Ketamine disrupts theta modulation of gamma in a computer model of hippocampus (Neymotin et al 2011)

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Accession:139421
"Abnormalities in oscillations have been suggested to play a role in schizophrenia. We studied theta-modulated gamma oscillations in a computer model of hippocampal CA3 in vivo with and without simulated application of ketamine, an NMDA receptor antagonist and psychotomimetic. Networks of 1200 multi-compartment neurons (pyramidal, basket and oriens-lacunosum moleculare, OLM, cells) generated theta and gamma oscillations from intrinsic network dynamics: basket cells primarily generated gamma and amplified theta, while OLM cells strongly contributed to theta. ..."
Reference:
1 . Neymotin SA, Lazarewicz MT, Sherif M, Contreras D, Finkel LH, Lytton WW (2011) Ketamine disrupts theta modulation of gamma in a computer model of hippocampus Journal of Neuroscience 31(32):11733-11743 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA3 pyramidal cell; Hippocampus CA3 basket cell; Hippocampus CA3 stratum oriens lacunosum-moleculare interneuron;
Channel(s): I L high threshold; I A; I K; I K,Ca;
Gap Junctions:
Receptor(s): GabaA; NMDA; Glutamate;
Gene(s): HCN1; HCN2;
Transmitter(s): Gaba; Glutamate;
Simulation Environment: NEURON; Python;
Model Concept(s): Oscillations; Synchronization; Therapeutics; Pathophysiology; Schizophrenia; Information transfer; Brain Rhythms;
Implementer(s): Lazarewicz, Maciej [mlazarew at gmu.edu]; Neymotin, Sam [samn at neurosim.downstate.edu];
Search NeuronDB for information about:  Hippocampus CA3 pyramidal cell; Hippocampus CA3 basket cell; GabaA; NMDA; Glutamate; I L high threshold; I A; I K; I K,Ca; Gaba; Glutamate;
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hpcdemo
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MyExp2Syn.mod *
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: $Id: MyExp2Syn.mod,v 1.3 2010/12/13 21:37:06 samn Exp $ 
COMMENT
Two state kinetic scheme synapse described by rise time tau1,
and decay time constant tau2. The normalized peak condunductance is 1.
Decay time MUST be greater than rise time.

The solution of A->G->bath with rate constants 1/tau1 and 1/tau2 is
 A = a*exp(-t/tau1) and
 G = a*tau2/(tau2-tau1)*(-exp(-t/tau1) + exp(-t/tau2))
	where tau1 < tau2

If tau2-tau1 -> 0 then we have a alphasynapse.
and if tau1 -> 0 then we have just single exponential decay.

The factor is evaluated in the
initial block such that an event of weight 1 generates a
peak conductance of 1.

Because the solution is a sum of exponentials, the
coupled equations can be solved as a pair of independent equations
by the more efficient cnexp method.

ENDCOMMENT

NEURON {
	POINT_PROCESS MyExp2Syn
	RANGE tau1, tau2, e, i, tgtid, synid, g
	NONSPECIFIC_CURRENT i
}

UNITS {
	(nA) = (nanoamp)
	(mV) = (millivolt)
	(uS) = (microsiemens)
}

PARAMETER {
	tau1=.1 (ms) <1e-9,1e9>
	tau2 = 10 (ms) <1e-9,1e9>
	e=0	(mV)
	tgtid = -1
	synid = -1
}

ASSIGNED {
	v (mV)
	i (nA)
	g (uS)
	factor
}

STATE {
	A (uS)
	B (uS)
}

INITIAL {
	LOCAL tp
	if (tau1/tau2 > .9999) {
		tau1 = .9999*tau2
	}
	A = 0
	B = 0
	tp = (tau1*tau2)/(tau2 - tau1) * log(tau2/tau1)
	factor = -exp(-tp/tau1) + exp(-tp/tau2)
	factor = 1/factor
}

BREAKPOINT {
	SOLVE state METHOD cnexp
	g = B - A
	i = g*(v - e)
}

DERIVATIVE state {
	A' = -A/tau1
	B' = -B/tau2
}

NET_RECEIVE(weight (uS),srcgid) {
	A = A + weight*factor
	B = B + weight*factor
}

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