Coincident signals in Olfactory Bulb Granule Cell spines (Aghvami et al 2019)

 Download zip file   Auto-launch 
Help downloading and running models
Accession:244687
"In the mammalian olfactory bulb, the inhibitory axonless granule cells (GCs) feature reciprocal synapses that interconnect them with the principal neurons of the bulb, mitral, and tufted cells. These synapses are located within large excitable spines that can generate local action potentials (APs) upon synaptic input (“spine spike”). Moreover, GCs can fire global APs that propagate throughout the dendrite. Strikingly, local postsynaptic Ca2+ entry summates mostly linearly with Ca2+ entry due to coincident global APs generated by glomerular stimulation, although some underlying conductances should be inactivated. We investigated this phenomenon by constructing a compartmental GC model to simulate the pairing of local and global signals as a function of their temporal separation ?t. These simulations yield strongly sublinear summation of spine Ca2+ entry for the case of perfect coincidence ?t = 0 ms. ..."
Reference:
1 . Aghvami SS, Müller M, Araabi BN, Egger V (2019) Coincidence Detection within the Excitable Rat Olfactory Bulb Granule Cell Spines. J Neurosci 39:584-595 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Dendrite; Channel/Receptor; Synapse;
Brain Region(s)/Organism: Olfactory bulb;
Cell Type(s): Olfactory bulb main interneuron granule MC GABA cell; Olfactory bulb main interneuron granule TC GABA cell;
Channel(s): Ca pump; I Calcium; I K; I Sodium;
Gap Junctions:
Receptor(s): NMDA; AMPA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON; Python;
Model Concept(s): Active Dendrites; Calcium dynamics; Coincidence Detection;
Implementer(s): Aghvami, S. Sara [ssa.aghvami at gmail.com];
Search NeuronDB for information about:  Olfactory bulb main interneuron granule MC GABA cell; Olfactory bulb main interneuron granule TC GABA cell; AMPA; NMDA; I K; I Sodium; I Calcium; Ca pump; Glutamate;
TITLE detailed model of glutamate AMPA receptors

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

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

	6-state gating model:
	similar to that suggested by
 	Patneau and Mayer, Neuron 6:785 (1991)
	Patneau et al, J Neurosci 13:3496 (1993)
  
	C ---- C1 -- C2 -- O
	       |     |
      	       D1    D2

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

  Based on voltage-clamp recordings of AMPA receptor-mediated currents in rat
  hippocampal slices (Xiang et al., J. Neurophysiol. 71: 2552-2556, 1994), this
  model was fit directly to experimental recordings in order to obtain the
  optimal values for the parameters (see Destexhe, Mainen and Sejnowski, 1996).

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

  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).

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

  See details in:

  Destexhe, A., Mainen, Z.F. and Sejnowski, T.J.  Kinetic models of 
  synaptic transmission.  In: Methods in Neuronal Modeling (2nd edition; 
  edited by Koch, C. and Segev, I.), MIT press, Cambridge, 1998, pp. 1-25.

  (electronic copy available at http://cns.iaf.cnrs-gif.fr)



  Alain Destexhe and Zach Mainen, 1995

-----------------------------------------------------------------------------
ENDCOMMENT

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

NEURON {
	POINT_PROCESS AMPA5
	POINTER C
	RANGE C0, C1, C2, D1, D2, O
	RANGE g, gmax, rb, i :i added by sara
	GLOBAL Erev
	GLOBAL Rb, Ru1, Ru2, Rd, Rr, Ro, Rc
	GLOBAL vmin, vmax
	NONSPECIFIC_CURRENT i
}

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

PARAMETER {

	Erev	= 0    (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	= 0.0059  (/ms)	: unbinding (1st site)
	Ru2	= 86  (/ms)	: unbinding (2nd site)		
	Rd	= 0.9   (/ms)	: desensitization
	Rr	= 0.064 (/ms)	: resensitization 
	Ro	= 2.7    (/ms)	: opening
	Rc	= 0.2    (/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
 	D1		: single glu bound, desensitized
 	D2		: double glu bound, desensitized
	O		: open state 2
}

INITIAL {
	C0=1
	C1=0
	C2=0
	D1=0
	D2=0
	O=0
}

BREAKPOINT {
	SOLVE kstates METHOD sparse

	g = gmax * O
	i = (1e-6) * g * (v - Erev)
}

KINETIC kstates {
	
	rb = Rb * C 

	~ C0  <-> C1	(rb,Ru1)
	~ C1 <-> C2	(rb,Ru2)
	~ C1 <-> D1	(Rd,Rr)
	~ C2 <-> D2	(Rd,Rr)
	~ C2 <-> O	(Ro,Rc)

	CONSERVE C0+C1+C2+D1+D2+O = 1
}


Loading data, please wait...