Thalamic quiescence of spike and wave seizures (Lytton et al 1997)

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Accession:9889
A phase plane analysis of a two cell interaction between a thalamocortical neuron (TC) and a thalamic reticularis neuron (RE).
Reference:
1 . Lytton WW, Contreras D, Destexhe A, Steriade M (1997) Dynamic interactions determine partial thalamic quiescence in a computer network model of spike-and-wave seizures. J Neurophysiol 77:1679-96 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism: Thalamus;
Cell Type(s): Thalamus geniculate nucleus (lateral) principal neuron; Thalamus reticular nucleus cell;
Channel(s): I T low threshold;
Gap Junctions:
Receptor(s): GabaA; Glutamate;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Temporal Pattern Generation; Oscillations; Calcium dynamics;
Implementer(s): Lytton, William [billl at neurosim.downstate.edu]; Destexhe, Alain [Destexhe at iaf.cnrs-gif.fr];
Search NeuronDB for information about:  Thalamus geniculate nucleus (lateral) principal neuron; Thalamus reticular nucleus cell; GabaA; Glutamate; I T low threshold; Gaba; Glutamate;
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lytton97
README
AMPA.mod
calciumpump_destexhe.mod *
GABAB1.mod
GABALOW.mod
gen.mod
HH_traub.mod *
IAHP_destexhe.mod
ICAN_destexhe.mod
Ih_old.mod *
IT_wang.mod
IT2_huguenard.mod
nmda.mod
passiv.mod
presyn.mod *
pulse.mod *
rand.mod
boxes.hoc *
declist.hoc *
decvec.hoc *
default.hoc *
directory
fig7.gif
geom.hoc
grvec.hoc
init.hoc
jnphys77_1679.pdf
local.hoc *
mosinit.hoc
network.hoc
nrnoc.hoc *
params.hoc
presyn.inc *
queue.inc *
run.hoc
simctrl.hoc *
snshead.inc *
synq.inc *
xtmp
                            
: $Id: IAHP_destexhe.mod,v 1.8 1994/10/27 21:26:59 billl Exp $
TITLE Slow Ca-dependent potassium current
:
:   Ca++ dependent K+ current IC responsible for slow AHP
:   Differential equations
:
:   Model of Destexhe, 1992.  Based on a first order kinetic scheme
:      <closed> + n cai <-> <open>	(alpha,beta)
:   Following this model, the activation fct will be half-activated at 
:   a concentration of Cai = (beta/alpha)^(1/n) = cac (parameter)
:   The mod file is here written for the case n=2 (2 binding sites)
:   ---------------------------------------------
:
:   This current models the "slow" IK[Ca] (IAHP): 
:      - potassium current
:      - activated by intracellular calcium
:      - NOT voltage dependent
:
:   A minimal value for the time constant has been added
:
:   Written by Alain Destexhe, Salk Institute, Nov 3, 1992
:

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

NEURON {
	SUFFIX iahp
	USEION k WRITE ik
	USEION ca READ cai
        RANGE gkbar, i
	GLOBAL beta, cac, m_inf, tau_m
}


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


PARAMETER {
	v		(mV)
	celsius	= 36	(degC)
	erev = -95		(mV)
	cai 	= 5e-5	(mM)		: initial [Ca]i = 50 nM
	gkbar	= .001	(mho/cm2)
	beta	= 2.5	(1/ms)		: backward rate constant
	cac	= 1e-4	(mM)		: middle point of activation fct
	taumin	= 1	(ms)		: minimal value of the time cst
}


STATE {
	m
}

ASSIGNED {
	ik	(mA/cm2)
	i	(mA/cm2)
	m_inf
	tau_m	(ms)
	tadj
}

BREAKPOINT { 
	SOLVE states METHOD runge
	i = gkbar * m*m * (v - erev)
	ik = i
}

DERIVATIVE states { 
	evaluate_fct(v,cai)

	m' = (m_inf - m) / tau_m
}

UNITSOFF
INITIAL {
	evaluate_fct(v,cai)
	m = m_inf
:
:  activation kinetics are assumed to be at 22 deg. C
:  Q10 is assumed to be 3
:
	tadj = 3 ^ ((celsius-22.0)/10)

}

PROCEDURE evaluate_fct(v(mV),cai(mM)) {  LOCAL car

	car = (cai/cac)^2

	m_inf = car / ( 1 + car )
	tau_m = 1 / beta / (1 + car) / tadj

        if(tau_m < taumin) { tau_m = taumin } 	: min value of time cst
}
UNITSON

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