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 CaGk
: Calcium activated K channel.
: Modified from Moczydlowski and Latorre (1983) J. Gen. Physiol. 82

UNITS {
	(molar) = (1/liter)
}

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


NEURON {
	SUFFIX cagk
	USEION nca READ ncai VALENCE 2
	USEION lca READ lcai VALENCE 2
	USEION tca READ tcai VALENCE 2
	USEION k READ ek WRITE ik
	RANGE gkbar,gkca, ik
	GLOBAL oinf, otau
}

UNITS {
	FARADAY = (faraday)  (kilocoulombs)
	R = 8.313424 (joule/degC)
}

PARAMETER {
	celsius		(degC)
	v		(mV)
	gkbar=.01	(mho/cm2)	: Maximum Permeability
	cai = 5.e-5	(mM)
	ek		(mV)

	d1 = .84
	d2 = 1.
	k1 = .48e-3	(mM)
	k2 = .13e-6	(mM)
	abar = .28	(/ms)
	bbar = .48	(/ms)
        st=1            (1)
	lcai		(mV)
	ncai		(mV)
	tcai		(mV)
}

ASSIGNED {
	ik		(mA/cm2)
	oinf
	otau		(ms)
        gkca          (mho/cm2)
}

INITIAL {
	cai= ncai + lcai + tcai
        rate(v,cai)
        o=oinf
}

STATE {	o }		: fraction of open channels

BREAKPOINT {
	SOLVE state METHOD cnexp
	gkca = gkbar*o^st
	ik = gkca*(v - ek)
}

DERIVATIVE state {	: exact when v held constant; integrates over dt step
	rate(v, cai)
	o' = (oinf - o)/otau
}

FUNCTION alp(v (mV), c (mM)) (1/ms) { :callable from hoc
	alp = c*abar/(c + exp1(k1,d1,v))
}

FUNCTION bet(v (mV), c (mM)) (1/ms) { :callable from hoc
	bet = bbar/(1 + c/exp1(k2,d2,v))
}

FUNCTION exp1(k (mM), d, v (mV)) (mM) { :callable from hoc
	exp1 = k*exp(-2*d*FARADAY*v/R/(273.15 + celsius))
}

PROCEDURE rate(v (mV), c (mM)) { :callable from hoc
	LOCAL a
	a = alp(v,c)
	otau = 1/(a + bet(v, c))
	oinf = a*otau
}


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