Inhibition of bAPs and Ca2+ spikes in a multi-compartment pyramidal neuron model (Wilmes et al 2016)

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Accession:187603
"Synaptic plasticity is thought to induce memory traces in the brain that are the foundation of learning. To ensure the stability of these traces in the presence of further learning, however, a regulation of plasticity appears beneficial. Here, we take up the recent suggestion that dendritic inhibition can switch plasticity of excitatory synapses on and off by gating backpropagating action potentials (bAPs) and calcium spikes, i.e., by gating the coincidence signals required for Hebbian forms of plasticity. We analyze temporal and spatial constraints of such a gating and investigate whether it is possible to suppress bAPs without a simultaneous annihilation of the forward-directed information flow via excitatory postsynaptic potentials (EPSPs). In a computational analysis of conductance-based multi-compartmental models, we demonstrate that a robust control of bAPs and calcium spikes is possible in an all-or-none manner, enabling a binary switch of coincidence signals and plasticity. ..."
Reference:
1 . Wilmes KA, Sprekeler H, Schreiber S (2016) Inhibition as a Binary Switch for Excitatory Plasticity in Pyramidal Neurons. PLoS Comput Biol 12:e1004768 [PubMed]
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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; Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal GLU cell; Neocortex V1 L6 pyramidal corticothalamic GLU cell;
Channel(s):
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: NEURON; Python;
Model Concept(s): Dendritic Action Potentials; Synaptic Plasticity; Synaptic Integration;
Implementer(s): Wilmes, Katharina A. [katharina.wilmes at googlemail.com];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; Neocortex V1 L6 pyramidal corticothalamic GLU cell;
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WilmesEtAl2016
mod_files
cad2.mod *
hh2.mod *
hh3.mod
it2.mod *
kap.mod *
kca.mod *
kdrca1.mod *
na3.mod *
na3dend.mod
na3shifted.mod *
sca.mod *
stdp_ca.mod
stdp_m.mod
                            
COMMENT

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)
} 

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
	gk = tadj*gbar*n
	ik = (1e-4) * gk * (v - ek)
} 

LOCAL nexp

PROCEDURE states() {   :Computes state variable n 
        rates(cai)      :             at the current v and dt.
        n = n + nexp*(ninf-n)

        VERBATIM
        return 0;
        ENDVERBATIM
}

PROCEDURE rates(cai(mM)) {  

        LOCAL tinc

        a = Ra * cai^caix
        b = Rb
        ntau = 1/(a+b)
	ninf = a*ntau

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

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