CA1 pyramidal neuron: depolarization block (Bianchi et al. 2012)

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Accession:143719
NEURON files from the paper: On the mechanisms underlying the depolarization block in the spiking dynamics of CA1 pyramidal neurons by D.Bianchi, A. Marasco, A.Limongiello, C.Marchetti, H.Marie,B.Tirozzi, M.Migliore (2012). J Comput. Neurosci. In press. DOI: 10.1007/s10827-012-0383-y. Experimental findings shown that under sustained input current of increasing strength neurons eventually stop firing, entering a depolarization block. We analyze the spiking dynamics of CA1 pyramidal neuron models using the same set of ionic currents on both an accurate morphological reconstruction and on its reduction to a single-compartment. The results show the specic ion channel properties and kinetics that are needed to reproduce the experimental findings, and how their interplay can drastically modulate the neuronal dynamics and the input current range leading to depolarization block.
Reference:
1 . Bianchi D, Marasco A, Limongiello A, Marchetti C, Marie H, Tirozzi B, Migliore M (2012) On the mechanisms underlying the depolarization block in the spiking dynamics of CA1 pyramidal neurons J Comput. Neurosci. 33:207-25 [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: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal cell;
Channel(s): I Na,t; I A; I K; I M; I h; I K,Ca; I_AHP;
Gap Junctions:
Receptor(s): GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON; Mathematica;
Model Concept(s): Simplified Models; Depolarization block; Bifurcation;
Implementer(s): Bianchi, Daniela [danielabianchi12 -at- gmail.com]; Limongiello, Alessandro [alessandro.limongiello at unina.it];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal cell; GabaA; AMPA; NMDA; I Na,t; I A; I K; I M; I h; I K,Ca; I_AHP; Gaba; Glutamate;
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Ca1_Bianchi
experiment
cad.mod *
cagk.mod *
cal.mod *
calH.mod *
car.mod *
cat.mod *
d3.mod *
h.mod *
kadist.mod *
kaprox.mod *
kca.mod *
kdr.mod *
km.mod *
na3.mod *
na3dend.mod *
na3notrunk.mod *
nap.mod *
nax.mod *
somacar.mod *
cell-setup.hoc
mosinit.hoc
sessio.ses
Simulation.hoc
                            
TITLE l-calcium channel
: l-type calcium channel


UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)

	FARADAY = 96520 (coul)
	R = 8.3134 (joule/degC)
	KTOMV = .0853 (mV/degC)
}

PARAMETER {
	v (mV)
	celsius= 34	(degC)
	gcalbar=0 (mho/cm2)
	ki=.001 (mM)
	cai = 50.e-6 (mM)
	cao = 2 (mM)
     	tfa = 5
      ggk
      eca = 140	
}


NEURON {
	SUFFIX cal
	USEION ca READ cai,cao WRITE ica
        RANGE gcalbar,cai, ica, gcal, ggk
        GLOBAL minf,taum
}

STATE {
	m
}

ASSIGNED {
	ica (mA/cm2)
        gcal (mho/cm2)
        minf
        taum  (ms)
}

INITIAL {
	rate(v)
	m = minf
}

BREAKPOINT {
	SOLVE state METHOD cnexp
	gcal = gcalbar*m*h2(cai)    
	ggk=ghk(v,cai,cao)
	ica = gcal*ggk

}

FUNCTION h2(cai(mM)) {
	h2 = ki/(ki+cai)
}


FUNCTION ghk(v(mV), ci(mM), co(mM)) (mV) {
        LOCAL nu,f
        f = KTF(celsius)/2
        nu = v/f
        ghk=-f*(1. - (ci/co)*exp(nu))*efun(nu)
}

FUNCTION KTF(celsius (DegC)) (mV) {
        KTF = ((25./293.15)*(celsius + 273.15))
}


FUNCTION efun(z) {
	if (fabs(z) < 1e-4) {
		efun = 1 - z/2
	}else{
		efun = z/(exp(z) - 1)
	}
}




FUNCTION alpm(v(mV)) {
	TABLE FROM -150 TO 150 WITH 200
	alpm = 0.055*(-27.01 - v)/(exp((-27.01-v)/3.8) - 1)
}


FUNCTION betm(v(mV)) {
        TABLE FROM -150 TO 150 WITH 200
        betm =0.94*exp((-63.01-v)/17)
}



DERIVATIVE state {  
        rate(v)
        m' = (minf - m)/taum
}

PROCEDURE rate(v (mV)) { :callable from hoc
        LOCAL a, b, qt
        a = alpm(v)
        taum = 1/(tfa*(a+betm(v))) : estimation of activation tau
        minf = a/(a+betm(v))       : estimation of activation steady state value

	
}

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