AP back-prop. explains threshold variability and rapid rise (McCormick et al. 2007, Yu et al. 2008)

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Accession:135839
This simple axon-soma model explained how the rapid rising phase in the somatic spike is derived from the propagated axon initiated spike, and how the somatic spike threshold variance is affected by spike propagation.
References:
1 . McCormick DA, Shu Y, Yu Y (2007) Hodgkin and Huxley model still standing? Nature 445:E1-E2 [PubMed]
2 . Yu Y, Shu Y, McCormick DA (2008) Cortical action potential backpropagation explains spike threshold variability and rapid-onset kinetics. J Neurosci 28:7260-72 [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: Neocortex;
Cell Type(s): Neocortex V1 L6 pyramidal corticothalamic cell; Neocortex V1 L2/6 pyramidal intratelencephalic cell;
Channel(s): I Na,t; I L high threshold; I T low threshold; I A; I K; I M; I h; I K,Ca; I_AHP;
Gap Junctions:
Receptor(s): GabaA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Detailed Neuronal Models;
Implementer(s):
Search NeuronDB for information about:  Neocortex V1 L6 pyramidal corticothalamic cell; Neocortex V1 L2/6 pyramidal intratelencephalic cell; GabaA; NMDA; I Na,t; I L high threshold; I T low threshold; I A; I K; I M; I h; I K,Ca; I_AHP;
/
McCormickEtAl2007YuEtAl2008
readme.txt
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 *
for_plot_spike.m
mosinit.hoc
neuron_soma.dat
Rapid_rising_somatic_spike_soma_axon.hoc
                            
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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