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 pyramidal corticothalamic L6 cell; Neocortex V1 pyramidal intratelencephalic L2-6 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 pyramidal corticothalamic L6 cell; Neocortex V1 pyramidal intratelencephalic L2-6 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;
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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
                            
:26 Ago 2002 Modification of original channel to allow variable time step and to correct an initialization error.
:    Done by Michael Hines(michael.hines@yale.e) and Ruggero Scorcioni(rscorcio@gmu.edu) at EU Advance Course in Computational Neuroscience. Obidos, Portugal
 



TITLE decay of internal calcium concentration
:
: Internal calcium concentration due to calcium currents and pump.
: Differential equations.
:
: Simple model of ATPase pump with 3 kinetic constants (Destexhe 92)
:     Cai + P <-> CaP -> Cao + P  (k1,k2,k3)
: A Michaelis-Menten approximation is assumed, which reduces the complexity
: of the system to 2 parameters: 
:       kt = <tot enzyme concentration> * k3  -> TIME CONSTANT OF THE PUMP
:	kd = k2/k1 (dissociation constant)    -> EQUILIBRIUM CALCIUM VALUE
: The values of these parameters are chosen assuming a high affinity of 
: the pump to calcium and a low transport capacity (cfr. Blaustein, 
: TINS, 11: 438, 1988, and references therein).  
:
: Units checked using "modlunit" -> factor 10000 needed in ca entry
:
: VERSION OF PUMP + DECAY (decay can be viewed as simplified buffering)
:
: All variables are range variables
:
:
: This mechanism was published in:  Destexhe, A. Babloyantz, A. and 
: Sejnowski, TJ.  Ionic mechanisms for intrinsic slow oscillations in
: thalamic relay neurons. Biophys. J. 65: 1538-1552, 1993)
:
: Written by Alain Destexhe, Salk Institute, Nov 12, 1992
:

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

NEURON {
	SUFFIX cad
	USEION ca READ ica, cai WRITE cai
	RANGE ca
	GLOBAL depth,cainf,taur
}

UNITS {
	(molar) = (1/liter)			: moles do not appear in units
	(mM)	= (millimolar)
	(um)	= (micron)
	(mA)	= (milliamp)
	(msM)	= (ms mM)
	FARADAY = (faraday) (coulomb)
}


PARAMETER {
	depth	= .1	(um)		: depth of shell
	taur	= 200	(ms)		: rate of calcium removal
	cainf	= 100e-6(mM)
	cai		(mM)
}

STATE {
	ca		(mM) <1e-5>
}

INITIAL {
	ca = cainf
	cai = ca
}

ASSIGNED {
	ica		(mA/cm2)
	drive_channel	(mM/ms)
}
	
BREAKPOINT {
	SOLVE state METHOD derivimplicit
}

DERIVATIVE state { 

	drive_channel =  - (10000) * ica / (2 * FARADAY * depth)
	if (drive_channel <= 0.) { drive_channel = 0. }	: cannot pump inward

	ca' = drive_channel + (cainf-ca)/taur
	cai = ca
}








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