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 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 mykca
	USEION ca READ cai
	USEION k READ ek WRITE ik
	RANGE gkbar,ik
	GLOBAL oinf, tau
}

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

PARAMETER {
      v		(mV)
	dt		(ms)
	ek		(mV)
	celsius = 20	(degC)
	gkbar = 0.01	(mho/cm2)	: Maximum Permeability
	cai = 1e-3	(mM)

      d1 =1
     	d2 = 1.5
	k1 = 0.18	(mM)
	k2 = 0.011	(mM)
	bbar = 0.28	(/ms)
	abar = 0.48	(/ms)


	:d1 = 0.84
	:d2 = 1
	:k1 = 0.18	(mM)
	:k2 = 0.011	(mM)
	:bbar = 0.28	(/ms)
	:abar = 0.48	(/ms)


        st=1            (1)
}

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

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

STATE {	o }		: fraction of open channels

BREAKPOINT {
	SOLVE state METHOD cnexp
	ik = gkbar*o^st*(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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