Cerebellar purkinje cell: interacting Kv3 and Na currents influence firing (Akemann, Knopfel 2006)

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Accession:80769
Purkinje neurons spontaneously generate action potentials in the absence of synaptic drive and thereby exert a tonic, yet plastic, input to their target cells in the deep cerebellar nuclei. Purkinje neurons express two ionic currents with biophysical properties that are specialized for high-frequency firing: resurgent sodium currents and potassium currents mediated by Kv3.3. Numerical simulations indicated that Kv3.3 increases the spontaneous firing rate via cooperation with resurgent sodium currents. We conclude that the rate of spontaneous action potential firing of Purkinje neurons is controlled by the interaction of Kv3.3 potassium currents and resurgent sodium currents. See paper for more and details.
Reference:
1 . Akemann W, Knöpfel T (2006) Interaction of Kv3 potassium channels and resurgent sodium current influences the rate of spontaneous firing of Purkinje neurons. J Neurosci 26:4602-12 [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:
Cell Type(s): Cerebellum Purkinje GABA cell;
Channel(s): I Na,t; I A; I K; I h; I K,Ca; I Calcium;
Gap Junctions:
Receptor(s):
Gene(s): Kv1.1 KCNA1; Kv4.3 KCND3; Kv3.3 KCNC3; HCN1;
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Ion Channel Kinetics; Oscillations; Action Potentials; Calcium dynamics;
Implementer(s): Akemann, Walther [akemann at brain.riken.jp];
Search NeuronDB for information about:  Cerebellum Purkinje GABA cell; I Na,t; I A; I K; I h; I K,Ca; I Calcium;
TITLE P-type calcium channel

COMMENT

NEURON implementation of a P-type calcium channel
Kinetical scheme: Hodgkin-Huxley (m), no inactivation

Modified from Khaliq et al., J. Neurosci. 23(2003)4899

Laboratory for Neuronal Circuit Dynamics
RIKEN Brain Science Institute, Wako City, Japan
http://www.neurodynamics.brain.riken.jp

Reference: Akemann and Knoepfel, J.Neurosci. 26 (2006) 4602
Date of Implementation: May 2005
Contact: akemann@brain.riken.jp

ENDCOMMENT

NEURON {
	SUFFIX CaP
	USEION ca READ cai, cao WRITE ica
	RANGE pcabar, ica
	GLOBAL minf, taum
	GLOBAL monovalConc, monovalPerm
}

UNITS {
	(mV) = (millivolt)
	(mA) = (milliamp)
	(nA) = (nanoamp)
	(pA) = (picoamp)
	(S)  = (siemens)
	(nS) = (nanosiemens)
	(pS) = (picosiemens)
	(um) = (micron)
	(molar) = (1/liter)
	(mM) = (millimolar)		
}

CONSTANT {
	q10 = 3
	F = 9.6485e4 (coulombs)
	R = 8.3145 (joule/kelvin)

	cv = 19 (mV)
	ck = 5.5 (mV)
}

PARAMETER {
	v (mV)
	celsius (degC)

	cai (mM)
	cao (mM)

	pcabar = 6e-5 (cm/s)
	monovalConc = 140 (mM)
	monovalPerm = 0
}

ASSIGNED {
	qt
	ica (mA/cm2)
      minf 
	taum (ms)
	T (kelvin)
	E (volt)
	zeta
}

STATE { m }

INITIAL {
	qt = q10^((celsius-22 (degC))/10 (degC))
	T = kelvinfkt( celsius )
	rates(v)
	m = minf
}

BREAKPOINT {
	SOLVE states METHOD cnexp
	ica = (1e3) * pcabar * m * ghk(v, cai, cao, 2)
}

DERIVATIVE states {
	rates(v)
	m' = (minf-m)/taum
}

FUNCTION ghk( v (mV), ci (mM), co (mM), z )  (coulombs/cm3) { 
	E = (1e-3) * v
      zeta = (z*F*E)/(R*T)	
	
	: ci = ci + (monovalPerm) * (monovalConc) :Monovalent permeability

	if ( fabs(1-exp(-zeta)) < 1e-6 ) {
	ghk = (1e-6) * (z*F) * (ci - co*exp(-zeta)) * (1 + zeta/2)
	} else {
	ghk = (1e-6) * (z*zeta*F) * (ci - co*exp(-zeta)) / (1-exp(-zeta))
	}
}

PROCEDURE rates( v (mV) ) {
	minf = 1 / ( 1 + exp(-(v+cv)/ck) )
	taum = (1e3) * taumfkt(v)/qt
}

FUNCTION taumfkt( v (mV) ) (s) {
	UNITSOFF
	if ( v > -50 ) {
	taumfkt = 0.000191 + 0.00376 * exp(-((v+41.9)/27.8)^2)
	} else {
	taumfkt = 0.00026367 + 0.1278 * exp(0.10327*v)
	}
	UNITSON
}

FUNCTION kelvinfkt( t (degC) )  (kelvin) {
	UNITSOFF
	kelvinfkt = 273.19 + t
	UNITSON
}

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