CA1 pyramidal neuron: rebound spiking (Ascoli et al.2010)

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Accession:126776
The model demonstrates that CA1 pyramidal neurons support rebound spikes mediated by hyperpolarization-activated inward current (Ih), and normally masked by A-type potassium channels (KA). Partial KA reduction confined to one or few branches of the apical tuft may be sufficient to elicit a local spike following a train of synaptic inhibition. These data suggest that the plastic regulation of KA can provide a dynamic switch to unmask post-inhibitory spiking in CA1 pyramidal neurons, further increasing the signal processing power of the CA1 synaptic microcircuitry.
Reference:
1 . Ascoli GA, Gasparini S, Medinilla V, Migliore M (2010) Local control of postinhibitory rebound spiking in CA1 pyramidal neuron dendrites. J Neurosci 30:6434-42 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Dendrite;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Na,t; I A; I h; I Potassium;
Gap Junctions:
Receptor(s): Gaba;
Gene(s):
Transmitter(s): Gaba;
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Activity Patterns; Dendritic Action Potentials; Active Dendrites; Detailed Neuronal Models; Action Potentials; Intrinsic plasticity; Synaptic Integration;
Implementer(s): Migliore, Michele [Michele.Migliore at Yale.edu];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; Gaba; I Na,t; I A; I h; I Potassium; Gaba;
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rebound
readme.html
h.mod
kadist.mod *
kaprox.mod *
kdrca1.mod *
na3n.mod *
naxn.mod *
4-ap.jpg
4-ap_plus_zd.jpg
control.jpg
fixnseg.hoc *
mod_func.c
mosinit.hoc
pc2b.hoc *
rebound.hoc
rebound.ses
                            
TITLE K-A channel from Klee Ficker and Heinemann
: modified to account for Dax A Current ----------
: M.Migliore Jun 1997

UNITS {
        (mA) = (milliamp)
        (mV) = (millivolt)
}

PARAMETER {
	celsius
        v (mV)
        gkabar=.008 (mho/cm2)
        vhalfn=-1   (mV)
        vhalfl=-56   (mV)
        a0l=0.05      (/ms)
        a0n=.1    (/ms)
        zetan=-1.8    (1)
        zetal=3    (1)
        gmn=0.39   (1)
        gml=1   (1)
        lmin=2  (mS)
        nmin=0.2  (mS)
        pw=-1    (1)
        tq=-40
        qq=5
        q10=5
        qtl=1
	ek
}


NEURON {
        SUFFIX kad
        USEION k READ ek WRITE ik
        RANGE gkabar,gka
        GLOBAL ninf,linf,taul,taun,lmin
}

STATE {
        n
        l
}

ASSIGNED {
        ik (mA/cm2)
        ninf
        linf      
        taul
        taun
        gka
}

BREAKPOINT {
        SOLVE states METHOD cnexp
        gka = gkabar*n*l
        ik = gka*(v-ek)

}

INITIAL {
	rates(v)
	n=ninf
	l=linf
}


FUNCTION alpn(v(mV)) {
LOCAL zeta
  zeta=zetan+pw/(1+exp((v-tq)/qq))
  alpn = exp(1.e-3*zeta*(v-vhalfn)*9.648e4/(8.315*(273.16+celsius))) 
}

FUNCTION betn(v(mV)) {
LOCAL zeta
  zeta=zetan+pw/(1+exp((v-tq)/qq))
  betn = exp(1.e-3*zeta*gmn*(v-vhalfn)*9.648e4/(8.315*(273.16+celsius))) 
}

FUNCTION alpl(v(mV)) {
  alpl = exp(1.e-3*zetal*(v-vhalfl)*9.648e4/(8.315*(273.16+celsius))) 
}

FUNCTION betl(v(mV)) {
  betl = exp(1.e-3*zetal*gml*(v-vhalfl)*9.648e4/(8.315*(273.16+celsius)))
 
}

DERIVATIVE states {  
        rates(v)
        n' = (ninf - n)/taun
        l' = (linf - l)/taul
}

PROCEDURE rates(v (mV)) { :callable from hoc
        LOCAL a,qt
        qt=q10^((celsius-24)/10)
        a = alpn(v)
        ninf = 1/(1 + a)
        taun = betn(v)/(qt*a0n*(1+a))
        if (taun<nmin) {taun=nmin}
        a = alpl(v)
        linf = 1/(1+ a)
        taul = 0.26*(v+50)/qtl
        if (taul<lmin/qtl) {taul=lmin/qtl}
}


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