Neocortical pyramidal neuron: deep; effects of dopamine (Durstewitz et al 2000)

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Accession:82849
"... Simulated dopamine strongly enhanced high, delay-type activity but not low, spontaneous activity in the model network. Furthermore the strength of an afferent stimulation needed to disrupt delay-type activity increased with the magnitude of the dopamine-induced shifts in network parameters, making the currently active representation much more stable. Stability could be increased by dopamine-induced enhancements of the persistent Na(+) and N-methyl-D-aspartate (NMDA) conductances. Stability also was enhanced by a reduction in AMPA conductances. The increase in GABA(A) conductances that occurs after stimulation of dopaminergic D1 receptors was necessary in this context to prevent uncontrolled, spontaneous switches into high-activity states (i.e., spontaneous activation of task-irrelevant representations). In conclusion, the dopamine-induced changes in the biophysical properties of intrinsic ionic and synaptic conductances conjointly acted to highly increase stability of activated representations in PFC networks and at the same time retain control over network behavior and thus preserve its ability to adequately respond to task-related stimuli. ..." See paper and references for more and details.
Reference:
1 . Durstewitz D, Seamans JK, Sejnowski TJ (2000) Dopamine-mediated stabilization of delay-period activity in a network model of prefrontal cortex. J Neurophysiol 83:1733-50 [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: Prefrontal cortex (PFC);
Cell Type(s): Neocortex V1 L6 pyramidal corticothalamic cell;
Channel(s): I Na,p; I Na,t; I L high threshold; I K; I Potassium;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Calcium dynamics;
Implementer(s): Durstewitz, Daniel [daniel.durstewitz at plymouth.ac.uk];
Search NeuronDB for information about:  Neocortex V1 L6 pyramidal corticothalamic cell; I Na,p; I Na,t; I L high threshold; I K; I Potassium;
: Persistent Na+ channel

NEURON {
	SUFFIX Nap
	USEION na READ ena WRITE ina
	RANGE gnapbar, ina, gna
	RANGE DA_alphamshift,DA_betamshift
	RANGE DA_alphahfactor, DA_betahfactor
}

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

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

PARAMETER {
	v (mV)
	dt (ms)
	gnapbar= 0.0022 (mho/cm2) <0,1e9>
	ena = 55 (mV)
	DA_alphamshift=0 : 2 for 100% DA, 0 otherwise
	DA_betamshift=0  : 5 for 100% DA,0 otherwise
	DA_alphahfactor=0: -.8e-5 for DA, 0 otherwise
	DA_betahfactor=0 : 0.014286-0.02 for DA, 0 otherwise
}

STATE {
	m h
}

ASSIGNED {
	ina (mA/cm2)
	minf hinf 
	mtau (ms)
	htau (ms)
	gna (mho/cm2)
	
}

INITIAL {
	rate(v)
	m = minf
	h = hinf
}

BREAKPOINT {
	SOLVE states METHOD cnexp
	gna = gnapbar*m*h
	ina = gna*(v-55)
	
}

DERIVATIVE states {
	rate(v)
	m' = (minf-m)/mtau
	h' = (hinf-h)/htau
}

UNITSOFF

FUNCTION malf( v){ LOCAL va 
	va=v+12+DA_alphamshift
	if (fabs(va)<1e-04){
	 va = va + 0.00001 }
	malf = (-0.2816*va)/(-1+exp(-va/9.3))
	
}


FUNCTION mbet(v(mV))(/ms) { LOCAL vb 
	vb=v-15+DA_betamshift
	if (fabs(vb)<1e-04){
	    vb = vb + 0.00001 }

	mbet = (0.2464*vb)/(-1+exp(vb/6))

}	


FUNCTION half(v(mV))(/ms) { LOCAL vc 
	vc=v+42.8477
	if (fabs(vc)<1e-04){
	   vc=vc+0.00001 }
        half= (2.8e-5+DA_alphahfactor)*(exp(-vc/4.0248))

}


FUNCTION hbet(v(mV))(/ms) { LOCAL vd
	vd=v-413.9284
	if (fabs(vd)<1e-04){
	vd=vd+0.00001 }
        hbet= (0.02+DA_betahfactor)/(1+exp(-vd/148.2589))
 
}




PROCEDURE rate(v (mV)) {LOCAL msum, hsum, ma, mb, ha, hb
	ma=malf(v) mb=mbet(v) ha=half(v) hb=hbet(v)
	
	msum = ma+mb
	minf = ma/msum
	mtau = 1/msum
	
	
	hsum = ha+hb
	hinf = ha/hsum
	htau = 1/hsum
}

	
UNITSON





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