Intracortical synaptic potential modulation by presynaptic somatic potential (Shu et al. 2006, 2007)

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Accession:135787
" ... Here we show that the voltage fluctuations associated with dendrosomatic synaptic activity propagate significant distances along the axon, and that modest changes in the somatic membrane potential of the presynaptic neuron modulate the amplitude and duration of axonal action potentials and, through a Ca21- dependent mechanism, the average amplitude of the postsynaptic potential evoked by these spikes. These results indicate that synaptic activity in the dendrite and soma controls not only the pattern of action potentials generated, but also the amplitude of the synaptic potentials that these action potentials initiate in local cortical circuits, resulting in synaptic transmission that is a mixture of triggered and graded (analogue) signals."
References:
1 . Shu Y, Duque A, Yu Y, Haider B, McCormick DA (2007) Properties of action-potential initiation in neocortical pyramidal cells: evidence from whole cell axon recordings. J Neurophysiol 97:746-60 [PubMed]
2 . Shu Y, Hasenstaub A, Duque A, Yu Y, McCormick DA (2006) Modulation of intracortical synaptic potentials by presynaptic somatic membrane potential. Nature 441:761-5 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Axon;
Brain Region(s)/Organism:
Cell Type(s): Neocortex V1 pyramidal corticothalamic L6 cell;
Channel(s): I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I_AHP; I_KD;
Gap Junctions:
Receptor(s): GabaA; AMPA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Detailed Neuronal Models; Action Potentials; Synaptic Integration;
Implementer(s):
Search NeuronDB for information about:  Neocortex V1 pyramidal corticothalamic L6 cell; GabaA; AMPA; NMDA; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I_AHP; I_KD;
/
ShuEtAl20062007
readme.txt
ampa5.mod *
ca.mod *
cad.mod
caL3d.mod *
capump.mod
gabaa5.mod *
Gfluct.mod *
ia.mod *
iahp.mod *
iahp2.mod *
ih.mod
im.mod *
kca.mod *
km.mod *
kv.mod *
na.mod *
NMDA_Mg.mod *
nmda5.mod *
release.mod *
2006_Nature.pdf
2006_Nature_supp.pdf
best_full_axon_decay.hoc
best_full_axon_spike_init.hoc
decay_constant.gif
for_decay.m
for_initiation.m
j4a.hoc *
j4a_removedendrite.hoc
j4a_removedendrite1.hoc
j7.hoc *
j8.hoc *
j8_removedendrite.hoc
lcAS3.hoc *
mosinit.hoc
spike_initiation.gif
                            
TITLE detailed model of GABA-A receptors

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

	Kinetic model of GABA-A receptors
	=================================

	5-state gating model from Busch and Sakmann (Cold Spring Harbor
	Symp. Quant. Biol. 55: 69-80, 1990)
  
	C -- C1 -- C2
	     |     |
      	     O1    O2

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

  Based on voltage-clamp recordings of GABAA receptor-mediated currents in rat
  hippocampal slices (Otis and Mody, Neuroscience 49: 13-32, 1992), this model
  was fit directly to experimental recordings in order to obtain the optimal
  values for the parameters (see Destexhe, Mainen and Sejnowski, 1996).

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

  This mod file does not include mechanisms for the release and time course
  of transmitter; it is to be used in conjunction with a sepearate mechanism
  to describe the release of transmitter and that provides the concentration
  of transmitter in the synaptic cleft (to be connected to pointer C here).

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

  See details in:

  Destexhe, A., Mainen, Z.F. and Sejnowski, T.J.  Kinetic models of 
  synaptic transmission.  In: Methods in Neuronal Modeling (2nd edition; 
  edited by Koch, C. and Segev, I.), MIT press, Cambridge, 1998, pp. 1-25.

  (electronic copy available at http://cns.iaf.cnrs-gif.fr)



  Written by Alain Destexhe, Laval University, 1995

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

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

NEURON {
	POINT_PROCESS GABAa5
	POINTER C
	RANGE C0, C1, C2, O1, O2
	RANGE g, gmax, f1, f2
	GLOBAL Erev, kf1, kf2, kb1, kb2, a1, b1, a2, b2
	NONSPECIFIC_CURRENT i
}

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

PARAMETER {

	Erev	= -80    (mV)	: reversal potential
	gmax	= 500  (pS)	: maximal conductance
	
: Rates

	: from Destexhe, Mainen and Sejnowski, 1996

	kf1	= 0.02   (/uM /ms)	: binding 		
	kf2	= 0.01   (/uM /ms)	: binding 		
	kb1	= 4.6	(/ms)	: unbinding		
	kb2	= 9.2	(/ms)	: unbinding		
	a1	= 3.3	(/ms)	: opening
	b1	= 9.8	(/ms)	: closing
	a2	= 10.6	(/ms)	: opening
	b2	= 0.41  (/ms)	: closing
}

COMMENT
	: from Busch and Sakmann

	kf1	= 0.2   (/uM /ms)	: binding 		
	kf2	= 0.1   (/uM /ms)	: binding 		
	kb1	= 3	(/ms)	: unbinding		
	kb2	= 6	(/ms)	: unbinding		
	a1	= 0.7	(/ms)	: opening
	b1	= 4	(/ms)	: closing
	a2	= 10	(/ms)	: opening
	b2	= 0.055 (/ms)	: closing
ENDCOMMENT

ASSIGNED {
	v		(mV)		: postsynaptic voltage
	i 		(nA)		: current = g*(v - Erev)
	g 		(pS)		: conductance
	C 		(mM)		: pointer to glutamate concentration

	f1		(/ms)    : binding
	f2		(/ms)    : binding
}

STATE {
	: Channel states (all fractions)
	C0		: unbound
	C1		: single bound
	C2		: double bound
	O1		: open
	O2		: open
}

INITIAL {
	C0 = 1
	C1 = 0
	C2 = 0
	O1 = 0
	O2 = 0
}

BREAKPOINT {
	SOLVE kstates METHOD sparse

	g = gmax * (O1+O2)
	i = (1e-6) * g * (v - Erev)
}

KINETIC kstates {
	
	f1 = kf1 * (1e3) * C 
	f2 = kf2 * (1e3) * C 

	~ C0 <-> C1	(f1,kb1)
	~ C1 <-> C2	(f2,kb2)
	~ C1 <-> O1	(a1,b1)
	~ C2 <-> O2	(a2,b2)

	CONSERVE C0+C1+C2+O1+O2 = 1
}


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