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.
Reference:
1 . Stadler K, Bierwirth C, Stoenica L, Battefeld A, Reetz O, Mix E, Schuchmann S, Velmans T, Ros (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-β-induced neuronal excitability changes in neocortical pyramidal neurons Journal of Neuroinflammation 11(1):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 pyramidal corticothalamic L6 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 pyramidal corticothalamic L6 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

na.mod

Sodium channel, Hodgkin-Huxley style kinetics.  

Kinetics were fit to data from Huguenard et al. (1988) and Hamill et
al. (1991)

qi is not well constrained by the data, since there are no points
between -80 and -55.  So this was fixed at 5 while the thi1,thi2,Rg,Rd
were optimized using a simplex least square proc

voltage dependencies are shifted approximately from the best
fit to give higher threshold

Author: Zach Mainen, Salk Institute, 1994, zach@salk.edu

May 2006: set the tha -28 mV, vshift 0 and thinf -55 mV to comply with measured 
Somatic Na+ kinetics in neocortex. Kole, ANU, 2006

ENDCOMMENT

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

NEURON {
	SUFFIX na
	USEION na READ ena WRITE ina
	RANGE m, h, gna, gbar
	GLOBAL tha, thi1, thi2, qa, qi, qinf, thinf
	RANGE minf, hinf, mtau, htau
	GLOBAL Ra, Rb, Rd, Rg
	GLOBAL q10, temp, tadj, vmin, vmax, vshift
}

PARAMETER {
	gbar = 1000   	(pS/um2)	: 0.12 mho/cm2
	vshift = 0	(mV)		: voltage shift (affects all)
								
	tha  = -28	(mV)		: v 1/2 for act		(-42)
	qa   = 9	(mV)			: act slope		
	Ra   = 0.182	(/ms)	: open (v)		
	Rb   = 0.124	(/ms)	: close (v)		

	thi1  = -50	(mV)		: v 1/2 for inact 	
	thi2  = -75	(mV)		: v 1/2 for inact 	
	qi   = 5	(mV)	        	: inact tau slope
	thinf  = -55	(mV)		: inact inf slope	
	qinf  = 6.2	(mV)		: inact inf slope
	Rg   = 0.0091	(/ms)	: inact (v)	
	Rd   = 0.024	(/ms)	: inact recov (v) 

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

	v 		(mV)
	dt		(ms)
	celsius		(degC)
	vmin = -120	(mV)
	vmax = 100	(mV)
}


UNITS {
	(mA) = (milliamp)
	(mV) = (millivolt)
	(pS) = (picosiemens)
	(um) = (micron)
} 

ASSIGNED {
	ina 		(mA/cm2)
	gna		(pS/um2)
	ena		(mV)
	minf 		hinf
	mtau (ms)	htau (ms)
	tadj
}
 

STATE { m h }

INITIAL { 
	trates(v+vshift)
	m = minf
	h = hinf
}

BREAKPOINT {
        SOLVE states METHOD cnexp
        gna = tadj*gbar*m*m*m*h
	ina = (1e-4) * gna * (v - ena)
} 

LOCAL mexp, hexp 

DERIVATIVE states {   :Computes state variables m, h, and n 
        trates(v+vshift)      :             at the current v and dt.
        m' =  (minf-m)/mtau
        h' =  (hinf-h)/htau
}

PROCEDURE trates(v) {  
                      
        
        TABLE minf,  hinf, mtau, htau
	DEPEND  celsius, temp, Ra, Rb, Rd, Rg, tha, thi1, thi2, qa, qi, qinf
	
	FROM vmin TO vmax WITH 199

	rates(v): not consistently executed from here if usetable == 1

:        tinc = -dt * tadj

:        mexp = 1 - exp(tinc/mtau)
:        hexp = 1 - exp(tinc/htau)
}


PROCEDURE rates(vm) {  
        LOCAL  a, b

	a = trap0(vm,tha,Ra,qa)
	b = trap0(-vm,-tha,Rb,qa)

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

	mtau = 1/tadj/(a+b)
	minf = a/(a+b)

		:"h" inactivation 

	a = trap0(vm,thi1,Rd,qi)
	b = trap0(-vm,-thi2,Rg,qi)
	htau = 1/tadj/(a+b)
	hinf = 1/(1+exp((vm-thinf)/qinf))
}


FUNCTION trap0(v,th,a,q) {
	if (fabs(v/th) > 1e-6) {
	        trap0 = a * (v - th) / (1 - exp(-(v - th)/q))
	} else {
	        trap0 = a * q
 	}
}	






Stadler K, Bierwirth C, Stoenica L, Battefeld A, Reetz O, Mix E, Schuchmann S, Velmans T, Ros (2014) Elevation in type I interferons inhibits HCN1 and slows cortical neuronal oscillations. Cereb Cortex 24:199-210[PubMed]

References and models cited by this paper

References and models that cite this paper

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(47 refs)

Reetz O, Stadler K, Strauss U (2014) Protein kinase C activation mediates interferon-β-induced neuronal excitability changes in neocortical pyramidal neurons Journal of Neuroinflammation 11(1):185[PubMed]

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   Pyramidal Neuron Deep: attenuation in dendrites (Stuart, Spruston 1998) [Model]

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