Status epilepticus alters dentate basket cell tonic inhibition (Yu J et al 2013)

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Accession:155602
Status epilepticus (SE) leads to changes in dentate inhibitory neuronal networks and alters synaptic and tonic inhibition in granule cells. Recently, we identified that one week after pilocarpine-induced status epilepticus, dentate fast-spiking basket cells (FS-BCs), which underlie fast perisomatic inhibition, show two distinct changes in inhibition: (1) enhanced tonic currents (IGABA) and (2)depolarizing shift in GABA reversal (EGABA) following SE. These two changes can have opposing effects on neuronal inhibition with increases in tonic GABA conductance (gGABA) reducing excitability when the GABA currents are shunting (or hyperpolarizing) and potentially enhancing excitability when GABA currents are depolarizing. The following model is used to examine the post-SE changes in tonic GABA conductance, together with the depolarized GABA reversal potential modify FS-BC excitability and dentate network activity.
Reference:
1 . Yu J, Proddutur A, Elgammal FS, Ito T, Santhakumar V (2013) Status epilepticus enhances tonic GABA currents and depolarizes GABA reversal potential in dentate fast-spiking basket cells. J Neurophysiol 109:1746-63 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism:
Cell Type(s): Dentate gyrus basket cell;
Channel(s):
Gap Junctions:
Receptor(s): GabaA;
Gene(s):
Transmitter(s): Gaba;
Simulation Environment: NEURON;
Model Concept(s): Epilepsy;
Implementer(s):
Search NeuronDB for information about:  GabaA; Gaba;
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YuEtAl2013
ReadMe.html
bgka.mod *
CaBK.mod *
ccanl.mod *
gap.mod
Gfluct2.mod *
gskch.mod *
hyperde3.mod *
ichan2.mod *
LcaMig.mod *
markov.mod *
nca.mod *
tca.mod *
tonic.mod *
fixed rseed Control -74 spill_ tonic 10uS with mossy kill.hoc
fixed rseed Pilo -54 spill_ tonic 10uS with mossy kill.hoc
mosinit.hoc
screenshot1.png
                            
TITLE l-calcium channel
: l-type calcium channel


UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(molar) = (1/liter)
	(mM) = (millimolar)
	FARADAY = 96520 (coul)
	R = 8.3134 (joule/degC)
	KTOMV = .0853 (mV/degC)
}

PARAMETER {
	v (mV)
	celsius 	(degC)
	glcabar		 (mho/cm2)
	ki=.001 (mM)
	cai (mM)
	cao (mM)
        tfa=1
}


NEURON {
	SUFFIX lca
	USEION lca READ elca WRITE ilca VALENCE 2
	USEION ca READ cai, cao VALENCE 2 
        RANGE glcabar, cai, ilca, elca
        GLOBAL minf,matu
}

STATE {
	m
}

ASSIGNED {
	ilca (mA/cm2)
        glca (mho/cm2)
        minf
        matu   (ms)
	elca (mV)   

}

INITIAL {
	rate(v)
	m = minf
	VERBATIM
	cai=_ion_cai;
	ENDVERBATIM
}

BREAKPOINT {
	SOLVE state METHOD cnexp
	glca = glcabar*m*m*h2(cai)
	ilca = glca*ghk(v,cai,cao)

}

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)/matu
}

PROCEDURE rate(v (mV)) { :callable from hoc
        LOCAL a
        a = alp(v)
        matu = 1/(tfa*(a + bet(v)))
        minf = tfa*a*matu
}
 



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