Lateral dendrodenditic inhibition in the Olfactory Bulb (David et al. 2008)

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Accession:116094
Mitral cells, the principal output neurons of the olfactory bulb, receive direct synaptic activation from primary sensory neurons. Shunting inhibitory inputs delivered by granule cell interneurons onto mitral cell lateral dendrites are believed to influence spike timing and underlie coordinated field potential oscillations. Lateral dendritic shunt conductances delayed spiking to a degree dependent on both their electrotonic distance and phase of onset. Recurrent inhibition significantly narrowed the distribution of mitral cell spike times, illustrating a tendency towards coordinated synchronous activity. This result suggests an essential role for early mechanisms of temporal coordination in olfaction. The model was adapted from Davison et al, 2003, but include additional noise mechanisms, long lateral dendrite, and specific synaptic point processes.
Reference:
1 . David F, Linster C, Cleland TA (2008) Lateral dendritic shunt inhibition can regularize mitral cell spike patterning. J Comput Neurosci 25:25-38 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network; Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Olfactory bulb;
Cell Type(s): Olfactory bulb main mitral GLU cell; Olfactory bulb main interneuron granule MC GABA cell;
Channel(s): I Na,t; I L high threshold; I A; I K; I K,Ca;
Gap Junctions:
Receptor(s): GabaA; AMPA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON; MATLAB;
Model Concept(s): Temporal Pattern Generation; Synchronization; Simplified Models; Active Dendrites; Olfaction;
Implementer(s):
Search NeuronDB for information about:  Olfactory bulb main mitral GLU cell; Olfactory bulb main interneuron granule MC GABA cell; GabaA; AMPA; I Na,t; I L high threshold; I A; I K; I K,Ca;
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DendroDendriticInhibition
ShortDendrite
cadecay.mod *
currentGauss.mod
flushf.mod *
GradGABAa.mod
ipscGauss.mod
kA.mod *
kca.mod *
kfasttab.mod *
kM.mod *
kslowtab.mod *
lcafixed.mod *
nafast.mod *
nagran.mod *
shuntInhib.mod *
stim2.mod
bulb.hoc
experiment_fig1cde.hoc
experiment_fig1fg.hoc
experiment_fig2bdf.hoc
experiment_fig3.hoc
experiment_fig4.hoc
experiment_fig5.hoc
experiment_fig6.hoc
fig1cde.ses
fig1fg.ses
fig2bdf.ses
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fig5.ses
fig6.ses
figure1cde.m
figure1fg.m
figure2bdf.m
figure3.m
figure4abcd.m
figure4ef.m
figure5.m
figure6.asv
figure6.m
fit_ML_normal.m
granule.tem
init.hoc
mathslib.hoc *
mitral.tem
mosinit.hoc *
parameters_fig1cde.hoc
parameters_fig1fg.hoc
parameters_fig2bdf.hoc
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parameters_fig4.hoc
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plot_normal.m
tabchannels.dat *
tabchannels.hoc
                            
COMMENT
-----------------------------------------------------------------------------

GradGABAa.mod
Graded ionotropic GABA-A synaptic mechanism

Simple synaptic mechanism for the thresholded, graded release of GABA
(e.g., in dendodendritic synapses).  

Thomas A. Cleland (tac29@cornell.edu) and Praveen Sethupathy
Cornell University
Summer 2003, January 2004
adapted by Francois David 2005
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There is a pointer called "PreActiv" which must be set to the (presynaptic) variable 
that is supposed to trigger synaptic release.  This variable is usually the
presynaptic voltage (mV) but it could be another variable, such as the presynaptic 
calcium concentration.

Once pre has crossed the threshold value given by Prethresh, a quantity of
C (i.e., GABA) is released which increases monotonically with (pre-Prethresh)
until Cmax (the maximum permissible concentration of GABA in the cleft) is
reached.  Postsynaptic conductance (g) is currently scaled directly to C such that 
g=gmax when C=Cmax.  

This mechanism is perfectly adequate for most network simulations; graded
release schema tend to be forgiving of kinetic imprecision.  It will, however,
be found wanting in studies of or critically depending upon GABA receptor kinetics.  

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ENDCOMMENT


NEURON {				
	POINT_PROCESS GradGABAa		
	POINTER PreActiv
	RANGE C, g, gmax, Erev, timestep, tau, g_inf, vref, thres, slop
	NONSPECIFIC_CURRENT i
}

UNITS {
	(nA) = (nanoamp)
	(mV) = (millivolt)
	(umho) = (micromho)
	(mM) = (milli/liter)
}

PARAMETER {

	Erev	 = -70	 (mV)			: reversal potential 
	gmax	 = 0	 (uS)			: maximum conductance
	tau 	 = 3 	 (ms)

	g_inf 	 = 0 	 (umho)
	vref     = 1    (mV)                    : sert juste a l'homogeneite des calculs
	thres    = -45  (mV) 
	slop	 = 0.2			 	: no unit	
}

ASSIGNED {
	v		(mV)		: postsynaptic voltage
	i 		(nA)		: current = g*(v - Erev)
	g 		(umho)		: conductance
	C				: analog of transmitter concentration or synapse activity
	PreActiv			: pointer to presynaptic variable
}

INITIAL {
	C = 0
	g = 0
}

BREAKPOINT { LOCAL delta_g
	  
	C = 1/(1+exp(4*slop*(thres-PreActiv)/vref))  : sigmoid 0.6/4 is the max slope at -45mV
					   	     : values fitted to get the wanted effect

	g_inf = gmax* C	
	delta_g = (dt/2) * (g_inf-g)/tau      : exponential function
					      : breakpoint called twice per time step then dt/2

	g = g + delta_g	

	:i=0

	i = (g*(v-Erev))
	:if ( i > 5 ){
	:	i=5	:to avoid bug
	:} 
	:optional to make the GABA conductnace  only inhibiting
	:if ( i < 0 ) {
	:	i=0	:to avoid bug 
	:}
}