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

 Download zip file   Auto-launch 
Help downloading and running models
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 transmitter release

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

 Simple (minimal?) model of transmitter release

 - single compartment, need calcium influx and efflux

 - Ca++ binds to a "fusion factor" protein F leading to an activated form FA.
   Assuming a cooperativity factor of 4 (see Augustine & charlton, 
   J Physiol. 381: 619-640, 1986), one obtains:

	F + 4 Cai <-> FA	(kb,ku)

 - FA binds to presynaptic vesicles and activates them according to:

	FA + V <-> VA		(k1,k2)

   VA represents the "activated vesicle" which is able to bind to the
   membrane and release transmitter.  Presynaptic vesicles (V) are 
   considered in excess.

 - VA releases nt transmitter molecules in the synaptic cleft

	VA  ->  nt T		(k3)

   This reaction is the slowest and a constant number of transmitter per 
   vesicule is considered (nt).  

 - Finally, T is hydrolyzed according to a first-order reaction

	T  ->  ...		(kh)


   References:

   Destexhe, A., Mainen, Z.F. and Sejnowski, T.J. Synthesis of models for
   excitable membranes, synaptic transmission and neuromodulation using a 
   common kinetic formalism, Journal of Computational Neuroscience 1: 
   195-230, 1994.

   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)

   For a more realistic model, see Yamada, WM & Zucker, RS. Time course
   of transmitter release calculated from simulations of a calcium
   diffusion model. Biophys. J. 61: 671-5682, 1992.


  Written by A. Destexhe, Salk Institute, December 1993; modified 1996

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


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

NEURON {
	SUFFIX rel
	USEION ca READ cai WRITE cai
	RANGE T,FA,CA,Fmax,Ves,b,u,k1,k2,k3,nt,kh
}

UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(mM) = (milli/liter)
}

PARAMETER {

	Ves = 0.1 	(mM)		: conc of vesicles
	Fmax = 0.001	(mM)		: conc of fusion factor F
	b = 1e16 	(/mM4-ms)	: ca binding to F
	u = 0.1  	(/ms)		: ca unbinding 
	k1 = 1000   	(/mM-ms)	: F binding to vesicle
	k2 = 0.1	(/ms)		: F unbinding to vesicle
	k3 = 4   	(/ms)		: exocytosis of T
	nt = 10000			: nb of molec of T per vesicle
	kh = 10  	(/ms)		: cst for hydolysis of T
}

ASSIGNED {
}

STATE {
	FA	(mM)
	VA	(mM)
	T	(mM)
	cai	(mM) 
}

INITIAL {
	FA = 0
	VA = 0
	T = 0
	cai = 1e-8
}

BREAKPOINT {
	SOLVE state METHOD derivimplicit : see http://www.neuron.yale.edu/phpBB/viewtopic.php?f=28&t=592
}

LOCAL bfc , kfv

DERIVATIVE state {

	bfc = b * (Fmax-FA-VA) * cai^4
	kfv = k1 * FA * Ves

	cai'	= - bfc + 4 * u * FA
	FA'	= bfc - u * FA - kfv + k2 * VA
	VA'	= kfv - (k2+k3) * VA
	T'	= nt * k3 * VA - kh * T
}	


Loading data, please wait...