Hodgkin Huxley Neuron Model

Theoretical Neuroscience
Assignment 1 - Part 2
Author: P.Somnath Sandeep
Submitted by: P.Somnath Sandeep
ID: 2015a1ps0651g
Acknowledgments: Ishaant Agarwal (in part, for (a), and (b)-(iii))
HH neuron model Matlab code (separately attached as a .m file as well), corresponding

plots, and answers to the questions uploaded on Moodle:
TNS HH Model Code

%Simulation Parameters
Final_Time=50; %Time duration of simulation (in milliseconds)
h=0.01; % Step Size for time (in ms)
Iext=; % External current (in microamps); Iext = [ 2 6 8 10 12 16 18 ]
% HH Model Parameters
Vr=-65; % in mV
gNa = 120; % in mS/cm^2
gK = 36; % in mS/cm^2
gL=0.3; % in mS/cm^2
eNa=55; % in mV (e-equilibrium potential)
eK=-72; %in mV
eL=-69.3114; % in mV
C=1; % in microF/cm^2 (capacitance)
%Expressions of rate constants: alpha, and beta for n,m, and h:

alphan= @(V) 0.01*(V+55)/(1-exp(-0.1*(V+55))) ;
alpham= @(V) 0.1*(V+40)/(1-exp(-0.1*(V+40))) ;
alphah= @(V) 0.07*exp(-0.05*(V+65));
betan= @(V) 0.125*exp(-0.0125*(V+65));

betam= @(V) 4*exp(-0.0556*(V+65));
betah= @(V) 1/(1+exp(-0.1*(V+35)));
fV= @(V,n,m,h) (1/C)*(-gNa*(m^3)*h*(V-eNa)-gK*(n^4)*(V-eK)-gL*(V-eL)+Iext);

fn=@(V,n) alphan(V)*(1-n)-betan(V)*n;
fm=@(V,m) alpham(V)*(1-m)-betam(V)*m;
fh=@(V,h) alphah(V)*(1-h)-betah(V)*h;
V1=Vr;
n1=alphan(Vr)/(alphan(Vr)+betan(Vr));
m1=alpham(Vr)/(alpham(Vr)+betam(Vr));
h1=alphah(Vr)/(alphah(Vr)+betah(Vr));
Y0= [V1;n1;m1;h1];
tspan= 0:0.01:50;
fun= @(t,V) [fV(V(1),V(2),V(3),V(4));fn(V(1),V(2));fm(V(1),V(3));fh(V(1),V(4))];
[time,out]=ode45(@(t,y) fun(t,y),tspan,Y0);
(i)
plot(time,out(:,1))
title({'Action Potential'})
xlabel('Time (in ms)')
ylabel('Membrane Potential (in mV)')
No, the neuron doesn’t spike for all the injected currents. When Iext = 2 the summation of
the action potentials doesn’t seem to reach the threshold value, enough to spike the
neuron.
(ii)
(a)
plot(time,out(:,2))
title({'Change in "n" with time'})
ylabel('Gating variable - n')
(ii)
(b)
plot(time,out(:,3))
title({'Change in "m" with time'})
ylabel('Gating variable - m')
(ii)
(c)
plot(time,out(:,4))
title({'Change in "h" with time'})
ylabel('Gating variable - h')
As the neuron spikes, due to the summation of actional potentials from the voltage-gated
channels reaching a certain threshold, m[Na+] gates open up. Initially, n(v) [K+], and m(v) [Na+]
increases, but h(v) [Na+] decreases, which implies that the K+ ion channels activate, whereas
the Na+ channels both activate, and deactivate. In part, this is also because the membrane is
much permeable to K+ than to Na+, the reason why the resting potential of the membrane is
close to that of the equilibrium potential of K+. Also, Tm [Na+] is much smaller than Th [Na+],
and Tn [K+]. This implies that Na+ ion channels need less time (Tm [Na+]) to activate, whereas
the time taken to deactivate the Na+ ion channels (Th [Na+]), or to activate K+ (Tn [K+])
channels is much higher. From the differential equations, Na+ conductance (gNa - m^3*h)
increase quicker than K+ conductance (gK - k^4). As a result, with the initial activation of Na+
ion voltage-gated channels, the conductance of Na+ through the membrane increases, resulting
in an increase of Na+ current (influx of the ions). The driving force (V-ENa) is large enough to
dominate the equation of membrane potential, and V increases towards the Na+ Nernst
membrane potential. This leads to increase m(v) which further increases Na+ activation. As V
approaches towards ENa, Na+ channels inactivate as Na+ driving force (V-ENa) decreases.
Around the same time, K+ channel activates with increase n(v), and the driving force for K+ is
also large. Similar to the Na+, K+ dominates the equation of the membrane potential, and
approaches K+ Nernst membrane potential causing the potential to drop down, and back to rest.
This change correlates to the drop in the spike.
This whole phenomenon corresponds to the strong depolarization of the membrane potential
causing Na+ ion channels to open up. This causes rapid Na+ influx, and leading more channels
to open up (local membrane potential increases causing more voltage-gated channels to open
up, until they are inactive). Once the influx of Na+ stops, causing sodium channels to close, the
K+ channels open up, annd close.
(iii) The time duration of the spike is approximately 5 ms, and from the plots, it looks like
takes around 5 ms for the neuron to return to its resting value.
(iv) Yes, the spikes are periodic for the injected currents starting from Iext = 8 μA.
(v) The frequency of spikes for Iext = 8 μA is around 50 Hz, and for Iext = 18 μA is around
80 Hz. Thus, the frequency(f) of the spikes seems directly proportional to the magnitude
of the injected current.
(vi) From the plots, the peak values don’t seem to change with a change in the injected
current. Since these are voltage-gated channels, the peak value depends only on voltage.
Change in the magnitude of injected current only affects the time taken to reach a certain
voltage, and not the peak value which is determined by voltage alone.

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Theoretical Neuroscience

HH neuron model Matlab code (separately attached as a .m file as well), corresponding

TNS HH Model Code

%Expressions of rate constants: alpha, and beta for n,m, and h:

betan= @(V) 0.125exp(-0.0125(V+65));

fV= @(V,n,m,h) (1/C)(-gNa(m^3)h(V-eNa)-gK(n^4)(V-eK)-gL*(V-eL)+Iext);

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