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]
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
datastore
pars
plots
poirazi-nmda-car
tests
validation-plots
README.txt
ampa_forti.mod
cacum.mod
cad.mod *
cagk.mod
cal.mod
calH.mod
car.mod
car_mag.mod
cat.mod
d3.mod *
h.mod
hha_old.mod
hha2.mod
kadist.mod
kaprox.mod
kca.mod
km.mod
nap.mod
nmda_andr.mod
somacar.mod
binaverages.m
bpap-cell.hoc
bpap-data.hoc
bpap-dendburst.hoc
bpap-graphics.hoc
bpap-gui.hoc
bpap-gui.ses
bpap-pars.hoc
bpap-record.hoc
bpap-run.hoc
bpap-scaling.hoc
bpap-sims.hoc
bpap-sims-cell1.hoc
bpap-sims-cell2.hoc
bpap-sims-scaling.hoc
bpap-somainj.hoc
bpap-spiketrain.hoc
ca1_mrg_cell1.hoc
ca1_mrg_cell2.hoc
ca1_poirazi.hoc
ChannelBlocker.hoc
CrossingFinder.hoc
epspsizes.hoc
figure-example.R
figures.R
figures-common.R
FileUtils.hoc
FormatFile.hoc
ghk.inc
GraphUtils.hoc
Integrator.hoc
Makefile
mosinit.hoc
NmdaAmpaSpineSynStim.hoc
NmdaAmpaSynStim.hoc
ObjectClass.hoc
plotscalingresults_pergroup1.m
plotscalingresults5.m
PointProcessDistributor.hoc
ReferenceAxis.hoc
removezeros.m
RPlot.hoc
scaling_plots.m
Segment.hoc
SimpleSpine.hoc
Spine.hoc
TreePlot.hoc
TreePlotArray.hoc
triexpsyn.inc
units.inc
utils.hoc
validate-bpap.hoc
VarList.hoc
VCaGraph.hoc
                            
TITLE Slow Ca-dependent potassium current
:
:   Ca++ dependent K+ current IC responsible for slow AHP
:   Differential equations
:
:   Model based on a first order kinetic scheme
:
:       + n cai <->     (alpha,beta)
:
:   Following this model, the activation fct will be half-activated at 
:   a concentration of Cai = (beta/alpha)^(1/n) = cac (parameter)
:
:   The mod file is here written for the case n=2 (2 binding sites)
:   ---------------------------------------------
:
:   This current models the "slow" IK[Ca] (IAHP): 
:      - potassium current
:      - activated by intracellular calcium
:      - NOT voltage dependent
:
:   A minimal value for the time constant has been added
:
:   Ref: Destexhe et al., J. Neurophysiology 72: 803-818, 1994.
:   See also: http://www.cnl.salk.edu/~alain , http://cns.fmed.ulaval.ca
:   modifications by Yiota Poirazi 2001 (poirazi@LNC.usc.edu)
:   taumin = 0.5 ms instead of 0.1 ms	

NEURON {
    SUFFIX kca
    USEION k READ ek WRITE ik
    USEION ca READ cai
    RANGE gk, gbar, m_inf, tau_m, gmax
    GLOBAL beta, cac
}

UNITS {
    (mA) = (milliamp)
    (mV) = (millivolt)
    (molar) = (1/liter)
    (mM) = (millimolar)
}

PARAMETER {
    v                (mV)
    celsius = 36     (degC)
    ek      = -80    (mV)
    cai     = 2.4e-5 (mM)           : initial [Ca]i
    gbar    = 0.01   (mho/cm2)
    beta    = 0.03   (1/ms)          : backward rate constant
    cac     = 0.025  (mM)            : middle point of activation fct
    taumin  = 0.5    (ms)            : minimal value of the time cst
}

STATE {m}        : activation variable to be solved in the DEs       

ASSIGNED {       : parameters needed to solve DE 
    ik      (mA/cm2)
    m_inf
    tau_m   (ms)
    tadj
    gk      (mho/cm2)
    gmax    (mho/cm2)
}
BREAKPOINT { 
    SOLVE states METHOD derivimplicit
    gk = gbar*m*m*m     : maximum channel conductance
    ik = gk*(v - ek)    : potassium current induced by this channel
    if (gk > gmax) {
        gmax = gk
    }
}

DERIVATIVE states { 
    evaluate_fct(v,cai)
    m' = (m_inf - m) / tau_m
}

INITIAL {
    :
    :  activation kinetics are assumed to be at 22 deg. C
    :  Q10 is assumed to be 3
    :
    tadj = 3 ^ ((celsius-22.0(degC))/10(degC)) : temperature-dependent adjastment factor
    evaluate_fct(v,cai)
    m = m_inf
    gk = gbar*m*m*m
    gmax = gk
}

PROCEDURE evaluate_fct(v(mV),cai(mM)) {  LOCAL car
    car = (cai/cac)^2
    m_inf = car / ( 1 + car )      : activation steady state value
    tau_m =  1 / beta / (1 + car) / tadj
    if(tau_m < taumin) { tau_m = taumin }   : activation min value of time cst
}

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