Action potential-evoked Na+ influx are similar in axon and soma (Fleidervish et al. 2010)

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"In cortical pyramidal neurons, the axon initial segment (AIS) is pivotal in synaptic integration. It has been asserted that this is because there is a high density of Na+ channels in the AIS. However, we found that action potential-associated Na+ flux, as measured by high-speed fluorescence Na+ imaging, was about threefold larger in the rat AIS than in the soma. Spike-evoked Na+ flux in the AIS and the first node of Ranvier was similar and was eightfold lower in basal dendrites. ... In computer simulations, these data were consistent with the known features of action potential generation in these neurons."
1 . Fleidervish IA, Lasser-Ross N, Gutnick MJ, Ross WN (2010) Na+ imaging reveals little difference in action potential-evoked Na+ influx between axon and soma. Nat Neurosci 13:852-60 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Neocortex;
Cell Type(s): Neocortex L5/6 pyramidal GLU cell; Neocortex L2/3 pyramidal GLU cell;
Channel(s): I Na,t; I K;
Gap Junctions:
Simulation Environment: NEURON;
Model Concept(s): Simplified Models; Active Dendrites; Action Potentials;
Implementer(s): Fleidervish, Ilya [ilya.fleidervish at];
Search NeuronDB for information about:  Neocortex L5/6 pyramidal GLU cell; Neocortex L2/3 pyramidal GLU cell; I Na,t; I K;
This is the readme for the model for the paper

Fleidervish IA, Lasser-Ross N, Gutnick MJ, Ross WN (2010) Na+ imaging
reveals little difference in action potential-evoked Na+ influx
between axon and soma. Nat Neurosci 13:852-60

These NEURON model files were contributed by Ilya Fleidervish.  The
NEURON simulator is available for free from
The number of sections and dt has been somewhat reduced from the
published ones to speed up the simulations.  Use of variable time step
has also been added since publication.  Unclick variable time step for
fixed if desired.

To run the model:

Either autolaunch from ModelDB (after NEURON is installed) and skip to
step 4 below or

under Windows

1. Run mknrndll and select MechanismsVer7.1 folder to make the dll.
2. run nrngui, then under File -> working dir:Move to the (working)
MechanismsVer7.1 directory to load nrnmech.dll
3. Load one of the session files in the top-level folder
4. Set [Na+]i=4 mmol/l, [Na+]o=151 mmol/l (e.g. go Tools-Distributed
Mechanisms-Viewers-Mechanisms (global)-na_ion)
5. Set EK=-85 mV (e.g. go Tools-Distributed
Mechanisms-Managers-Homogenous Spec and select MechType-k_ion)
6. Push Init & Run to start the simulation

under Linux
1. compile the mod files with 
nrnivmodl MechanismsVer7.1
2. load one of the session files either by choosing one after starting
nrngui mosinit.hoc
or starting with one of them directly, e.g. nrngui
3. follow the windows instructions above from step 4.

under Mac OS X
1.  drag and drop the MechanismsVer7.1 file onto the mknrndll icon
2.  drag and drop the mosinit.hoc file onto the nrngui icon
3.  follow the windows instructions above from step 4.

Notes about the figures:

Fig. 3A:

A simplified compartmental model that encompasses the fundamental
morphological features of a layer 5 pyramidal neuron. In the model,
the first 50 um of the axonal length are assumed to be uncovered by
the myelin sheath and to possess a uniform Na+ channel density about
threefold higher than that of the soma.  The subsequent, myelinated
segment possesses no Na+ channels.  In addition to Hodgkin-Huxley type
Na+ and K+ conductances, the model incorporates longitudinal diffusion
of Na+ ions between neighboring compartments with a diffusion
coefficient of 0.6 um2 ms; no mechanism for Na+ extrusion is
included. Thus, the spatio-temporal patterns of the simulated [Na+]i
transients solely reflects transmembrane influx into the 'active'
compartments that possess Na+ channels (soma and AIS) and Na+
diffusion into compartments that either possess no Na+ channels
(myelinated segments) or are large sinks because they have a
relatively small surface-to-volume ratio (soma).  The model closely
mimicks experimentally observed changes in SBFI fluorescence during a
single action potential.

Fig. 4B 10 APs and 100 APs 

Na+ transients in models with different process-to-soma ratios of Na+
channel density. When Na+ channel density in the process is set equal
to that in the soma (default value, 250 pS/um2), during the AP trains
[Na+]i in the process rises more significantly because of its higher
surface-to-volume ratio.  If we will keep somatic Na+ channel density
constant and vary Na+ channel density in the process (AIS hh_Cs_scaled
in Biophysics menu of the CellBuilder), we can find out that the basal
dendrite Na+ channel density has to be 0.1-0.3-fold larger than the
somatic density and the AIS density has to be one- to threefold larger
than the somatic density to match the experimentally determined

Fig. 6B

Simulated changes in [Na+]i elicited by a single action potential
plotted against distance from the axon hillock.  Because the nodes are
small, Na+ ions diffuse laterally almost as quickly as they enter
across the nodal membrane.  Simulation shows that diffusion-mediated
[Na+]i equilibration between the nodal and internodal volumes should
be nearly complete in milliseconds and that more than 90% of Na+ ions
that enter a 1-um-long node were already in the internodal region
within 10 ms of the peak of the action potential. In contrast, 10 ms
after an action potential in the 48-um-long AIS, dissipation of the
Na+ gradient was minimal. Default values for Na+ channel desnsity: AIS
gnabar_hh_Cs_scaled = 800 pS/um2, node gnabar_hh_Cs_scaled = 1200
pS/um2.  The latter value could be changed to 1600 pS/um2 and to 8000
pS/um2 to obtain the model of panel C, right.

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