A two-layer biophysical olfactory bulb model of cholinergic neuromodulation (Li and Cleland 2013)

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Accession:149739
This is a two-layer biophysical olfactory bulb (OB) network model to study cholinergic neuromodulation. Simulations show that nicotinic receptor activation sharpens mitral cell receptive field, while muscarinic receptor activation enhances network synchrony and gamma oscillations. This general model suggests that the roles of nicotinic and muscarinic receptors in OB are both distinct and complementary to one another, together regulating the effects of ascending cholinergic inputs on olfactory bulb transformations.
Reference:
1 . Li G, Cleland TA (2013) A two-layer biophysical model of cholinergic neuromodulation in olfactory bulb. J Neurosci 33:3037-58 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism:
Cell Type(s): Olfactory bulb main mitral cell; Olfactory bulb main interneuron periglomerular cell; Olfactory bulb main interneuron granule MC cell;
Channel(s): I Na,p; I L high threshold; I T low threshold; I A; I M; I h; I K,Ca; I CAN; I Sodium; I Calcium; I Potassium; I_Ks; I Cl, leak; I Ca,p;
Gap Junctions:
Receptor(s): Nicotinic; GabaA; Muscarinic; AMPA; NMDA;
Gene(s):
Transmitter(s): Acetylcholine;
Simulation Environment: NEURON; MATLAB;
Model Concept(s): Sensory processing; Sensory coding; Neuromodulation; Olfaction;
Implementer(s): Li, Guoshi [guoshi_li at med.unc.edu];
Search NeuronDB for information about:  Olfactory bulb main mitral cell; Olfactory bulb main interneuron periglomerular cell; Olfactory bulb main interneuron granule MC cell; Nicotinic; GabaA; Muscarinic; AMPA; NMDA; I Na,p; I L high threshold; I T low threshold; I A; I M; I h; I K,Ca; I CAN; I Sodium; I Calcium; I Potassium; I_Ks; I Cl, leak; I Ca,p; Acetylcholine;
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Readme.txt
cadecay.mod *
cadecay2.mod *
Caint.mod *
Can.mod *
CaPN.mod *
CaT.mod *
GradeAMPA.mod *
GradeGABA.mod *
GradNMDA.mod *
hpg.mod *
kAmt.mod *
KCa.mod *
KDRmt.mod *
kfasttab.mod *
kM.mod *
KS.mod *
kslowtab.mod *
LCa.mod *
nafast.mod *
NaP.mod *
Naxn.mod *
Nicotin.mod *
nmdanet.mod *
OdorInput.mod *
Background.hoc
Connect.hoc
GC_def.hoc
GC_save.hoc *
GC_Stim.hoc
Input.hoc
MC_def.hoc
MC_save.hoc
MC_Stim.hoc
mod_func.c
mosinit.hoc
OB.hoc
Parameter.hoc
PG_def.hoc
PG_save.hoc *
PG_Stim.hoc
SaveData.hoc
tabchannels.dat *
tabchannels.hoc
                            
: $Id: fvpre.mod,v 1.10 2003/07/29 23:37:22 billl Exp $
COMMENT
synapse taken from Wang, X.-J. and Buzsaki G. (1996) Gamma oscillations by
synaptic inhibition in a hippocampal interneuronal network.  
J. Neurosci. 16, 6402-6413.
ENDCOMMENT
					       
NEURON {
  POINT_PROCESS gradNMDA
  RANGE gmax, g, i, alpha, beta, thetasyn,e, sigma
  GLOBAL mg
  NONSPECIFIC_CURRENT i
  POINTER vpre
}

UNITS {
  (nA) = (nanoamp)
  (mV) = (millivolt)
  (uS) = (microsiemens)
}

PARAMETER {
  gmax  = 1e-3 (uS)
  alpha = 0.0163 (/ms)   : 61.3 ms 
  beta  = 0.00292 (/ms)  :  343 ms
  e     = 0	  (mV)    : reserval potential
  thetasyn = 0 (mV)   : spike threshold
  mg       = 1   (mM) : external magnesium concentration
  sigma    = 2  : !!!
}

ASSIGNED { vpre (mV)
           v (mV) 
		   i (nA)
		   g (uS)
	       B       : magnesium block
}

STATE { s }

INITIAL {
  s =  alpha*F(vpre)/(alpha*F(vpre)+beta)
}

BREAKPOINT {
  SOLVE state METHOD cnexp
  B = mgblock(v)
  g = gmax*s*B
  i = g*(v - e)
}

DERIVATIVE state {
  s' = alpha*F(vpre)*(1-s) - beta*s
}

FUNCTION F (v1 (mV)) {
  F = 1/(1 + exp(-(v1-thetasyn)/sigma))
}  

FUNCTION mgblock(v(mV)) {
        TABLE 
        DEPEND mg
        FROM -140 TO 80 WITH 1000
        : from Jahr & Stevens
        mgblock = 1 / (1 + exp(0.062 (/mV) * -v) * (mg / 3.57 (mM)))
}