Firing neocortical layer V pyramidal neuron (Reetz et al. 2014; Stadler et al. 2014)

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Accession:168148
Neocortical Layer V model with firing behaviour adjusted to in vitro observations. The model was used to investigate the effects of IFN and PKC on the excitability of neurons (Stadler et al 2014, Reetz et al. 2014). The model contains new channel simulations for HCN1, HCN2 and the big calcium dependent potassium channel BK.
Reference:
1 . Stadler K, Bierwirth C, Stoenica L, Battefeld A, Reetz O, Mix E, Schuchmann S, Velmans T, Rosenberger K, Bräuer AU, Lehnardt S, Nitsch R, Budt M, Wolff T, Kole MH, Strauss U (2014) Elevation in type I interferons inhibits HCN1 and slows cortical neuronal oscillations. Cereb Cortex 24:199-210 [PubMed]
2 . Reetz O, Stadler K, Strauss U (2014) Protein kinase C activation mediates interferon-ß-induced neuronal excitability changes in neocortical pyramidal neurons. J Neuroinflammation 11:185 [PubMed]
Citations  Citation Browser
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 V1 L6 pyramidal corticothalamic GLU cell;
Channel(s): I Na,p; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I Sodium; I Calcium; I Mixed; I Potassium; I Q;
Gap Junctions:
Receptor(s):
Gene(s): HCN1; HCN2;
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Activity Patterns; Detailed Neuronal Models; Action Potentials; Signaling pathways;
Implementer(s): Stadler, Konstantin [konstantin.stadler at ntnu.no];
Search NeuronDB for information about:  Neocortex V1 L6 pyramidal corticothalamic GLU cell; I Na,p; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I Sodium; I Calcium; I Mixed; I Potassium; I Q;
COMMENT

changed from (AS Oct0899)
ca.mod to lead to thalamic ca current inspired by destexhe and huguenrd
Uses fixed eca instead of GHK eqn

LVA Ca?

ENDCOMMENT

INDEPENDENT {t FROM 0 TO 1 WITH 1 (ms)}

NEURON {
	SUFFIX it2
	USEION ca READ eca WRITE ica
	RANGE m, h, gca, gcabar
	RANGE minf, hinf, mtau, htau, inactF, actF
	GLOBAL  vshift,vmin,vmax, v12m, v12h, vwm, vwh, am, ah, vm1, vm2, vh1, vh2, wm1, wm2, wh1, wh2
}

PARAMETER {
	gcabar = 0.0008 (mho/cm2)	: 0.12 mho/cm2
	vshift = 0	(mV)		: voltage shift (affects all)

	cao  = 2.5	(mM)	        : external ca concentration
	cai		(mM)
						 
	v 		(mV)
	dt		(ms)
	celsius		(degC)
	vmin = -120	(mV)
	vmax = 100	(mV)

	v12m=50         	(mV)
	v12h=78         	(mV)
	vwm =7.4         	(mV)
	vwh=5.0         	(mV)
	am=3         	(mV)
	ah=85         	(mV)
	vm1=25         	(mV)
	vm2=100         	(mV)
	vh1=46         	(mV)
	vh2=405         	(mV)
	wm1=20         	(mV)
	wm2=15         	(mV)
	wh1=4         	(mV)
	wh2=50         	(mV)


}


UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(pS) = (picosiemens)
	(um) = (micron)
	(molar) = (1/liter)
	(mM) 	= (millimolar)
	FARADAY = (faraday) (coulomb)
	R = (k-mole) (joule/degC)
	PI	= (pi) (1)
} 

ASSIGNED {
	ica 		(mA/cm2)
	gca		(pS/um2)
	eca		(mV)
	minf 		hinf
	mtau (ms)	htau (ms)
	tadj
}
 

STATE { m h }

INITIAL { 
	trates(v+vshift)
	m = minf
	h = hinf
}

BREAKPOINT {
        SOLVE states
        gca = gcabar*m*m*h
	ica = gca * (v - eca)
} 

LOCAL mexp, hexp

PROCEDURE states() {
        trates(v+vshift)      
        m = m + mexp*(minf-m)
        h = h + hexp*(hinf-h)
	VERBATIM
	return 0;
	ENDVERBATIM
}


PROCEDURE trates(v) {  
                      
        LOCAL tinc
        TABLE minf, mexp, hinf, hexp
	DEPEND dt	
	FROM vmin TO vmax WITH 199

	rates(v): not consistently executed from here if usetable == 1

        tinc = -dt 

        mexp = 1 - exp(tinc/mtau)
        hexp = 1 - exp(tinc/htau)
}


PROCEDURE rates(v_) {  
        LOCAL  a, b

	minf = 1.0 / ( 1 + exp(-(v_+v12m)/vwm) )
	hinf = 1.0 / ( 1 + exp((v_+v12h)/vwh) )

	mtau = ( am + 1.0 / ( exp((v_+vm1)/wm1) + exp(-(v_+vm2)/wm2) ) ) 
	htau = ( ah + 1.0 / ( exp((v_+vh1)/wh1) + exp(-(v_+vh2)/wh2) ) ) 
}