L5 PFC microcircuit used to study persistent activity (Papoutsi et al. 2014, 2013)

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Accession:155057
Using a heavily constrained biophysical model of a L5 PFC microcircuit we investigate the mechanisms that underlie persistent activity emergence (ON) and termination (OFF) and search for the minimum network size required for expressing these states within physiological regimes.
References:
1 . Papoutsi A, Sidiropoulou K, Cutsuridis V, Poirazi P (2013) Induction and modulation of persistent activity in a layer V PFC microcircuit model. Front Neural Circuits 7:161 [PubMed]
2 . Papoutsi A, Sidiropoulou K, Poirazi P (2014) Dendritic nonlinearities reduce network size requirements and mediate ON and OFF states of persistent activity in a PFC microcircuit model. PLoS Comput Biol 10:e1003764 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Dendrite; Connectionist Network;
Brain Region(s)/Organism: Neocortex;
Cell Type(s): Neocortex L5/6 pyramidal GLU cell;
Channel(s): I Na,p; I Na,t; I L high threshold; I A; I CAN; I Potassium; I R; I_AHP;
Gap Junctions:
Receptor(s): GabaA; GabaB; AMPA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Active Dendrites; Working memory;
Implementer(s): Papoutsi, Athanasia [athpapoutsi at gmail.com];
Search NeuronDB for information about:  Neocortex L5/6 pyramidal GLU cell; GabaA; GabaB; AMPA; NMDA; I Na,p; I Na,t; I L high threshold; I A; I CAN; I Potassium; I R; I_AHP;
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L5microcircuit
mechanism
ampa.mod
ampain.mod
cadyn.mod
cal.mod
can.mod
car.mod
cat.mod
gabaa.mod *
gabaain.mod
gabab.mod
h.mod
ican.mod
iks.mod
kadist.mod
kca.mod
kct.mod
kdr.mod *
naf.mod
nap.mod
netstim.mod *
NMDA.mod
NMDA_syn.mod
sinclamp.mod *
vecstim.mod *
                            
TITLE Kct current

COMMENT Equations from Shao L.R., Halvorsrud R., Borg-Graham L., Storm J.F. The role of BK-type Ca2_-dependent K+ channels in spike broadening during repetitive firing in rat hippocampal pyramidal cells J.Physiology (1999),521:135-146   
		  The Krasnow Institute
		  George Mason University
Copyright	  Maciej Lazarewicz, 2001
		  (mlazarew@gmu.edu)
		  All rights reserved.
ENDCOMMENT

NEURON {
	SUFFIX iC
	USEION k READ ko, ki WRITE ik		
	USEION ca READ cai   
	RANGE  gkcbar,ik
}

UNITS {
	(molar) = (1/liter)
	(mM)	= (millimolar)
	(S)  	= (siemens)
	(mA) 	= (milliamp)
	(mV) 	= (millivolt)
}

PARAMETER {
        gkcbar	= 0	 (S/cm2)
	:gkbar	= 1.0e-3 (S/cm2)
}

ASSIGNED {
        v       (mV)
        cai	(mM)     :26/10/04   htan se sxolio
	celsius		 (degC)
	ek		(mV)
	ik	(mA/cm2)
	k1	(/ms)
	k2	(/ms)
	k3	(/ms)
	k4	(/ms)
	q10	(1)
	ko	(mM)
	ki	(mM)
}

STATE { cst ost ist }

BREAKPOINT { 
	SOLVE kin METHOD sparse
	ek=25*log(ko/ki)		:Changed, added, 23/04/2010, Nassi
	ik = gkcbar * ost *( v - ek ) 
}

INITIAL {
	SOLVE kin STEADYSTATE sparse
}

KINETIC kin {
	rates(v, cai)
	~cst<->ost  (k3,k4)
	~ost<->ist  (k1,0.0)
	~ist<->cst  (k2,0.0)
	CONSERVE cst+ost+ist=1
}

:change feb8th for pfc
:PROCEDURE rates( v(mV), cani(mM)) {
PROCEDURE rates( v(mV), cai(mM)) {
:	 k1=alp( 0.1, v,  -10.0,   1.0 ) : original
	 k1=alp( 0.01, v,  -10.0,   1.0 ) :increases the current
	 k2=alp( 0.1, v, -120.0, -10.0 ) :original (0.1, -120, -10)
:	 k3=alpha( 0.001, 1.0, v, -20.0, 7.0 ) *1.0e8* ( cai*1.0(/mM) )^3  :original
	 k3=alpha( 0.001, 1.0, v, -20.0, 7.0 ) *1.0e8* (cai*1.0(/mM) )^3
	 :k3 changes the attenuation
	 k4=alp( 0.2, v, -44.0,  -5.0 ) :original
:	 k4=alp( 0.2, v, -44.0,  -5.0 )
}

FUNCTION alpha( tmin(ms), tmax(ms), v(mV), vhalf(mV), k(mV) )(/ms){
        alpha = 1.0 / ( tmin + 1.0 / ( 1.0 / (tmax-tmin) + exp((v-vhalf)/k)*1.0(/ms) ) )
}

FUNCTION alp( tmin(ms), v(mV), vhalf(mV), k(mV) )(/ms){
        alp = 1.0 / ( tmin + exp( -(v-vhalf) / k )*1.0(ms) )
}










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