Impact of dendritic atrophy on intrinsic and synaptic excitability (Narayanan & Chattarji, 2010)

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Accession:147867
These simulations examined the atrophy induced changes in electrophysiological properties of CA3 pyramidal neurons. We found these neurons change from bursting to regular spiking as atrophy increases. Region-specific atrophy induced region-specific increases in synaptic excitability in a passive dendritic tree. All dendritic compartments of an atrophied neuron had greater synaptic excitability and a larger voltage transfer to the soma than the control neuron.
Reference:
1 . Narayanan R, Chattarji S (2010) Computational analysis of the impact of chronic stress on intrinsic and synaptic excitability in the hippocampus. J Neurophysiol 103:3070-83 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Synapse; Dendrite;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA3 pyramidal GLU cell;
Channel(s): I Na,t; I L high threshold; I N; I T low threshold; I A; I K; I M; I h; I K,Ca; I Calcium; I_AHP;
Gap Junctions:
Receptor(s): AMPA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Active Dendrites; Influence of Dendritic Geometry; Detailed Neuronal Models; Action Potentials; Conductance distributions;
Implementer(s): Narayanan, Rishikesh [rishi at iisc.ac.in];
Search NeuronDB for information about:  Hippocampus CA3 pyramidal GLU cell; AMPA; I Na,t; I L high threshold; I N; I T low threshold; I A; I K; I M; I h; I K,Ca; I Calcium; I_AHP; Glutamate;
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CA3Atrophy
Input
README.html
ampa.mod
borgkm.mod *
cadiv.mod *
cagk.mod *
cal2.mod *
can2.mod *
cat.mod *
h.mod
kad.mod
kahp.mod *
kap.mod
kdr.mod *
nahh.mod *
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Fig1D.hoc
Fig2D-E.hoc
Fig2F-G.hoc
Menu.png
mosinit.hoc
neuron.que
Neurons.inp
                            
TITLE I-h channel from Magee 1998
: Modified to make it slower according to SfN 2006 Poster 342.23.
: The peak activation time constant of Ih is around 100ms, around
: twice slower than that at CA1. And vhalf is around -89 mV, which
: is similar to what one sees in CA1 dendrites

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

}

PARAMETER {
	v 		(mV)
        ehd  		(mV)        
	celsius 	(degC)
	ghdbar=.0001 	(mho/cm2)
        vhalfl=-89   	(mV)
	kl=-8
        vhalft=-75   	(mV)
        a0t=0.005      	(/ms) :original 0.011
        zetat=2.2    	(1)
        gmt=.4   	(1)
	q10=4.5
	qtl=1
}

NEURON {
	SUFFIX hd
	NONSPECIFIC_CURRENT i
        RANGE ghdbar, vhalfl
        GLOBAL linf,taul
}

STATE {
        l
}

ASSIGNED {
	i (mA/cm2)
        linf      
        taul
        ghd
}

INITIAL {
	rate(v)
	l=linf
}

BREAKPOINT {
	SOLVE states METHOD cnexp
	ghd = ghdbar*l
	i = ghd*(v-ehd)

}

FUNCTION alpt(v(mV)) {
  alpt = exp(0.0378*zetat*(v-vhalft)) 
}

FUNCTION bett(v(mV)) {
  bett = exp(0.0378*zetat*gmt*(v-vhalft)) 
}

DERIVATIVE states {     : exact when v held constant; integrates over dt step
        rate(v)
        l' =  (linf - l)/taul
}

PROCEDURE rate(v (mV)) { :callable from hoc
        LOCAL a,qt
        qt=q10^((celsius-33)/10)
        a = alpt(v)
        linf = 1/(1 + exp(-(v-vhalfl)/kl))
:       linf = 1/(1+ alpl(v))
        taul = bett(v)/(qtl*qt*a0t*(1+a))
}

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