuroepithelial cells through viral vectors or homologous recombination.Neural stem cells can be induced to differentiate into mature, physiologically active neurons and glia, and can be assessed in an undifferentiated or differentiated state and after engraftment.Stem-cell models allow the analysis of neuronal and glial subtypes simultaneously, and they can be assessed using current microarray technologies as well as other conventional activity and expression assays. Stem cells, of course, also have their disadvantages.Examples of how stem cells can be used to model specific neurodegenerative conditions are given.Further experimentation with stem cells and establishment of disease models will provide an important system to test signal-transduction pathways and disease mechanisms in human cells before clinical trials are attempted.Human stem-cell models should be used in parallel with current transgenic animal models as each approach has important strengths.}, - language = {en}, - number = {2}, - urldate = {2021-07-28}, - journal = {Nature Reviews Genetics}, - author = {Jakel, Rebekah J. and Schneider, Bernard L. and Svendsen, Clive N.}, - month = feb, - year = {2004}, - pages = {136--144}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\Y2RP9SSZ\\Jakel et al. - 2004 - Using human neural stem cells to model neurologica.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\W9M4YE6R\\nrg1268.html:text/html}, + + +@Article{Rush2006, + author = {Rush, Anthony M. and Dib-Hajj, Sulayman D. and Liu, Shujun and Cummins, Theodore R. and Black, Joel A. and Waxman, Stephen G.}, + title = {A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons}, + doi = {10.1073/pnas.0602813103}, + number = {21}, + pages = {8245--8250}, + url = {https://www.pnas.org/doi/10.1073/pnas.0602813103}, + urldate = {2022-03-05}, + volume = {103}, + file = {Full Text PDF:https\://www.pnas.org/doi/pdf/10.1073/pnas.0602813103:application/pdf}, + groups = {Jan}, + journal = {Proceedings of the National Academy of Sciences}, + month = may, + publisher = {Proceedings of the National Academy of Sciences}, + year = {2006}, } -@article{goversen_immature_2018, - title = {The immature electrophysiological phenotype of {iPSC}-{CMs} still hampers in vitro drug screening: {Special} focus on {IK1}}, - volume = {183}, - issn = {0163-7258}, - shorttitle = {The immature electrophysiological phenotype of {iPSC}-{CMs} still hampers in vitro drug screening}, - url = {https://www.sciencedirect.com/science/article/pii/S0163725817302383}, - doi = {10.1016/j.pharmthera.2017.10.001}, - abstract = {Preclinical drug screens are not based on human physiology, possibly complicating predictions on cardiotoxicity. Drug screening can be humanised with in vitro assays using human induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs). However, in contrast to adult ventricular cardiomyocytes, iPSC-CMs beat spontaneously due to presence of the pacemaking current If and reduced densities of the hyperpolarising current IK1. In adult cardiomyocytes, IK1 finalises repolarisation by stabilising the resting membrane potential while also maintaining excitability. The reduced IK1 density contributes to proarrhythmic traits in iPSC-CMs, which leads to an electrophysiological phenotype that might bias drug responses. The proarrhythmic traits can be suppressed by increasing IK1 in a balanced manner. We systematically evaluated all studies that report strategies to mature iPSC-CMs and found that only few studies report IK1 current densities. Furthermore, these studies did not succeed in establishing sufficient IK1 levels as they either added too little or too much IK1. We conclude that reduced densities of IK1 remain a major flaw in iPSC-CMs, which hampers their use for in vitro drug screening.}, - language = {en}, - urldate = {2021-07-28}, - journal = {Pharmacology \& Therapeutics}, - author = {Goversen, Birgit and van der Heyden, Marcel A. G. and van Veen, Toon A. B. and de Boer, Teun P.}, - month = mar, - year = {2018}, - keywords = {Arrhythmia, Cardiac electrophysiology, CiPA, I, iPSC-CMs, Safety pharmacology}, - pages = {127--136}, - file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\ATGB4836\\Goversen et al. - 2018 - The immature electrophysiological phenotype of iPS.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\UTKW4TK4\\S0163725817302383.html:text/html}, +@Article{zuberi_novel_1999, + author = {Zuberi, S. M. and Eunson, L. H. and Spauschus, A. and De Silva, R. and Tolmie, J. and Wood, N. W. and McWilliam, R. C. and Stephenson, J. P. B. and Kullmann, D. M. and Hanna, M. G.}, + title = {A novel mutation in the human voltage-gated potassium channel gene ({Kv1}.1) associates with episodic ataxia type 1 and sometimes with partial epilepsy}, + doi = {10.1093/brain/122.5.817}, + issn = {0006-8950}, + number = {5}, + pages = {817--825}, + url = {https://doi.org/10.1093/brain/122.5.817}, + urldate = {2021-06-10}, + volume = {122}, + abstract = {Episodic ataxia type 1 (EA1) is a rare autosomal dominant disorder characterized by brief episodes of ataxia associated with continuous interattack myokymia. Point mutations in the human voltage-gated potassium channel (Kv1.1) gene on chromosome 12p13 have recently been shown to associate with EA1. A Scottish family with EA1 harbouring a novel mutation in this gene is reported. Of the five affected individuals over three generations, two had partial epilepsy in addition to EA1. The detailed clinical, electrophysiological and molecular genetic findings are presented. The heterozygous point mutation is located at nucleotide position 677 and results in a radical amino acid substitution at a highly conserved position in the second transmembrane domain of the potassium channel. Functional studies indicated that mutant subunits exhibited a dominant negative effect on potassium channel function and would be predicted to impair neuronal repolarization. Potassium channels determine the excitability of neurons and blocking drugs are proconvulsant. A critical review of previously reported EA1 families shows an over-representation of epilepsy in family members with EA1 compared with unaffected members. These observations indicate that this mutation is pathogenic and suggest that the epilepsy in EA1 may be caused by the dysfunctional potassium channel. It is possible that such dysfunction may be relevant to other epilepsies in man.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SEX9BDH8\\Zuberi et al. - 1999 - A novel mutation in the human voltage-gated potass.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Q6HMRVKV\\296621.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\Y5C7TN83\\296621.html:text/html}, + journal = {Brain}, + month = may, + year = {1999}, } -@incollection{maan_carbamazepine_2021, - address = {Treasure Island (FL)}, - title = {Carbamazepine}, - copyright = {Copyright © 2021, StatPearls Publishing LLC.}, - url = {http://www.ncbi.nlm.nih.gov/books/NBK482455/}, - abstract = {Carbamazepine is used to manage and treat epilepsy, trigeminal neuralgia, and acute manic and mixed episodes in bipolar I disorder. Indications for epilepsy are specifically for partial seizures with complex symptomatology (psychomotor, temporal lobe), generalized tonic seizures (grand mal), and mixed seizure patterns. This activity will highlight off-label uses, mechanism of action, dosing, adverse effects, contraindications, and other key factors regarding carbamazepine.}, - language = {eng}, - urldate = {2021-07-28}, - booktitle = {{StatPearls}}, - publisher = {StatPearls Publishing}, - author = {Maan, Jasdave S. and Duong, Truc vi H. and Saadabadi, Abdolreza}, - year = {2021}, - file = {Printable HTML:C\:\\Users\\nilsk\\Zotero\\storage\\69GFVCY7\\NBK482455.html:text/html}, +@Article{rajakulendran_episodic_2007, + author = {Rajakulendran, Sanjeev and Schorge, Stephanie and Kullmann, Dimitri M. and Hanna, Michael G.}, + title = {Episodic ataxia type 1: {A} neuronal potassium channelopathy}, + doi = {10.1016/j.nurt.2007.01.010}, + issn = {1878-7479}, + language = {en}, + number = {2}, + pages = {258--266}, + url = {https://doi.org/10.1016/j.nurt.2007.01.010}, + urldate = {2021-06-10}, + volume = {4}, + abstract = {Episodic ataxia type 1 is a paroxysmal neurological disorder characterized by short-lived attacks of recurrent midline cerebellar dysfunction and continuous motor activity. Mutations in KCN1A, the gene encoding Kv1.1, a voltage-gated neuronal potassium channel, are associated with the disorder. Although rare, the syndrome highlights the fundamental features of genetic ion-channel diseases and serves as a useful model for understanding more common paroxysmal disorders, such as epilepsy and migraine. This review examines our current understanding of episodic ataxia type 1, focusing on its clinical and genetic features, pathophysiology, and treatment.}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\TCNZXIXP\\Rajakulendran et al. - 2007 - Episodic ataxia type 1 A neuronal potassium chann.pdf:application/pdf}, + journal = {Neurotherapeutics}, + month = apr, + shorttitle = {Episodic ataxia type 1}, + year = {2007}, } -@misc{noauthor_rilutek_2018, - type = {Text}, - title = {Rilutek}, - url = {https://www.ema.europa.eu/en/medicines/human/EPAR/rilutek}, - abstract = {Rilutek}, - language = {en}, - urldate = {2021-07-28}, - journal = {European Medicines Agency}, - month = sep, - year = {2018}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\5QA4JVU2\\rilutek.html:text/html}, +@Article{ponce_expression_2018, + author = {Ponce, Arturo and Castillo, Aida and Hinojosa, Lorena and Martinez‐Rendon, Jacqueline and Cereijido, Marcelino}, + title = {The expression of endogenous voltage‐gated potassium channels in {HEK293} cells is affected by culture conditions}, + doi = {10.14814/phy2.13663}, + issn = {2051-817X}, + number = {8}, + pages = {e13663}, + url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5903699/}, + urldate = {2021-07-28}, + volume = {6}, + abstract = {HEK293 cells are widely used as a host for expression of heterologous proteins; yet, little care has been taken to characterize their endogenous membrane components, including ion channels. In this work, we aimed to describe the biophysical and pharmacological properties of endogenous, voltage‐dependent potassium currents (IKv). We also examined how its expression depends on culture conditions. We used the electrophysiological technique of whole‐cell patch clamp to record ion currents from HEK293 cells. We found that HEK cells express endogenous, voltage‐dependent potassium currents. We also found that diverse culture conditions, such as the passage number, the cell density, the type of serum that complements the culture media and the substratum, affect the magnitude and shape of IKv, resulting from the relative contribution of fast, slow, and noninactivating component currents. Incubation of cells in mature monolayers with trypsin–EDTA, notoriously reduces the magnitude and modifies the shape of voltage‐dependent potassium endogenous currents; nonetheless HEK cells recover IKv′s magnitude and shape within 6 h after replating, with a process that requires synthesis of new mRNA and protein subunits, as evidenced by the fact that actinomycin D and cycloheximide, inhibitors of synthesis of mRNA and protein, respectively, impair the recovery of IKv after trypsinization. In addition to be useful as a model expression system, HEK293 may be useful to understand how cells regulate the density of ion channels on the membrane.}, + file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3EW2NAWL\\Ponce et al. - 2018 - The expression of endogenous voltage‐gated potassi.pdf:application/pdf}, + journal = {Physiological Reports}, + month = apr, + pmcid = {PMC5903699}, + pmid = {29665277}, + year = {2018}, +} + +@Article{rutecki_neuronal_1992, + author = {Rutecki, P. A.}, + title = {Neuronal excitability: voltage-dependent currents and synaptic transmission}, + issn = {0736-0258}, + language = {eng}, + number = {2}, + pages = {195--211}, + volume = {9}, + abstract = {Neuronal membrane excitability and the synaptic connections among neurons produce behavior and cognition. The intracellular compartment of neurons is negatively charged relative to the extracellular space, and this charge, as well as current flow, is produced by ions. From the perspective of charged ions, the lipid bilayer of the neuronal membrane acts as a capacitor, and transmembrane glycoprotein pores or channels act as resistors. The open and closed states of ionic channels determine the membrane potential. At equilibrium, the lowest resistance or greatest permeability is for potassium, and the resting membrane potential is close to the equilibrium potential for potassium. When a channel is opened, permeable ions diffuse down their electrochemical gradients and the membrane potential is changed. Channels are gated (opened or closed) by voltage, neurotransmitters, and second messengers. The neuron integrates synaptic potentials produced by transmitter-gated channel activity and either generates a subthreshold potential, or a suprathreshold depolarization that generates an action potential or a burst of action potentials. Action potential generation is mediated by a large, brief sodium influx that is followed by activation of a voltage-dependent potassium eflux. The pattern of action potential firing is dependent on the interaction of a repertoire of voltage-dependent ion conductances. The action potential is the main signaling mechanism to activate synaptic transmission at axon terminals. Synaptic transmission is graded depending on the amount of calcium entering the presynaptic terminal. The number of action potentials, or the shape of the action potential, will determine the amount of calcium entering the terminal and the efficacy of synaptic transmission. Presynaptic ion channels may also be controlled by neurotransmitters or modulators and affect synaptic transmission by altering the amount of calcium influx.}, + journal = {Journal of Clinical Neurophysiology: Official Publication of the American Electroencephalographic Society}, + keywords = {Animals, Synapses, Membrane Potentials, Synaptic Transmission, Humans, Axons, Central Nervous System, Dendrites, Ion Channels, Neuromuscular Junction, Neurotransmitter Agents, Synaptic Membranes}, + month = apr, + shorttitle = {Neuronal excitability}, + year = {1992}, +} + +@Article{czitrom_one-factor-at--time_1999, + author = {Czitrom, Veronica}, + title = {One-{Factor}-at-a-{Time} versus {Designed} {Experiments}}, + doi = {10.2307/2685731}, + issn = {0003-1305}, + number = {2}, + pages = {126--131}, + url = {https://www.jstor.org/stable/2685731}, + urldate = {2021-06-02}, + volume = {53}, + abstract = {Many engineers and scientists perform one-factor-at-a-time (OFAT) experiments. They will continue to do so until they understand the advantages of designed experiments over OFAT experiments, and until they learn to recognize OFAT experiments so they can avoid them. A very effective way to illustrate the advantages of designed experiments, and to show ways in which OFAT experiments present themselves in real life, is to introduce real examples of OFAT experiments and then demonstrate why a designed experiment would have been better. Three engineering examples of OFAT experiments are presented, as well as designed experiments that would have been better. The three examples have been successfully used in an industrial workshop and can also be used in academic courses.}, + file = {Submitted Version:C\:\\Users\\nilsk\\Zotero\\storage\\GW8BJJXX\\Czitrom - 1999 - One-Factor-at-a-Time versus Designed Experiments.pdf:application/pdf}, + journal = {The American Statistician}, + year = {1999}, +} + +@Article{van_dyke_hereditary_1975, + author = {Van Dyke, D. H. and Griggs, R. C. and Murphy, M. J. and Goldstein, M. N.}, + title = {Hereditary myokymia and periodic ataxia}, + doi = {10.1016/0022-510X(75)90191-4}, + issn = {0022-510X}, + language = {en}, + number = {1}, + pages = {109--118}, + url = {https://www.sciencedirect.com/science/article/pii/0022510X75901914}, + urldate = {2021-06-10}, + volume = {25}, + abstract = {A kindred in which at least 11 individuals in 3 consecutive generations have continuous muscle movement, i.e., myokymia, and periodic ataxia, has been studied. Three patients, a 24-year-old woman, her 4-year-old son and her 27-year-old sister, have been studied in detail. The disorder is inherited as an autosomal-dominant trait and presents in early childhood with attacks of ataxia of 1–2 min in duration, with associated jerking movements of the head, arms and legs. Attacks are provoked by abrupt postural change, emotional stimulus, and caloric-vestibular stimulation. At the age of 12 years approximately, facial and extremity myokymia appears. Physical findings include large calves, normal muscle strength and widespread myokymia of face, hands, arms and legs with a hand posture resembling carpopedal spasm. EMG studies at rest showed continuous spontaneous activity of otherwise normal motor units. Nerve conduction velocities were normal. Gastrocnemius biopsy in 2 patients showed fiber type grouping and small angular fibers, and was consistent with denervation. Histographic analysis of the biopsies demonstrated enlargement of both fiber types, particularly of Type I fibers. These findings are consistent with chronic denervation and an abnormality of motor neuron population or firing. The myokymia described here is of interest not only because of its genetic association with a movement disorder, but also because the muscle findings support a peripheral basis for the muscle movements.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\GZD6WJU6\\Van Dyke et al. - 1975 - Hereditary myokymia and periodic ataxia.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\XQD53H6D\\0022510X75901914.html:text/html}, + journal = {Journal of the Neurological Sciences}, + month = may, + year = {1975}, } -@misc{merck_sharp__dohme_msd_nodate, - title = {{MSD} {Manual} {Professional} {Edition}}, - url = {https://www.msdmanuals.com/professional}, - abstract = {Now Free Online - The Professional Version of the MSD Manuals (known as the Merck Manuals in US \& Canada) is the global standard in medical reference for Doctors \& Students - since 1899.}, - language = {en}, - urldate = {2021-07-28}, - journal = {MSD Manual Professional Edition}, - author = {{Merck Sharp \& Dohme}}, - file = {Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\P2RCSDET\\professional.html:text/html}, + + + +@Article{ermentrout_type_1996, + author = {Ermentrout, Bard}, + title = {Type {I} {Membranes}, {Phase} {Resetting} {Curves}, and {Synchrony}}, + doi = {10.1162/neco.1996.8.5.979}, + issn = {0899-7667}, + note = {\_eprint: https://direct.mit.edu/neco/article-pdf/8/5/979/813352/neco.1996.8.5.979.pdf}, + number = {5}, + pages = {979--1001}, + url = {https://doi.org/10.1162/neco.1996.8.5.979}, + volume = {8}, + abstract = {Type I membrane oscillators such as the Connor model (Connor et al. 1977) and the Morris-Lecar model (Morris and Lecar 1981) admit very low frequency oscillations near the critical applied current. Hansel et al. (1995) have numerically shown that synchrony is difficult to achieve with these models and that the phase resetting curve is strictly positive. We use singular perturbation methods and averaging to show that this is a general property of Type I membrane models. We show in a limited sense that so called Type II resetting occurs with models that obtain rhythmicity via a Hopf bifurcation. We also show the differences between synapses that act rapidly and those that act slowly and derive a canonical form for the phase interactions.}, + journal = {Neural Computation}, + month = jul, + year = {1996}, +} + +@Article{tsaur_differential_1992, + author = {Tsaur, Meei-Ling and Sheng, Morgan and Lowenstein, Daniel H. and Jan, Yuh Nung and Jan, Lily Yeh}, + title = {Differential expression of {K}+ channel {mRNAs} in the rat brain and down-regulation in the hippocampus following seizures}, + doi = {10.1016/0896-6273(92)90127-Y}, + issn = {0896-6273}, + language = {en}, + number = {6}, + pages = {1055--1067}, + url = {https://www.sciencedirect.com/science/article/pii/089662739290127Y}, + urldate = {2021-06-12}, + volume = {8}, + abstract = {K+ channels are major determinants of membrane excitability. Differences in neuronal excitability within the nervous system may arise from differential expression of K+ channel genes, regulated spatially in a cell type-specific manner, or temporally in response to neuronal activity. We have compared the distribution of mRNAs of three K+ channel genes, Kv1.1, Kv1.2, and Kv4.2 in rat brain, and examined activity-dependent changes following treatment with the convulsant drug pentylenetetrazole. Both regional and cell type-specific differences of K+ channel gene expression were found. In addition, seizure activity caused a reduction of Kv1.2 and Kv4.2 mRNAs in the dentate granule cells of the hippocampus, raising the possibility that K+ channel gene regulation may play a role in long-term neuronal plasticity.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\AV3MLGZ2\\Tsaur et al. - 1992 - Differential expression of K+ channel mRNAs in the.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\BAQZSPTI\\089662739290127Y.html:text/html}, + journal = {Neuron}, + month = jun, + year = {1992}, +} + +@Article{veh_immunohistochemical_1995, + author = {Veh, Rüdiger W. and Lichtinghagen, Ralf and Sewing, Sabine and Wunder, Frank and Grumbach, Isabella M. and Pongs, Olaf}, + title = {Immunohistochemical {Localization} of {Five} {Members} of the {KV1} {Channel} {Subunits}: {Contrasting} {Subcellular} {Locations} and {Neuron}-specific {Co}-localizations in {Rat} {Brain}}, + doi = {10.1111/j.1460-9568.1995.tb00641.x}, + issn = {1460-9568}, + language = {en}, + number = {11}, + pages = {2189--2205}, + url = {https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1460-9568.1995.tb00641.x}, + urldate = {2021-06-10}, + volume = {7}, + abstract = {A large variety of potassium channels is involved in regulating integration and transmission of electrical signals in the nervous system. Different types of neurons, therefore, require specific patterns of potassium channel subunit expression and specific regulation of subunit coassembly into heteromultimeric channels, as well as subunit-specific sorting and segregation. This was investigated by studying in detail the expression of six different α-subunits of voltage-gated potassium channels in the rat hippocampus, cerebellum, olfactory bulb and spinal cord, combining in situ hybridization and immunocytochemistry. Specific polyclonal antibodies were prepared for five α-subunits (KV1.1, KV1.2, KV1.3, KV1.4, KV1.6) of the Shaker-related subfamily of rat Kv channels, which encode delayed-rectifier type and rapidly inactivating A-type potassium channels. Their distribution was compared to that of an A-type potassium channel (KV3.4), belonging to the Shaw-related subfamily of rat Kv channels. Our results show that these Kv channel α-subunits are differentially expressed in rat brain neurons. We did not observe in various neurons a stereotypical distribution of Kv channel α-subunits to dendritic and axonal compartments, but a complex differential subcellular subunit distribution. The different Kv channel subunits are targeted either to presynaptic or to postsynaptic domains, depending on neuronal cell type. Thus, distinct combinations of Kv1 α-subunits are co-localized in different neurons. The implications of these findings are that both differential expression and assembly as well as subcellular targeting of Kv channel α-subunits may contribute to Kv channel diversity and thereby to presynaptic and postsynaptic membrane excitability.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\FBDVD9YW\\Veh et al. - 1995 - Immunohistochemical Localization of Five Members o.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\2DYEMJUC\\Veh et al. - 1995 - Immunohistochemical Localization of Five Members o.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\TCXWZH3V\\j.1460-9568.1995.tb00641.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\CQNWEC4V\\j.1460-9568.1995.tb00641.html:text/html}, + journal = {European Journal of Neuroscience}, + keywords = {potassium channels, hybridization, in situ, rat brain}, + shorttitle = {Immunohistochemical {Localization} of {Five} {Members} of the {KV1} {Channel} {Subunits}}, + year = {1995}, +} + +@Article{brew_hyperexcitability_2003, + author = {Brew, Helen M. and Hallows, Janice L. and Tempel, Bruce L.}, + title = {Hyperexcitability and reduced low threshold potassium currents in auditory neurons of mice lacking the channel subunit {Kv1}.1}, + doi = {10.1111/j..2003.t01-1-00001.x}, + issn = {1469-7793}, + language = {en}, + number = {1}, + pages = {1--20}, + url = {https://physoc.onlinelibrary.wiley.com/doi/abs/10.1111/j..2003.t01-1-00001.x}, + urldate = {2021-06-14}, + volume = {548}, + abstract = {A low voltage-activated potassium current, IKL, is found in auditory neuron types that have low excitability and precisely preserve the temporal pattern of activity present in their presynaptic inputs. The gene Kcna1 codes for Kv1.1 potassium channel subunits, which combine in expression systems to produce channel tetramers with properties similar to those of IKL, including sensitivity to dendrotoxin (DTX). Kv1.1 is strongly expressed in neurons with IKL, including auditory neurons of the medial nucleus of the trapezoid body (MNTB). We therefore decided to investigate how the absence of Kv1.1 affected channel properties and function in MNTB neurons from mice lacking Kcna1. We used the whole cell version of the patch clamp technique to record from MNTB neurons in brainstem slices from Kcna1-null (−/−) mice and their wild-type (+/+) and heterozygous (+/−) littermates. There was an IKL in voltage-clamped −/− MNTB neurons, but it was about half the amplitude of the IKL in +/+ neurons, with otherwise similar properties. Consistent with this, −/− MNTB neurons were more excitable than their +/+ counterparts; they fired more than twice as many action potentials (APs) during current steps, and the threshold current amplitude required to generate an AP was roughly halved. +/− MNTB neurons had excitability and IKL amplitudes identical to the +/+ neurons. The IKL remaining in −/− neurons was blocked by DTX, suggesting the underlying channels contained subunits Kv1.2 and/or Kv1.6 (also DTX-sensitive). DTX increased excitability further in the already hyperexcitable −/− MNTB neurons, suggesting that −/−IKL limited excitability despite its reduced amplitude in the absence of Kv1.1 subunits.}, + copyright = {© 2003 The Journal of Physiology © 2003 The Physiological Society}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\KHZTN5RA\\Brew et al. - 2003 - Hyperexcitability and reduced low threshold potass.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\SRKME4BH\\j..2003.t01-1-00001.html:text/html}, + journal = {The Journal of Physiology}, + year = {2003}, +} + +@Article{isacoff_evidence_1990, + author = {Isacoff, Ehud Y. and Jan, Yuh Nung and Jan, Lily Yeh}, + title = {Evidence for the formation of heteromultimeric potassium channels in {Xenopus} oocytes}, + doi = {10.1038/345530a0}, + issn = {1476-4687}, + language = {en}, + number = {6275}, + pages = {530--534}, + url = {https://www.nature.com/articles/345530a0}, + urldate = {2021-06-12}, + volume = {345}, + abstract = {POTASSIUM channels show a wide range of functional diversity1–3. Nerve cells typically express a number of K+. channels that differ in their kinetics, single-channel conductance, pharmacology, and sensitivity to voltage and second messengers. The cloning of the Shaker gene in Drosophila4–7, and of related genes8–14, has revealed that the encoded K+ channel polypeptides resemble one of the four internally homologous domains of the α-subunits of Na+ channels and Ca2+ channels15–18, indicating that K+ channels may form by the co-assembly of several polypeptides. In this report we provide evidence that the Shaker A-type K+ channels expressed in Xenopus oocytes contain several Shaker polypeptides, that heteromultimeric channels may form through assembly of different channel polypeptides, that the kinetics or pharmacology of some heteromultimeric channels differ from those of homomultimeric channels, and that channel polypeptides from the fruit fly can co-assemble with homologous polypeptides from the rat. We suggest that heteromultimer formation may increase K+ channel diversity beyond even the level expected from the large number of K+ channel genes and alternative splicing products4,5,19–25.}, + copyright = {1990 Nature Publishing Group}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7W7QWWF8\\Isacoff et al. - 1990 - Evidence for the formation of heteromultimeric pot.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4S7NC3QA\\345530a0.html:text/html}, + journal = {Nature}, + month = jun, + year = {1990}, +} + +@Article{roeper_nip_1998, + author = {Roeper, Jochen and Sewing, Sabine and Zhang, Ying and Sommer, Tobias and Wanner, Siegmund G. and Pongs, Olaf}, + title = {{NIP} domain prevents {N}-type inactivation in voltage-gated potassium channels}, + doi = {10.1038/34916}, + issn = {1476-4687}, + language = {en}, + number = {6665}, + pages = {390--393}, + url = {https://www.nature.com/articles/34916}, + urldate = {2021-06-07}, + volume = {391}, + abstract = {Shaker-related voltage-gated K+ (Kv) channels1,2 are assembled from ion-conducting Kvα subunits, which are integral membrane proteins, and auxiliary Kvβ subunits. This leads to the formation of highly diverse heteromultimeric Kv channels that mediate outward currents with a wide range of time courses for inactivation. Two principal inactivation mechanisms have been recognized1: C-type inactivation correlated with carboxy-terminal Kvα-subunit structures3, and N-type inactivation conferred by ‘ball’ domains in the amino termini of certain Kvα4,5 and Kvβ6 subunits. Assembly of heteromultimers with one or more Kvα4,7- and/or Kvβ6 ball domains appears to be an essential principle of the generation of A-type Kv channel diversity. Here we show that, unexpectedly, the presence of Kvα- or Kvβ-ball domains does not dominate the gating phenotype in heteromultimers containing Kv1.6α subunits. These heteromultimers mediate non-inactivating currents because of the dominant-negative activity of a new type of N-type inactivation-prevention (NIP) domain present in the Kv1.6 amino terminus. Mutations in the NIP domain lead to loss of function, and its transfer to another Kvα subunit leads to gain of function. Our discovery of the NIP domain, which neutralizes the activity of Kvα- and Kvβ-inactivation gates, establishes a new determinant for the gating behaviour of heteromultimeric Kv channels.}, + copyright = {1998 Macmillan Magazines Ltd.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\BPJPQVJA\\Roeper et al. - 1998 - NIP domain prevents N-type inactivation in voltage.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8V4C3VA2\\34916.html:text/html}, + journal = {Nature}, + month = jan, + year = {1998}, +} + +@Article{ransdell_neurons_2013, + author = {Ransdell, Joseph L. and Nair, Satish S. and Schulz, David J.}, + title = {Neurons within the {Same} {Network} {Independently} {Achieve} {Conserved} {Output} by {Differentially} {Balancing} {Variable} {Conductance} {Magnitudes}}, + number = {24}, + pages = {9950--9956}, + volume = {33}, + file = {Neurons within the Same Network Independently Achieve Conserved Output by Differentially Balancing Variable Conductance Magnitudes | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\YM4JHXV4\\9950.html:text/html}, + journal = {Journal of Neuroscience}, + month = jun, + year = {2013}, +} + +@Article{zhang_specific_1999, + author = {Zhang, Chuan-Li and Messing, Albee and Chiu, Shing Yan}, + title = {Specific {Alteration} of {Spontaneous} {GABAergic} {Inhibition} in {Cerebellar} {Purkinje} {Cells} in {Mice} {Lacking} the {Potassium} {Channel} {Kv1}.1}, + doi = {10.1523/JNEUROSCI.19-08-02852.1999}, + issn = {0270-6474, 1529-2401}, + language = {en}, + number = {8}, + pages = {2852--2864}, + url = {https://www.jneurosci.org/content/19/8/2852}, + urldate = {2021-06-10}, + volume = {19}, + abstract = {In the cerebellum, the basket cell innervation on Purkinje cells provides a major GABAergic inhibitory control of the single efferent output from the cerebellum. The Shaker-type K channel Kv1.1 is localized at the axon arborization preceding the terminal of the basket cells and is therefore a potential candidate for regulating the GABAergic inhibition. In this study, we directly assess this role of Kv1.1 by electrophysiological analysis of Kv1.1 null mutant mice. Whole-cell patch-clamp recordings of spontaneous IPSCs (sIPSCs) were made from Purkinje cells in thin cerebellar slices from postnatal day (P)10–15 Kv1.1-null mutants using wild-type littermates as controls. The null mutation confers a very specific change in the sIPSC: the frequency increases about twofold, without accompanying changes in the mean and variance of its amplitude distribution. The frequency and amplitude of the miniature IPSCs (mIPSCs) are unaffected. Spontaneous firing rate of the basket cells is unaltered. Evoked IPSC does not show multiple activity in the mutants. Motor skills tests show that Kv1.1 null mice display a compromised ability to maintain balance on a thin stationary rod. We conclude that the Kv1.1 null mutation results in a persistent elevation of the tonic inhibitory tone on the cerebellum Purkinje cell efferent and that this is not fully compensated for by residual Shaker-type channels. We further suggest that the increase in inhibitory tone in the mutants might underlie the behavioral deficits. At the cellular level, we propose that Kv1.1 deletion enhances excitability of the basket cells by selectively enhancing the likelihood of action potential propagation past axonal branch points.}, + copyright = {Copyright © 1999 Society for Neuroscience}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\CAKAQZ6X\\Zhang et al. - 1999 - Specific Alteration of Spontaneous GABAergic Inhib.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\8MH5FK92\\2852.html:text/html}, + journal = {Journal of Neuroscience}, + keywords = {mouse, GABA, cerebellum, Purkinje cell, homologous recombination, potassium channel gene}, + month = apr, + year = {1999}, +} + +@Article{khaliq_relative_2006, + author = {Khaliq, Zayd M. and Raman, Indira M.}, + title = {Relative {Contributions} of {Axonal} and {Somatic} {Na} {Channels} to {Action} {Potential} {Initiation} in {Cerebellar} {Purkinje} {Neurons}}, + number = {7}, + pages = {1935--1944}, + volume = {26}, + file = {Relative Contributions of Axonal and Somatic Na Channels to Action Potential Initiation in Cerebellar Purkinje Neurons | Journal of Neuroscience:C\:\\Users\\nilsk\\Zotero\\storage\\A2ZU9LSD\\1935.html:text/html}, + journal = {Journal of Neuroscience}, + month = feb, + year = {2006}, +} + +@Article{otsuka_conductance-based_2004, + author = {Otsuka, Takeshi and Abe, Takafumi and Tsukagawa, Takahisa and Song, Wen-Jie}, + title = {Conductance-{Based} {Model} of the {Voltage}-{Dependent} {Generation} of a {Plateau} {Potential} in {Subthalamic} {Neurons}}, + doi = {10.1152/jn.00508.2003}, + issn = {0022-3077}, + number = {1}, + pages = {255--264}, + url = {https://journals.physiology.org/doi/full/10.1152/jn.00508.2003}, + urldate = {2021-03-31}, + volume = {92}, + abstract = {Because the subthalamic nucleus (STN) acts as a driving force of the basal ganglia, it is important to know how the activities of STN neurons are regulated. Previously, we have reported that a subset of STN neurons generates a plateau potential in a voltage-dependent manner. These plateau potentials can be evoked only when the cell is hyperpolarized. Here, to examine the mechanism of the voltage-dependent generation of the plateau potential in STN neurons, we constructed a conductance-based model of the plateau-generating STN neuron based on experimental observations and compared simulation results with recordings in slices. The model consists of a single compartment containing a Na+ current, a delayed-rectifier K+ current, an A-type K+ current, an L-like long-lasting Ca2+ current, a T-type Ca2+ current, a Ca2+-dependent K+ current, and a leak current. Our simulation results showed that a plateau potential in the model could be induced in a voltage-dependent manner that depended on the inactivation properties of L-like long-lasting Ca2+ current. The model could also reproduce the generation of a plateau potential as a rebound potential after termination of hyperpolarizing current injection. In addition, we tested the stability of simulated plateau potentials against inhibitory perturbation and found that the model showed similar properties observed for the plateau potentials of STN neurons in slices. The effects of K+ channel blockade by TEA and intracellular Ca2+ ion chelation by BAPTA on the plateau duration were also tested in the model and were found to match experimental observations. Thus our STN neuron model could qualitatively reproduce a number of experimental observations on plateau potentials. Our results suggest that the inactivation of L-type Ca2+ channels plays an important role in the voltage-dependent generation of the plateau potential.}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\YYMYAXMJ\\Otsuka et al. - 2004 - Conductance-Based Model of the Voltage-Dependent G.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\NIZRIRNC\\jn.00508.html:text/html}, + journal = {Journal of Neurophysiology}, + month = jul, + year = {2004}, +} + +@Article{zhou_temperature-sensitive_1998, + author = {Zhou, Lei and Zhang, Chuan-Li and Messing, Albee and Chiu, Shing Yan}, + title = {Temperature-{Sensitive} {Neuromuscular} {Transmission} in {Kv1}.1 {Null} {Mice}: {Role} of {Potassium} {Channels} under the {Myelin} {Sheath} in {Young} {Nerves}}, + doi = {10.1523/JNEUROSCI.18-18-07200.1998}, + issn = {0270-6474, 1529-2401}, + language = {en}, + number = {18}, + pages = {7200--7215}, + url = {https://www.jneurosci.org/content/18/18/7200}, + urldate = {2021-06-10}, + volume = {18}, + abstract = {In mammalian myelinated nerves, the internodal axon that is normally concealed by the myelin sheath expresses a rich repertoire of K channel subtypes thought to be important in modulating action potential propagation. The function of myelin-covered K channels at transition zones, however, has remained unexplored. Here we show that deleting the voltage-sensitive potassium channel Kv1.1 from mice confers a marked temperature-sensitivity to neuromuscular transmission in postnatal day 14 (P14)–P21 mice. Using immunofluorescence and electrophysiology, we examined contributions of four regions of the peripheral nervous system to the mutant phenotype: the nerve trunk, the myelinated segment preceding the terminal, the presynaptic terminal membrane itself, and the muscle. We conclude that the temperature-sensitive neuromuscular transmission is accounted for solely by a deficiency in Kv1.1 normally concealed in the myelinated segments just preceding the terminal. This paper demonstrates that under certain situations of physiological stress, the functional role of myelin-covered K channels is dramatically enhanced as the transition zone at the neuromuscular junction is approached.}, + copyright = {Copyright © 1998 Society for Neuroscience}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\SCRRDKGM\\Zhou et al. - 1998 - Temperature-Sensitive Neuromuscular Transmission i.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FQBN6Q2X\\7200.html:text/html}, + journal = {Journal of Neuroscience}, + keywords = {mouse, end plate, homologous recombination, myelinated nerves, nerve conduction, potassium channel gene}, + month = sep, + shorttitle = {Temperature-{Sensitive} {Neuromuscular} {Transmission} in {Kv1}.1 {Null} {Mice}}, + year = {1998}, +} + +@Article{xu_kv2_1997, + author = {Xu, Jia and Li, Min}, + title = {Kvβ2 {Inhibits} the {Kvβ1}-mediated {Inactivation} of {K}+ {Channels} in {Transfected} {Mammalian} {Cells}}, + doi = {10.1074/jbc.272.18.11728}, + issn = {0021-9258}, + language = {en}, + number = {18}, + pages = {11728--11735}, + url = {https://www.sciencedirect.com/science/article/pii/S0021925818405091}, + urldate = {2021-06-12}, + volume = {272}, + abstract = {Cloned auxiliary β-subunits (e.g.Kvβ1) modulate the kinetic properties of the pore-forming α-subunits of a subset of Shaker-like potassium channels. Coexpression of the α-subunit and Kvβ2, however, induces little change in channel properties. Since more than one β-subunit has been found in individual K+ channel complexes and expression patterns of different β-subunits overlap in vivo, it is important to test the possible physical and/or functional interaction(s) between different β-subunits. In this report, we show that both Kvβ2 and Kvβ1 recognize the same region on the pore-forming α-subunits of the Kv1 Shaker-like potassium channels. In the absence of α-subunits the Kvβ2 polypeptide interacts with additional β-subunit(s) to form either a homomultimer with Kvβ2 or a heteromultimer with Kvβ1. When coexpressing α-subunits and Kvβ1 in the presence of Kvβ2, we find that Kvβ2 is capable of inhibiting the Kvβ1-mediated inactivation. Using deletion analysis, we have localized the minimal interaction region that is sufficient for Kvβ2 to associate with both α-subunits and Kvβ1. This mapped minimal interaction region is necessary and sufficient for inhibiting the Kvβ1-mediated inactivation, consistent with the notion that the inhibitory activity of Kvβ2 results from the coassembly of Kvβ2 with compatible α-subunits and possibly with Kvβ1. Together, these results provide biochemical evidence that Kvβ2 may profoundly alter the inactivation activity of another β-subunit by either differential subunit assembly or by competing for binding sites on α-subunits, which indicates that Kvβ2 is capable of serving as an important determinant in regulating the kinetic properties of K+currents.}, + file = {ScienceDirect Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\RVNNHGE9\\Xu and Li - 1997 - Kvβ2 Inhibits the Kvβ1-mediated Inactivation of K+.pdf:application/pdf;ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\EG8EMIEK\\S0021925818405091.html:text/html}, + journal = {Journal of Biological Chemistry}, + month = may, + year = {1997}, } -@article{lehmann_modeling_2020, - title = {Modeling chemotherapy induced peripheral neuropathy ({CIPN}) in vitro: {Prospects} and limitations}, - volume = {326}, - issn = {0014-4886}, - shorttitle = {Modeling chemotherapy induced peripheral neuropathy ({CIPN}) in vitro}, - url = {https://www.sciencedirect.com/science/article/pii/S0014488619302870}, - doi = {10.1016/j.expneurol.2019.113140}, - abstract = {Neuronal cell cultures have been used as an essential tool for studying pathomechanisms of toxicity of chemotherapeutic drugs and to develop neuroprotective approaches. They offer the opportunity to dissect disease mechanisms and molecular pathways while allowing precise control of a variety of confounding factors of the physio-chemical environment. As such, a growing number of in vitro studies are published each year to decipher mechanisms of neurotoxicity of taxanes, vinca alcaloids, proteasome inhibitors and platin derivatives and/or to test neuroprotective strategies. Here, we provide a review of cell culture techniques and outcome measures that have been used in the past or are currently employed to model chemotherapy induced neuropathy in vitro. Furthermore, we discuss their advantages as well as their limitations and ways to enhance efficiency and reproducibility of cell culture studies in the field of toxic neuropathy.}, - language = {en}, - urldate = {2021-07-28}, - journal = {Experimental Neurology}, - author = {Lehmann, Helmar C. and Staff, Nathan P. and Hoke, Ahmet}, - month = apr, - year = {2020}, - keywords = {Cell culture conditions, Cell culture technique, CIPN, Dorsal root ganglion neuron, Neuronal cell culture, Neurotoxicology, Regeneration, Stem cell, Viability}, - pages = {113140}, - file = {ScienceDirect Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\CNF4A9I2\\S0014488619302870.html:text/html}, + +@Article{Gnecchi2021, + author = {Gnecchi, Massimiliano and Sala, Luca and Schwartz, Peter J}, + title = {Precision {Medicine} and cardiac channelopathies: when dreams meet reality}, + doi = {10.1093/eurheartj/ehab007}, + issn = {0195-668X}, + number = {17}, + pages = {1661--1675}, + url = {https://doi.org/10.1093/eurheartj/ehab007}, + urldate = {2022-03-06}, + volume = {42}, + abstract = {Precision Medicine (PM) is an innovative approach that, by relying on large populations’ datasets, patients’ genetics and characteristics, and advanced technologies, aims at improving risk stratification and at identifying patient-specific management through targeted diagnostic and therapeutic strategies. Cardiac channelopathies are being progressively involved in the evolution brought by PM and some of them are benefiting from these novel approaches, especially the long QT syndrome. Here, we have explored the main layers that should be considered when developing a PM approach for cardiac channelopathies, with a focus on modern in vitro strategies based on patient-specific human-induced pluripotent stem cells and on in silico models. PM is where scientists and clinicians must meet and integrate their expertise to improve medical care in an innovative way but without losing common sense. We have indeed tried to provide the cardiologist’s point of view by comparing state-of-the-art techniques and approaches, including revolutionary discoveries, to current practice. This point matters because the new approaches may, or may not, exceed the efficacy and safety of established therapies. Thus, our own eagerness to implement the most recent translational strategies for cardiac channelopathies must be tempered by an objective assessment to verify whether the PM approaches are indeed making a difference for the patients. We believe that PM may shape the diagnosis and treatment of cardiac channelopathies for years to come. Nonetheless, its potential superiority over standard therapies should be constantly monitored and assessed before translating intellectually rewarding new discoveries into clinical practice.}, + file = {:Gnecchi2021 - Precision Medicine and Cardiac Channelopathies_ When Dreams Meet Reality.pdf:PDF}, + groups = {Jan}, + journal = {European Heart Journal}, + month = may, + shorttitle = {Precision {Medicine} and cardiac channelopathies}, + year = {2021}, } -@article{ponce_expression_2018, - title = {The expression of endogenous voltage‐gated potassium channels in {HEK293} cells is affected by culture conditions}, - volume = {6}, - issn = {2051-817X}, - url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5903699/}, - doi = {10.14814/phy2.13663}, - abstract = {HEK293 cells are widely used as a host for expression of heterologous proteins; yet, little care has been taken to characterize their endogenous membrane components, including ion channels. In this work, we aimed to describe the biophysical and pharmacological properties of endogenous, voltage‐dependent potassium currents (IKv). We also examined how its expression depends on culture conditions. We used the electrophysiological technique of whole‐cell patch clamp to record ion currents from HEK293 cells. We found that HEK cells express endogenous, voltage‐dependent potassium currents. We also found that diverse culture conditions, such as the passage number, the cell density, the type of serum that complements the culture media and the substratum, affect the magnitude and shape of IKv, resulting from the relative contribution of fast, slow, and noninactivating component currents. Incubation of cells in mature monolayers with trypsin–EDTA, notoriously reduces the magnitude and modifies the shape of voltage‐dependent potassium endogenous currents; nonetheless HEK cells recover IKv′s magnitude and shape within 6 h after replating, with a process that requires synthesis of new mRNA and protein subunits, as evidenced by the fact that actinomycin D and cycloheximide, inhibitors of synthesis of mRNA and protein, respectively, impair the recovery of IKv after trypsinization. In addition to be useful as a model expression system, HEK293 may be useful to understand how cells regulate the density of ion channels on the membrane.}, - number = {8}, - urldate = {2021-07-28}, - journal = {Physiological Reports}, - author = {Ponce, Arturo and Castillo, Aida and Hinojosa, Lorena and Martinez‐Rendon, Jacqueline and Cereijido, Marcelino}, - month = apr, - year = {2018}, - pmid = {29665277}, - pmcid = {PMC5903699}, - pages = {e13663}, - file = {PubMed Central Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\3EW2NAWL\\Ponce et al. - 2018 - The expression of endogenous voltage‐gated potassi.pdf:application/pdf}, + + + +@Article{ERMENTROUT2002, + author = {G.Bard Ermentrout and Carson C. Chow}, + title = {Modeling neural oscillations}, + doi = {https://doi.org/10.1016/S0031-9384(02)00898-3}, + issn = {0031-9384}, + number = {4}, + pages = {629-633}, + url = {https://www.sciencedirect.com/science/article/pii/S0031938402008983}, + volume = {77}, + abstract = {A brief review of oscillatory activity in neurons and networks is given. Conditions required for neural oscillations are provided. Three mathematical methods for studying the coupling between neural oscillators are described: (i) weak coupling, (ii) firing time maps, and (iii) leaky integrate-and-fire methods. Several applications from macroscopic motor behavior to slice phenomena are provided.}, + journal = {Physiology \& Behavior}, + keywords = {Neural oscillators, Synchronization, Mathematical models}, + year = {2002}, +} + +@Article{verma_computational_2020, + author = {Verma, Parul and Kienle, Achim and Flockerzi, Dietrich and Ramkrishna, Doraiswami}, + title = {Computational analysis of a {9D} model for a small {DRG} neuron}, + doi = {10.1007/s10827-020-00761-6}, + issn = {1573-6873}, + language = {en}, + number = {4}, + pages = {429--444}, + url = {https://doi.org/10.1007/s10827-020-00761-6}, + urldate = {2021-06-17}, + volume = {48}, + abstract = {Small dorsal root ganglion (DRG) neurons are primary nociceptors which are responsible for sensing pain. Elucidation of their dynamics is essential for understanding and controlling pain. To this end, we present a numerical bifurcation analysis of a small DRG neuron model in this paper. The model is of Hodgkin-Huxley type and has 9 state variables. It consists of a Nav1.7 and a Nav1.8 sodium channel, a leak channel, a delayed rectifier potassium, and an A-type transient potassium channel. The dynamics of this model strongly depend on the maximal conductances of the voltage-gated ion channels and the external current, which can be adjusted experimentally. We show that the neuron dynamics are most sensitive to the Nav1.8 channel maximal conductance (\${\textbackslash}overline \{g\}\_\{1.8\}\$). Numerical bifurcation analysis shows that depending on \${\textbackslash}overline \{g\}\_\{1.8\}\$and the external current, different parameter regions can be identified with stable steady states, periodic firing of action potentials, mixed-mode oscillations (MMOs), and bistability between stable steady states and stable periodic firing of action potentials. We illustrate and discuss the transitions between these different regimes. We further analyze the behavior of MMOs. As the external current is decreased, we find that MMOs appear after a cyclic limit point. Within this region, bifurcation analysis shows a sequence of isolated periodic solution branches with one large action potential and a number of small amplitude peaks per period. For decreasing external current, the number of small amplitude peaks is increasing and the distance between the large amplitude action potentials is growing, finally tending to infinity and thereby leading to a stable steady state. A closer inspection reveals more complex concatenated MMOs in between these periodic MMO branches, forming Farey sequences. Lastly, we also find small solution windows with aperiodic oscillations which seem to be chaotic. The dynamical patterns found here—as consequences of bifurcation points regulated by different parameters—have potential translational significance as repetitive firing of action potentials imply pain of some form and intensity; manipulating these patterns by regulating the different parameters could aid in investigating pain dynamics.}, + file = {Springer Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\8VBIHVFQ\\Verma et al. - 2020 - Computational analysis of a 9D model for a small D.pdf:application/pdf}, + journal = {Journal of Computational Neuroscience}, + month = nov, + year = {2020}, } -@article{lauxmann_therapeutic_2021, - title = {Therapeutic potential of sodium channel blockers as targeted therapy approach in {KCNA1}-associated episodic ataxia ({EA1}) and a comprehensive review of the literature}, - volume = {In Press}, - issn = {1664-2295}, - url = {https://www.frontiersin.org/articles/10.3389/fneur.2021.703970/abstract}, - doi = {10.3389/fneur.2021.703970}, - abstract = {Among genetic paroxysmal movement disorders, variants in ion channel coding genes constitute a major subgroup. Loss-of-function (LOF) variants in KCNA1, the coding gene for KV1.1 channels, are associated with episodic ataxia type 1 (EA1), characterized by seconds to minutes-lasting attacks including gait incoordination, limb ataxia, truncal instability, dysarthria, nystagmus, tremor, occasionally seizures, but also persistent neuromuscular symptoms like myokymia or neuromyotonia. Standard treatment has not been developed yet and different treatment efforts need to be systematically evaluated. Personalized therapeutic regimens tailored to disease-causing pathophysiological mechanisms may offer the specificity required to overcome limitations in therapy. Toward this aim, we (i) reviewed all available clinical reports on treatment response and functional consequences of KCNA1 variants causing EA1, (ii) examined the potential effects on neuronal excitability of all variants using a predictive scoring system for ion channel variants based on single compartment conductance-based models, (iii) set out to assess a variety of SCBs (Phenytoin, lamotrigine, carbamazepine, and riluzole) regarding their potential to restore the identified underlying pathophysiological mechanisms of KV1.1 channels and (iv) provide a comprehensive review of the literature considering all types of episodic ataxia. Reviewing the treatment efforts of EA1 patients revealed moderate response to acetazolamide and exhibited the strength of sodium channel blockers (SCBs) in the treatment of EA1 patients. Biophysical dysfunction of Kv1.1 channels is typically based on depolarizing shifts of steady-state activation, leading to a loss-of-function of KCNA1 variant channels. Our model predicts a broadening of the action potentials, a lowered rheobase to more hyperpolarized potentials and an increase of the firing rate. Predicted effects of phenytoin, carbamazepine and riluzole could partially restore the altered gating properties of dysfunctional variant channels. These data strengthen the great potential of SCBs by contributing to functional compensation of dysfunctional Kv1.1 channels, propose riluzole as a new drug repurposing candidate and highlight the role of personalized approaches to develop standard care for EA1 patients. These results could have implications for clinical practice in future and highlight the need for the development of individualized and targeted therapies for episodic ataxia and genetic paroxysmal disorders in general.}, - language = {English}, - urldate = {2021-07-28}, - journal = {Frontiers in Neurology}, - author = {Lauxmann, Stephan and Sonnenberg, Lukas and Koch, Nils A. and Boßelmann, Christian Malte and Winter, Natalie and Schwarz, Niklas and Wuttke, Thomas Volkmar and Hedrich, Ulrike B. S. and Liu, Yuanyuan and Lerche, Holger and Benda, Jan and Kegele, Josua}, - year = {2021}, - keywords = {conduction-based model, episodic ataxia, Kcna1, KV1.1, Paroxysmal movement disorders, precision medicine, Riluzole, Sodium Channel Blockers, Voltage-gated potassium channels}, + + +@Article{Musto2020, + author = {Musto, Elisa and Gardella, Elena and Møller, Rikke S.}, + title = {Recent advances in treatment of epilepsy-related sodium channelopathies}, + doi = {10.1016/j.ejpn.2019.12.009}, + issn = {1090-3798}, + language = {en}, + pages = {123--128}, + series = {Epilepsy \& {Neurodevelopmental} {Disorders}}, + url = {https://www.sciencedirect.com/science/article/pii/S1090379819304295}, + urldate = {2022-03-03}, + volume = {24}, + abstract = {Voltage-gated sodium channels (VGSCs) play a crucial role in generation of action potentials. Pathogenic variants in the five human brain expressed VGSC genes, SCN1A, SCN2A, SCN3A, SCN8A and SCN1B have been associated with a spectrum of epilepsy phenotypes and neurodevelopmental disorders. In the last decade, next generation sequencing techniques have revolutionized the way we diagnose these channelopathies, which is paving the way towards precision medicine. Knowing the functional effect (Loss-of-function versus Gain-of-function) of a variant is not only important for understanding the underlying pathophysiology, but it is particularly crucial to orient therapeutic decisions. Here we provide a review of the literature dealing with treatment options in epilepsy-related sodium channelopathies, including the current and emerging medications.}, + file = {ScienceDirect Full Text PDF:https\://www.sciencedirect.com/science/article/pii/S1090379819304295/pdfft?md5=b62b2d62314c96f68a012a8a5c17a268&pid=1-s2.0-S1090379819304295-main.pdf&isDTMRedir=Y:application/pdf}, + groups = {Jan}, + journal = {European Journal of Paediatric Neurology}, + keywords = {Epilepsy, SCN1A, SCN2A, SCN8A, SCN1B}, + month = jan, + year = {2020}, } -@article{johannesen_genotype-phenotype_2021, - title = {Genotype-phenotype correlations in {SCN8A}-related disorders reveal prognostic and therapeutic implications}, - copyright = {© 2021, Posted by Cold Spring Harbor Laboratory. This pre-print is available under a Creative Commons License (Attribution-NoDerivs 4.0 International), CC BY-ND 4.0, as described at http://creativecommons.org/licenses/by-nd/4.0/}, - url = {https://www.medrxiv.org/content/10.1101/2021.03.22.21253711v1}, - doi = {10.1101/2021.03.22.21253711}, - abstract = {{\textless}h3{\textgreater}Abstract{\textless}/h3{\textgreater} {\textless}p{\textgreater}We report detailed functional analyses and genotype-phenotype correlations in 433 individuals carrying disease-causing variants in \textit{SCN8A}, encoding the voltage-gated Na$^{\textrm{+}}$ channel Na$_{\textrm{V}}$1.6. Five different clinical subgroups could be identified: 1) Benign familial infantile epilepsy (BFIE) (n=17, normal cognition, treatable seizures), 2) intermediate epilepsy (n=36, mild ID, partially pharmacoresponsive), 3) developmental and epileptic encephalopathy (DEE, n=191, severe ID, majority pharmacoresistant), 4) generalized epilepsy (n=21, mild to moderate ID, frequently with absence seizures), and 5) affected individuals without epilepsy (n=25, mild to moderate ID). Groups 1-3 presented with early-onset (median: four months) focal or multifocal seizures and epileptic discharges, whereas the onset of seizures in group 4 was later (median: 39 months) with generalized epileptic discharges. The epilepsy was not classifiable in 143 individuals. We performed functional studies expressing missense variants in ND7/23 neuroblastoma cells and primary neuronal cultures using recombinant tetrodotoxin insensitive human Na$_{\textrm{V}}$1.6 channels and whole-cell patch clamping. Two variants causing DEE showed a strong gain-of-function (GOF, hyperpolarising shift of steady-state activation, strongly increased neuronal firing rate), and one variant causing BFIE or intermediate epilepsy showed a mild GOF (defective fast inactivation, less increased firing). In contrast, all three variants causing generalized epilepsy induced a loss-of-function (LOF, reduced current amplitudes, depolarising shift of steady-state activation, reduced neuronal firing). Including previous studies, functional effects were known for 165 individuals. All 133 individuals carrying GOF variants had either focal (76, groups 1-3), or unclassifiable epilepsy (37), whereas 32 with LOF variants had either generalized (14), no (11) or unclassifiable (5) epilepsy; only two had DEE. Computational modeling in the GOF group revealed a significant correlation between the severity of the electrophysiological and clinical phenotypes. GOF variant carriers responded significantly better to sodium channel blockers (SCBs) than to other anti-seizure medications, and the same applied for all individuals of groups 1-3.{\textless}/p{\textgreater}{\textless}p{\textgreater}In conclusion, our data reveal clear genotype-phenotype correlations between age at seizure onset, type of epilepsy and gain- or loss-of-function effects of \textit{SCN8A} variants. Generalized epilepsy with absence seizures is the main epilepsy phenotype of LOF variant carriers and the extent of the electrophysiological dysfunction of the GOF variants is a main determinant of the severity of the clinical phenotype in focal epilepsies. Our pharmacological data indicate that SCBs present a therapeutic treatment option in early onset \textit{SCN8A}-related focal epilepsy.{\textless}/p{\textgreater}}, - language = {en}, - urldate = {2021-07-29}, - journal = {medRxiv}, - author = {Johannesen, Katrine M. and Liu, Yuanyuan and Gjerulfsen, Cathrine E. and Koko, Mahmoud and Sonnenberg, Lukas and Schubert, Julian and Fenger, Christina D. and Eltokhi, Ahmed and Rannap, Maert and Koch, Nils A. and Lauxmann, Stephan and Krüger, Johanna and Kegele, Josua and Canafoglia, Laura and Franceschetti, Silvana and Mayer, Thomas and Rebstock, Johannes and Zacher, Pia and Ruf, Susanne and Alber, Michael and Sterbova, Katalin and Lassuthová, Petra and Vlckova, Marketa and Lemke, Johannes R. and Krey, Ilona and Heine, Constanze and Wieczorek, Dagmar and Kroell-Seger, Judith and Lund, Caroline and Klein, Karl Martin and Au, PY Billie and Rho, Jong M. and Ho, Alice W. and Masnada, Silvia and Veggiotti, Pierangelo and Giordano, Lucio and Accorsi, Patrizia and Hoei-Hansen, Christina E. and Striano, Pasquale and Zara, Federico and Verhelst, Helene and S.Verhoeven, Judith and Zwaag, Bert van der and Harder, Aster V. E. and Brilstra, Eva and Pendziwiat, Manuela and Lebon, Sebastian and Vaccarezza, Maria and Le, Ngoc Minh and Christensen, Jakob and Schmidt-Petersen, Mette U. and Grønborg, Sabine and Scherer, Stephen W. and Howe, Jennifer and Fazeli, Walid and Howell, Katherine B. and Leventer, Richard and Stutterd, Chloe and Walsh, Sonja and Gerard, Marion and Gerard, Bénédicte and Matricardi, Sara and Bonardi, Claudia M. and Sartori, Stefano and Berger, Andrea and Hoffman-Zacharska, Dorota and Mastrangelo, Massimo and Darra, Francesca and Vøllo, Arve and Motazacker, M. Mahdi and Lakeman, Phillis and Nizon, Mathilde and Betzler, Cornelia and Altuzarra, Cecilia and Caume, Roseline and Roubertie, Agathe and Gélisse, Philippe and Marini, Carla and Guerrini, Renzo and Bilan, Frederic and Tibussek, Daniel and Koch-Hogrebe, Margarete and Perry, M. Scott and Ichikawa, Shoji and Dadali, Elena and Sharkov, Artem and Mishina, Irina and Abramov, Mikhail and Kanivets, Ilya and Korostelev, Sergey and Kutsev, Sergey and Wain, Karen E. and Eisenhauer, Nancy and Wagner, Monisa and Savatt, Juliann M. and Müller-Schlüter, Karen and Bassan, Haim and Borovikov, Artem and Nassogne, Marie-Cecile and Destrée, Anne and Schoonjans, An-Sofie and Meuwissen, Marije and Buzatu, Marga and Jansen, Anna and Scalais, Emmanuel and Srivastava, Siddharth and Tan, Wen-Hann and Olson, Heather E. and Loddenkemper, Tobias and Poduri, Annapurna and Helbig, Katherine L. and Helbig, Ingo and Fitzgerald, Mark P. and Goldberg, Ethan M. and Roser, Timo and Borggraefe, Ingo and Brünger, Tobias and May, Patrick and Lal, Dennis and Lederer, Damien and Rubboli, Guido and Lesca, Gaetan and Hedrich, Ulrike BS and Benda, Jan and Gardella, Elena and Lerche, Holger and Møller, Rikke S.}, - month = mar, - year = {2021}, - pages = {2021.03.22.21253711}, - file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\473Q4W4Z\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\I4ATHYDV\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\5BLXZ69T\\Johannesen et al. - 2021 - Genotype-phenotype correlations in SCN8A-related d.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\4UWL4V5H\\2021.03.22.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\E7KCJBEZ\\2021.03.22.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\FS6JAG82\\2021.03.22.html:text/html}, +@Article{zhao_common_2020, + author = {Zhao, Juan and Petitjean, Dimitri and Haddad, Georges A. and Batulan, Zarah and Blunck, Rikard}, + title = {A {Common} {Kinetic} {Property} of {Mutations} {Linked} to {Episodic} {Ataxia} {Type} 1 {Studied} in the {Shaker} {Kv} {Channel}}, + doi = {10.3390/ijms21207602}, + language = {en}, + number = {20}, + pages = {7602}, + url = {https://www.mdpi.com/1422-0067/21/20/7602}, + urldate = {2021-06-10}, + volume = {21}, + abstract = {(1) Background: Episodic ataxia type 1 is caused by mutations in the KCNA1 gene encoding for the voltage-gated potassium channel Kv1.1. There have been many mutations in Kv1.1 linked to episodic ataxia reported and typically investigated by themselves or in small groups. The aim of this article is to determine whether we can define a functional parameter common to all Kv1.1 mutants that have been linked to episodic ataxia. (2) Methods: We introduced the disease mutations linked to episodic ataxia in the drosophila analog of Kv1.1, the Shaker Kv channel, and expressed the channels in Xenopus oocytes. Using the cut-open oocyte technique, we characterized the gating and ionic currents. (3) Results: We found that the episodic ataxia mutations variably altered the different gating mechanisms described for Kv channels. The common characteristic was a conductance voltage relationship and inactivation shifted to less polarized potentials. (4) Conclusions: We suggest that a combination of a prolonged action potential and slowed and incomplete inactivation leads to development of ataxia when Kv channels cannot follow or adapt to high firing rates.}, + copyright = {http://creativecommons.org/licenses/by/3.0/}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\A2Q2B2UZ\\Zhao et al. - 2020 - A Common Kinetic Property of Mutations Linked to E.pdf:application/pdf;Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\7DVZLKI7\\Zhao et al. - 2020 - A Common Kinetic Property of Mutations Linked to E.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\2EXHPJBW\\7602.html:text/html;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\V8EV5IKK\\7602.html:text/html}, + journal = {International Journal of Molecular Sciences}, + keywords = {electrophysiology, episodic ataxia, gating, voltage-gated potassium channel}, + month = jan, + year = {2020}, +} + +@Article{manganas_identification_2001, + author = {Manganas, Louis N. and Wang, Qiang and Scannevin, Robert H. and Antonucci, Dana E. and Rhodes, Kenneth J. and Trimmer, James S.}, + title = {Identification of a trafficking determinant localized to the {Kv1} potassium channel pore}, + doi = {10.1073/pnas.241403898}, + issn = {0027-8424, 1091-6490}, + language = {en}, + number = {24}, + pages = {14055--14059}, + url = {https://www.pnas.org/content/98/24/14055}, + urldate = {2021-06-12}, + volume = {98}, + abstract = {The repertoire of Kv1 potassium channels expressed in presynaptic terminals of mammalian central neurons is shaped by intrinsic trafficking signals that determine surface-expression efficiencies of homomeric and heteromeric Kv1 channel complexes. Here, we show that a determinant controlling surface expression of Kv1 channels is localized to the highly conserved pore region. Point-mutation analysis revealed two residues as critical for channel trafficking, one in the extracellular “turret” domain and one in the region distal to the selectivity filter. Interestingly, these same residues also form the binding sites for polypeptide neurotoxins. Our findings demonstrate a previously uncharacterized function for the channel-pore domain as a regulator of channel trafficking.}, + copyright = {Copyright © 2001, The National Academy of Sciences}, + file = {Full Text PDF:C\:\\Users\\nilsk\\Zotero\\storage\\USC4WDPI\\Manganas et al. - 2001 - Identification of a trafficking determinant locali.pdf:application/pdf;Snapshot:C\:\\Users\\nilsk\\Zotero\\storage\\9M7UBRBX\\14055.html:text/html}, + journal = {Proceedings of the National Academy of Sciences}, + month = nov, + year = {2001}, }

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