Firing neocortical layer V pyramidal neuron (Reetz et al. 2014; Stadler et al. 2014)

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Accession:168148
Neocortical Layer V model with firing behaviour adjusted to in vitro observations. The model was used to investigate the effects of IFN and PKC on the excitability of neurons (Stadler et al 2014, Reetz et al. 2014). The model contains new channel simulations for HCN1, HCN2 and the big calcium dependent potassium channel BK.
References:
1 . Stadler K, Bierwirth C, Stoenica L, Battefeld A, Reetz O, Mix E, Schuchmann S, Velmans T, Rosenberger K, Bräuer AU, Lehnardt S, Nitsch R, Budt M, Wolff T, Kole MH, Strauss U (2014) Elevation in type I interferons inhibits HCN1 and slows cortical neuronal oscillations. Cereb Cortex 24:199-210 [PubMed]
2 . Reetz O, Stadler K, Strauss U (2014) Protein kinase C activation mediates interferon-ß-induced neuronal excitability changes in neocortical pyramidal neurons. J Neuroinflammation 11:185 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism: Neocortex;
Cell Type(s): Neocortex V1 L6 pyramidal corticothalamic GLU cell;
Channel(s): I Na,p; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I Sodium; I Calcium; I Mixed; I Potassium; I Q;
Gap Junctions:
Receptor(s):
Gene(s): HCN1; HCN2;
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Activity Patterns; Detailed Neuronal Models; Action Potentials; Signaling pathways;
Implementer(s): Stadler, Konstantin [konstantin.stadler at ntnu.no];
Search NeuronDB for information about:  Neocortex V1 L6 pyramidal corticothalamic GLU cell; I Na,p; I Na,t; I L high threshold; I A; I K; I M; I h; I K,Ca; I Sodium; I Calcium; I Mixed; I Potassium; I Q;
COMMENT
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

kca.mod

Calcium-dependent potassium channel
Based on
Pennefather (1990) -- sympathetic ganglion cells
taken from
Reuveni et al (1993) -- neocortical cells

Author: Zach Mainen, Salk Institute, 1995, zach@salk.edu
	
ENDCOMMENT

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

NEURON {
	SUFFIX kca
	USEION k READ ek WRITE ik
	USEION ca READ cai
	RANGE n, gk, gbar
	RANGE ninf, ntau
	GLOBAL Ra, Rb, caix
	GLOBAL q10, temp, tadj, vmin, vmax
}

UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(pS) = (picosiemens)
	(um) = (micron)
	(molar) = (1/liter)
	(mM) 	= (millimolar)
} 

PARAMETER {
	gbar = 10   	(pS/um2)	: 0.03 mho/cm2
	v 		(mV)
	cai  		(mM)
	caix = 1	
									
	Ra   = 0.01	(/ms)		: max act rate  
	Rb   = 0.02	(/ms)		: max deact rate 

	dt		(ms)
	celsius		(degC)
	temp = 23	(degC)		: original temp 	
	q10  = 2.3			: temperature sensitivity

	vmin = -120	(mV)
	vmax = 100	(mV)
} 


ASSIGNED {
	a		(/ms)
	b		(/ms)
	ik 		(mA/cm2)
	gk		(pS/um2)
	ek		(mV)
	ninf
	ntau 		(ms)	
	tadj
}
 

STATE { n }

INITIAL { 
	rates(cai)
	n = ninf
}

BREAKPOINT {
        SOLVE states METHOD cnexp
	gk = tadj*gbar*n
	ik = (1e-4) * gk * (v - ek)
} 

LOCAL nexp

DERIVATIVE states {   :Computes state variable n 
        rates(cai)      :             at the current v and dt.
        n' =  (ninf-n)/ntau

}

PROCEDURE rates(cai(mM)) {  

        

        a = Ra * cai^caix
        b = Rb

        tadj = q10^((celsius - temp)/10)

        ntau = 1/tadj/(a+b)
	ninf = a/(a+b)

 
:        tinc = -dt * tadj
:        nexp = 1 - exp(tinc/ntau)
}












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