D2 dopamine receptor modulation of interneuronal activity (Maurice et al. 2004)

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Accession:98005
"... Using a combination of electrophysiological, molecular, and computational approaches, the studies reported here show that D2 dopamine receptor modulation of Na+ currents underlying autonomous spiking contributes to a slowing of discharge rate, such as that seen in vivo. Four lines of evidence support this conclusion. ... Fourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slowing of pacemaker discharge. These studies establish a cellular mechanism linking dopamine and the reduction in striatal cholinergic interneuron activity seen in the initial stages of associative learning." See paper for more and details.
Reference:
1 . Maurice N, Mercer J, Chan CS, Hernandez-Lopez S, Held J, Tkatch T, Surmeier DJ (2004) D2 dopamine receptor-mediated modulation of voltage-dependent Na+ channels reduces autonomous activity in striatal cholinergic interneurons. J Neurosci 24:10289-301 [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:
Cell Type(s): Neostriatum interneuron ACh cell;
Channel(s): I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium;
Gap Junctions:
Receptor(s): D2;
Gene(s): D2 DRD2; HCN1; HCN2;
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Activity Patterns; Action Potentials; Parkinson's;
Implementer(s): Held, Joshua [j-held at northwestern.edu];
Search NeuronDB for information about:  Neostriatum interneuron ACh cell; D2; I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium;
:Migliore file Modify by Maciej Lazarewicz (mailto:mlazarew@gmu.edu) May/16/2001

TITLE l-calcium channel
: l-type calcium channel

: copy by josh

NEURON {
	SUFFIX cal_ch
	USEION ca READ cai,cao WRITE ica
        RANGE  gbar,ica
	GLOBAL vhm, vcm
	GLOBAL Ctm, atm, btm, tm0, vhtm
        GLOBAL minf,tau
}

UNITS {
	(mA) 	= 	(milliamp)
	(mV) 	= 	(millivolt)
	FARADAY =  	(faraday)  (kilocoulombs)
	R 	= 	(k-mole) (joule/degC)
	KTOMV 	= .0853 (mV/degC)
}

PARAMETER {
	v (mV)
	celsius = 6.3	(degC)
	gbar	= .003 	(mho/cm2)
	ki	= .001 	(mM)
	cai 		(mM)
	cao 		(mM)
        tfa	= 1
	vhm = -1.5
	vcm = 5.6
	Ctm = 3
	atm = 12
	btm = 11
	tm0 = 0
	vhtm = -2
}

STATE { m }

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

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

INITIAL {
	rate(v)
	m = minf
}

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 alp(v(mV)) (1/ms) {
	TABLE FROM -150 TO 150 WITH 200
	alp = 15.69*(-1.0*v+81.5)/(exp((-1.0*v+81.5)/10.0)-1.0)
}

FUNCTION bet(v(mV)) (1/ms) {
	TABLE FROM -150 TO 150 WITH 200
	bet = 0.29*exp(-v/10.86)
}

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

PROCEDURE rate(v (mV)) { :callable from hoc
        LOCAL a

        a    = alp(v)
        :tau  = 1/(tfa*(a + bet(v)))
        :minf = tfa*a*tau
	tau = Ctm/(exp((v-vhtm)/atm) + exp((vhtm-v)/btm)) + tm0
	minf = 1/(1+exp(-(v-vhm)/vcm))
}
 













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