Impact of dendritic atrophy on intrinsic and synaptic excitability (Narayanan & Chattarji, 2010)

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Accession:147867
These simulations examined the atrophy induced changes in electrophysiological properties of CA3 pyramidal neurons. We found these neurons change from bursting to regular spiking as atrophy increases. Region-specific atrophy induced region-specific increases in synaptic excitability in a passive dendritic tree. All dendritic compartments of an atrophied neuron had greater synaptic excitability and a larger voltage transfer to the soma than the control neuron.
Reference:
1 . Narayanan R, Chattarji S (2010) Computational analysis of the impact of chronic stress on intrinsic and synaptic excitability in the hippocampus. J Neurophysiol 103:3070-83 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Synapse; Dendrite;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA3 pyramidal cell;
Channel(s): I Na,t; I L high threshold; I N; I T low threshold; I A; I K; I M; I h; I K,Ca; I Calcium; I_AHP;
Gap Junctions:
Receptor(s): AMPA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Active Dendrites; Influence of Dendritic Geometry; Detailed Neuronal Models; Action Potentials; Conductance distributions;
Implementer(s): Narayanan, Rishikesh [rishi at mbu.iisc.ernet.in];
Search NeuronDB for information about:  Hippocampus CA3 pyramidal cell; AMPA; I Na,t; I L high threshold; I N; I T low threshold; I A; I K; I M; I h; I K,Ca; I Calcium; I_AHP; Glutamate;
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CA3Atrophy
Input
README.html
ampa.mod
borgkm.mod *
cadiv.mod *
cagk.mod *
cal2.mod *
can2.mod *
cat.mod *
h.mod
kad.mod
kahp.mod *
kap.mod
kdr.mod *
nahh.mod *
0.png
25.png
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Fig1D.hoc
Fig2D-E.hoc
Fig2F-G.hoc
Menu.png
mosinit.hoc
neuron.que
Neurons.inp
                            
TITLE CaGk
: Calcium activated K channel.
: Modified from Moczydlowski and Latorre (1983) J. Gen. Physiol. 82

UNITS {
	(molar) = (1/liter)
}

UNITS {
	(mV) =	(millivolt)
	(mA) =	(milliamp)
	(mM) =	(millimolar)
}


NEURON {
	SUFFIX cagk
	USEION ca READ cai
	USEION k READ ek WRITE ik
	RANGE gkbar,gkca
	GLOBAL oinf, tau
}

UNITS {
	FARADAY = (faraday)  (kilocoulombs)
	R = 8.313424 (joule/degC)
}

PARAMETER {
	celsius		(degC)
	v		(mV)
	gkbar=.01	(mho/cm2)	: Maximum Permeability
	cai = 5.e-5	(mM)
	ek		(mV)

	d1 = .84
	d2 = 1.
	k1 = .48e-3	(mM)
	k2 = .13e-6	(mM)
	abar = .28	(/ms)
	bbar = .48	(/ms)
        st=1            (1)
}

ASSIGNED {
	ik		(mA/cm2)
	oinf
	tau		(ms)
        gkca          (mho/cm2)
}

INITIAL {
        rate(v,cai)
        o=oinf
}

STATE {	o }		: fraction of open channels

BREAKPOINT {
	SOLVE state METHOD cnexp
	gkca = gkbar*o^st
	ik = gkca*(v - ek)
}

DERIVATIVE state {	: exact when v held constant; integrates over dt step
	rate(v, cai)
	o' = (oinf - o)/tau
}

FUNCTION alp(v (mV), c (mM)) (1/ms) { :callable from hoc
	alp = c*abar/(c + exp1(k1,d1,v))
}

FUNCTION bet(v (mV), c (mM)) (1/ms) { :callable from hoc
	bet = bbar/(1 + c/exp1(k2,d2,v))
}

FUNCTION exp1(k (mM), d, v (mV)) (mM) { :callable from hoc
	exp1 = k*exp(-2*d*FARADAY*v/R/(273.15 + celsius))
}

PROCEDURE rate(v (mV), c (mM)) { :callable from hoc
	LOCAL a
	a = alp(v,c)
	tau = 1/(a + bet(v, c))
	oinf = a*tau
}


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