CA1 pyramidal neuron: synaptically-induced bAP predicts synapse location (Sterratt et al. 2012)

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Accession:144490
This is an adaptation of Poirazi et al.'s (2003) CA1 model that is used to measure BAP-induced voltage and calcium signals in spines after simulated Schaffer collateral synapse stimulation. In the model, the peak calcium concentration is highly correlated with soma-synapse distance under a number of physiologically-realistic suprathreshold stimulation regimes and for a range of dendritic morphologies. There are also simulations demonstrating that peak calcium can be used to set up a synaptic democracy in a homeostatic manner, whereby synapses regulate their synaptic strength on the basis of the difference between peak calcium and a uniform target value.
Reference:
1 . Sterratt DC, Groen MR, Meredith RM, van Ooyen A (2012) Spine calcium transients induced by synaptically-evoked action potentials can predict synapse location and establish synaptic democracy. PLoS Comput Biol 8:e1002545 [PubMed]
Citations  Citation Browser
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): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Na,t; I L high threshold; I T low threshold; I A; I K; I M; I Mixed; I R; I_AHP;
Gap Junctions:
Receptor(s): AMPA; NMDA;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Dendritic Action Potentials; Synaptic Plasticity;
Implementer(s): Sterratt, David ; Groen, Martine R [martine.groen at gmail.com];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; AMPA; NMDA; I Na,t; I L high threshold; I T low threshold; I A; I K; I M; I Mixed; I R; I_AHP;
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bpap
CA1_multi
mechanism
cad.mod *
cagk.mod *
cal.mod *
calH.mod *
car.mod *
cat.mod *
d3.mod *
gabaa.mod *
gabab.mod *
glutamate.mod *
h.mod *
hha_old.mod *
hha2.mod *
kadist.mod *
kaprox.mod *
kca.mod *
km.mod *
nap.mod *
nmda.mod *
somacar.mod *
mosinit.hoc.old *
mosinit.poirazi.hoc *
                            
COMMENT
km.mod
Potassium channel, Hodgkin-Huxley style kinetics
Based on I-M (muscarinic K channel)
Slow, noninactivating
Author: Zach Mainen, Salk Institute, 1995, zach@salk.edu
	
ENDCOMMENT

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

NEURON {
	SUFFIX km
	USEION k READ ek WRITE ik
	RANGE n, gk, gbar
	RANGE ninf, ntau
	GLOBAL Ra, Rb
	GLOBAL q10, temp, tadj, vmin, vmax
}

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

PARAMETER {
	v 		(mV)
	dt		(ms)
	gbar = 10   	(pS/um2)	: 0.03 mho/cm2
	tha  = -30	(mV)		: v 1/2 for inf
	qa   = 9	(mV)		: inf slope		
	Ra   = 0.001	(/ms)		: max act rate  (slow)
	Rb   = 0.001	(/ms)		: max deact rate  (slow)
	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 { 
	trates(v)
	n = ninf
}

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

LOCAL nexp

PROCEDURE states() {   : Computes state variable n 
        trates(v)      : at the current v and dt.
        n = n + nexp*(ninf-n)
        VERBATIM
        return 0;
        ENDVERBATIM
}

PROCEDURE trates(v) {  :Computes rate and other constants at current v.
                       :Call once from HOC to initialize inf at resting v.
        LOCAL tinc
        TABLE ninf, nexp
	DEPEND dt, celsius, temp, Ra, Rb, tha, qa
	
	FROM vmin TO vmax WITH 199

	rates(v): not consistently executed from here if usetable_hh == 1
        tadj = q10^((celsius - temp)/10)  :temperature adjastment
        tinc = -dt * tadj
        nexp = 1 - exp(tinc/ntau)
}


PROCEDURE rates(v) {  :Computes rate and other constants at current v.
                      :Call once from HOC to initialize inf at resting v.

        a = Ra * (v - tha) / (1 - exp(-(v - tha)/qa))
        b = -Rb * (v - tha) / (1 - exp((v - tha)/qa))
        ntau = 1/(a+b)
	ninf = a*ntau
}