updated spacing in Fig 1 and section numbering in diff tex file

Figures/diversity_in_firing.py

@@ -100,7 +100,7 @@ def plot_spike_train(ax, model='RS Pyramidal', stop=750):
     ax.set_xlabel('Time [s]')
     ax.set_ylim(-85, 60)
     ax.axis('off')
-    ax.set_title(model, fontsize=7)
+    ax.set_title(model, fontsize=7, y=1.1)
 
 
 def plot_fI(ax, model='RS Pyramidal'):
@@ -254,7 +254,7 @@ add_scalebar(ax12_spikes, matchx=False, matchy=False, hidex=True, hidey=True, si
 # add subplot labels
 for i in range(0,len(models)):
     # spike_axs[i].text(-0.18, 1.08, string.ascii_uppercase[i], transform=spike_axs[i].transAxes, size=10, weight='bold')
-    spike_axs[i].text(-0.572, 1.2, string.ascii_uppercase[i], transform=spike_axs[i].transAxes, size=10, weight='bold')
+    spike_axs[i].text(-0.572, 1.3, string.ascii_uppercase[i], transform=spike_axs[i].transAxes, size=10, weight='bold')
 # save
 fig.set_size_inches(cm2inch(21,15))
 fig.savefig('./Figures/diversity_in_firing_diagram.jpg', dpi=300, bbox_inches='tight') #pdf # eps

Frontiers_manuscript/For_Submission/Koch_frontiers_diff.tex

@@ -1,7 +1,7 @@
 \documentclass[utf8]{FrontiersinHarvard} 
 %DIF LATEXDIFF DIFFERENCE FILE
 %DIF DEL Koch_Frontiers.tex           Mon Mar 27 10:08:50 2023
-%DIF ADD Koch_Frontiers_revised.tex   Mon Apr 24 18:53:51 2023
+%DIF ADD Koch_Frontiers_revised.tex   Tue Apr 25 10:43:03 2023
 \DeclareUnicodeCharacter{03B2}{\(\beta\)}
 \DeclareUnicodeCharacter{03B1}{\(\alpha\)}
 \DeclareUnicodeCharacter{00C5}{\AA}
@@ -113,6 +113,7 @@ $^{3}$Department of Neurology and Epileptology, Hertie Institute for Clinical Br
 \end{abstract}
 \DIFaddbegin 
 
+\setcounter{section}{0}
 \DIFaddend \section{Introduction}
 The properties and combinations of voltage-gated ion channels are vital in determining neuronal excitability \citep{bernard_channelopathies_2008, carbone_ion_2020, rutecki_neuronal_1992, pospischil_minimal_2008}. However, ion channel function can be disturbed, for instance through genetic alterations, resulting in altered neuronal firing behavior \citep{carbone_ion_2020}. In recent years, next generation sequencing has led to an increase in the discovery of clinically relevant ion channel mutations and has provided the basis for pathophysiological studies of genetic epilepsies, pain disorders, dyskinesias, intellectual disabilities, myotonias, and periodic paralyses \citep{bernard_channelopathies_2008, carbone_ion_2020}.
 Ongoing efforts of many research groups have contributed to the current understanding of underlying disease mechanism in channelopathies. However, a complex pathophysiological landscape has emerged for many channelopathies and is likely a reason for limited therapeutic success with standard care.              

Frontiers_manuscript/For_Submission/Koch_frontiers_revised.tex

@@ -66,6 +66,7 @@ $^{3}$Department of Neurology and Epileptology, Hertie Institute for Clinical Br
  \keyFont{ \section{Keywords:} Channelopathy, Epilepsy, Ataxia, Potassium Current, Neuronal Simulations, Conductance-based Models, Neuronal heterogeneity } 
 \end{abstract}
 
+\setcounter{section}{0}
 \section{Introduction}
 The properties and combinations of voltage-gated ion channels are vital in determining neuronal excitability \citep{bernard_channelopathies_2008, carbone_ion_2020, rutecki_neuronal_1992, pospischil_minimal_2008}. However, ion channel function can be disturbed, for instance through genetic alterations, resulting in altered neuronal firing behavior \citep{carbone_ion_2020}. In recent years, next generation sequencing has led to an increase in the discovery of clinically relevant ion channel mutations and has provided the basis for pathophysiological studies of genetic epilepsies, pain disorders, dyskinesias, intellectual disabilities, myotonias, and periodic paralyses \citep{bernard_channelopathies_2008, carbone_ion_2020}.
 Ongoing efforts of many research groups have contributed to the current understanding of underlying disease mechanism in channelopathies. However, a complex pathophysiological landscape has emerged for many channelopathies and is likely a reason for limited therapeutic success with standard care.              
@@ -80,7 +81,7 @@ In this study, we therefore investigated how the outcome of ionic current kineti
 
 \section{Material and Methods}
 All modelling and simulation was done in parallel with custom written Python 3.8  (Python Programming Language; RRID:SCR\_008394) software, run on a Cent-OS 7 server with an Intel(R) Xeon (R) E5-2630 v2 CPU.
-    
+
 \subsection{Different Neuron Models}
 A set of single-compartment, conductance-based neuronal models representing the major classes of cortical and thalamic neurons including regular spiking pyramidal (RS pyramidal; model D), regular spiking inhibitory (RS inhibitory; model B), and fast spiking (FS; model C) neurons were used \citep{pospischil_minimal_2008}. Additionally,  a \Kv current (\IKv; \citealt{ranjan_kinetic_2019}) was added to each of these models (RS pyramidal +\Kv; model H, RS inhibitory +\Kv; model E, and FS +\Kv; model G respectively). A cerebellar stellate cell model from \citet{alexander_cerebellar_2019} is used (Cb stellate; model A) in this study. This neuron model was also extended by a \Kv current \citep{ranjan_kinetic_2019}, either in addition to the A-type potassium current (Cb stellate +\Kv; model F) or by replacing the A-type potassium current (Cb stellate \(\Delta\)\Kv; model J). A subthalamic nucleus (STN; model L) neuron model as described by \citet{otsuka_conductance-based_2004} was also used. The STN neuron model (model L) was  additionally extended by a \Kv current \citep{ranjan_kinetic_2019}, either in addition to the A-type potassium current (STN +\Kv; model I) or by replacing the A-type potassium current (STN \(\Delta\)\Kv; model K). Model letter naming corresponds to panel lettering in Figure \ref{fig:diversity_in_firing}. The anatomical origin of each model is shown in Figure \ref{fig:diversity_in_firing}~M. The properties and maximal conductances of each model are detailed in Table \ref{tab:g} and depicted in Figure \ref{fig:model_g}. The gating properties are unaltered from the original Cb stellate (model A)  and STN (model L) models \citep{alexander_cerebellar_2019, otsuka_conductance-based_2004}. For enabling the comparison of models with the typically reported electrophysiological data fitting reported and for ease of further gating curve manipulations, a modified Boltzmann function
 \begin{equation}\label{eqn:Boltz}