Synaptic transmission at the calyx of Held (Graham et al 2001)

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Accession:19747
This model allows the user to investigate faciliation and depression in a complex Monte Carlo model of the calyx of Held, a giant synapse in the mammalian auditory system (Graham et al, 2001)
Reference:
1 . Graham BP, Wong AYC, Forsythe ID (2001) A computational model of synaptic transmission at the calyx of Held Neurocomputing 38:37-42
Model Information (Click on a link to find other models with that property)
Model Type: Synapse;
Brain Region(s)/Organism:
Cell Type(s):
Channel(s):
Gap Junctions:
Receptor(s): Glutamate;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Facilitation; Depression; Vestibular;
Implementer(s): Graham, Bruce [B.Graham at cs.stir.ac.uk];
Search NeuronDB for information about:  Glutamate; Glutamate;
TITLE Model of AMPA receptors

COMMENT
-----------------------------------------------------------------------------

    Kinetic model of AMPA receptors
    ===============================

    6-state gating model:
    (scheme 1 from Raman and Trussell, Neuron 9:173-186, 1992)
        2 open states provide dual exponential response.
  
               O1
               |
    C -- C1 -- C2 -- O2
               |
               D

-----------------------------------------------------------------------------

  This mod file does not include mechanisms for the release and time course
  of transmitter; it is to be used in conjunction with a sepearate mechanism
  to describe the release of transmitter and that provides the concentration
  of transmitter in the synaptic cleft (to be connected to pointer C here).

  Default parameters are set for a miniature EPSC.

  Code based on Destexhe's ampa5.mod

B. Graham, Dept. of Computing Science & Maths, University of Stirling
(Contact: b.graham@cs.stir.ac.uk)
(previously IANC, Division of Informatics, University of Edinburgh)

CNS 2000 Version (19/11/02)
-----------------------------------------------------------------------------
ENDCOMMENT

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

NEURON {
    POINT_PROCESS AMPA
    POINTER C
    RANGE C0, C1, C2, D, O1, O2
    RANGE g, gmax, rb
    GLOBAL Erev
    GLOBAL Rb, Ru1, Ru2, Rd, Rr, Ro1, Rc1, Ro2, Rc2
    GLOBAL vmin, vmax
    NONSPECIFIC_CURRENT i
}

UNITS {
    (nA) = (nanoamp)
    (mV) = (millivolt)
    (pS) = (picosiemens)
    (umho) = (micromho)
    (mM) = (milli/liter)
    (uM) = (micro/liter)
}

PARAMETER {

    Erev    = 7    (mV) : reversal potential
    gmax    = 500  (pS)  : maximal conductance
    vmin = -120 (mV)
    vmax = 100  (mV)
    
: Rates

    Rb  = 13   (/mM /ms): binding 
                : diffusion limited (DO NOT ADJUST)
    Ru1 = 0.3  (/ms)    : unbinding (1st site)
    Ru2 = 200  (/ms)    : unbinding (2nd site)      
    Rd  = 30.0   (/ms)  : desensitization
    Rr  = 0.02 (/ms)    : resensitization 
    Ro1 = 100    (/ms)  : opening (fast)
    Rc1 = 2    (/ms)  : closing
    Ro2 = 2    (/ms)   : opening (slow)
    Rc2 = 0.25    (/ms) : closing
}

ASSIGNED {
    v       (mV)    : postsynaptic voltage
    i       (nA)    : current = g*(v - Erev)
    g       (pS)    : conductance
    C       (mM)    : pointer to glutamate concentration
    rb      (/ms)   : binding
}

STATE {
    : Channel states (all fractions)
    C0      : unbound
    C1      : single glu bound
    C2      : double glu bound
    D       : single glu bound, desensitized
    O1      : open state 1
    O2      : open state 2
}

INITIAL {
    C0=1
    C1=0
    C2=0
    D=0
    O1=0
    O2=0
}

BREAKPOINT {
    SOLVE kstates METHOD sparse

    g = gmax * (O1 + O2)
    i = (1e-6) * g * (v - Erev)
}

KINETIC kstates {
    
    rb = Rb * C 

    ~ C0  <-> C1    (rb,Ru1)
    ~ C1 <-> C2 (rb,Ru2)
    ~ C2 <-> D  (Rd,Rr)
    ~ C2 <-> O1 (Ro1,Rc1)
    ~ C2 <-> O2 (Ro2,Rc2)

    CONSERVE C0+C1+C2+D+O1+O2 = 1
}

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