Thalamocortical and Thalamic Reticular Network (Destexhe et al 1996)

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Accession:3343
NEURON model of oscillations in networks of thalamocortical and thalamic reticular neurons in the ferret. (more applications for a model quantitatively identical to previous DLGN model; updated for NEURON v4 and above)
Reference:
1 . Destexhe A, Bal T, McCormick DA, Sejnowski TJ (1996) Ionic mechanisms underlying synchronized oscillations and propagating waves in a model of ferret thalamic slices. J Neurophysiol 76:2049-70 [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 GLU cell; Thalamus reticular nucleus GABA cell;
Channel(s): I Na,t; I T low threshold; I K,leak; I h;
Gap Junctions:
Receptor(s): GabaA; GabaB; AMPA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Activity Patterns; Oscillations; Synchronization; Spatio-temporal Activity Patterns; Sleep; Calcium dynamics; Spindles;
Implementer(s): Destexhe, Alain [Destexhe at iaf.cnrs-gif.fr];
Search NeuronDB for information about:  Thalamus geniculate nucleus/lateral principal GLU cell; Thalamus reticular nucleus GABA cell; GabaA; GabaB; AMPA; I Na,t; I T low threshold; I K,leak; I h;
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DLGN_NEW
README
ampa.mod
cadecay.mod *
gabaa.mod
gabab.mod
HH2.mod *
Ih.mod *
IT.mod *
IT2.mod *
kleak.mod *
Fbic.oc
FbicL.oc
Fdelta.oc
FdeltaL.oc
Fspin.oc
FspinL.oc
mosinit.hoc *
RE.tem
rundemo.hoc
TC.tem
                            
TITLE simple GABAb receptors

COMMENT
-----------------------------------------------------------------------------

	Kinetic model of GABA-B receptors
	=================================

  MODEL OF SECOND-ORDER G-PROTEIN TRANSDUCTION AND FAST K+ OPENING
  WITH COOPERATIVITY OF G-PROTEIN BINDING TO K+ CHANNEL

  PULSE OF TRANSMITTER

  SIMPLE KINETICS WITH NO DESENSITIZATION

	Features:

  	  - peak at 100 ms; time course fit to Tom Otis' PSC
	  - SUMMATION (psc is much stronger with bursts)


	Approximations:

	  - single binding site on receptor	
	  - model of alpha G-protein activation (direct) of K+ channel
	  - G-protein dynamics is second-order; simplified as follows:
		- saturating receptor
		- no desensitization
		- Michaelis-Menten of receptor for G-protein production
		- "resting" G-protein is in excess
		- Quasi-stat of intermediate enzymatic forms
	  - binding on K+ channel is fast


	Kinetic Equations:

	  dR/dt = K1 * T * (1-R-D) - K2 * R

	  dG/dt = K3 * R - K4 * G

	  R : activated receptor
	  T : transmitter
	  G : activated G-protein
	  K1,K2,K3,K4 = kinetic rate cst

  n activated G-protein bind to a K+ channel:

	n G + C <-> O		(Alpha,Beta)

  If the binding is fast, the fraction of open channels is given by:

	O = G^n / ( G^n + KD )

  where KD = Beta / Alpha is the dissociation constant

-----------------------------------------------------------------------------

  Parameters estimated from patch clamp recordings of GABAB PSP's in
  rat hippocampal slices (Otis et al, J. Physiol. 463: 391-407, 1993).

-----------------------------------------------------------------------------

  PULSE MECHANISM

  Kinetic synapse with release mechanism as a pulse.  

  Warning: for this mechanism to be equivalent to the model with diffusion 
  of transmitter, small pulses must be used...

  see details at http://cns.iaf.cnrs-gif.fr

  Written by A. Destexhe, 1995
  27-11-2002: the pulse is implemented using a counter, which is more
	stable numerically (thanks to Yann LeFranc)

-----------------------------------------------------------------------------
ENDCOMMENT



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

NEURON {
	POINT_PROCESS GABAb_S
	POINTER pre
	RANGE C, R, G, g, gmax, lastrelease, TimeCount
	NONSPECIFIC_CURRENT i
	GLOBAL Cmax, Cdur, Prethresh, Deadtime
	GLOBAL K1, K2, K3, K4, KD, Erev
}
UNITS {
	(nA) = (nanoamp)
	(mV) = (millivolt)
	(umho) = (micromho)
	(mM) = (milli/liter)
}

PARAMETER {
	dt		(ms)
	Cmax	= 0.5	(mM)		: max transmitter concentration
	Cdur	= 0.3	(ms)		: transmitter duration (rising phase)
	Prethresh = 0 			: voltage level nec for release
	Deadtime = 1	(ms)		: mimimum time between release events
:
:	From Kfit with long pulse (5ms 0.5mM)
:
	K1	= 0.52	(/ms mM)	: forward binding rate to receptor
	K2	= 0.0013 (/ms)		: backward (unbinding) rate of receptor
	K3	= 0.098 (/ms)		: rate of G-protein production
	K4	= 0.033 (/ms)		: rate of G-protein decay
	KD	= 100			: dissociation constant of K+ channel
	n	= 4			: nb of binding sites of G-protein on K+
	Erev	= -95	(mV)		: reversal potential (E_K)
	gmax		(umho)		: maximum conductance
}


ASSIGNED {
	v		(mV)		: postsynaptic voltage
	i 		(nA)		: current = g*(v - Erev)
	g 		(umho)		: conductance
	C		(mM)		: transmitter concentration
	Gn
	pre 				: pointer to presynaptic variable
	lastrelease	(ms)		: time of last spike
	TimeCount	(ms)		: time counter
}


STATE {
	R				: fraction of activated receptor
	G				: fraction of activated G-protein
}


INITIAL {
	C = 0
	lastrelease = -9e9

	R = 0
	G = 0
	TimeCount=-1
}

BREAKPOINT {
	SOLVE bindkin METHOD cnexp
	Gn = G^n
	g = gmax * Gn / (Gn+KD)
	i = g*(v - Erev)
}


DERIVATIVE bindkin {

	release()		: evaluate the variable C

	R' = K1 * C * (1-R) - K2 * R
	G' = K3 * R - K4 * G

}


PROCEDURE release() {
	:will crash if user hasn't set pre with the connect statement 

        TimeCount=TimeCount-dt       		: time since last release ended

						: ready for another release?
	if (TimeCount < -Deadtime) {
		if (pre > Prethresh) {		: spike occured?
			C = Cmax			: start new release
			lastrelease = t
			TimeCount=Cdur
		}
						
	} else if (TimeCount > 0) {		: still releasing?
	
		: do nothing
	
	} else if (C == Cmax) {			: in dead time after release
		C = 0.
	}

}

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