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]
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 GLU cell; Olfactory bulb main interneuron periglomerular GABA cell; Olfactory bulb main interneuron granule MC GABA 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 GLU cell; Olfactory bulb main interneuron periglomerular GABA cell; Olfactory bulb main interneuron granule MC GABA 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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SP
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
                            
TITLE Calcium decay
: as described in Bhalla and Bower, J. Neurophysiol. 69:1948-1983 (1993)
: Andrew Davison, The Babraham Institute, 1998
: partially based on cadecay.mod by Alain Destexhe, Salk Institute 1995.

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

NEURON{
	SUFFIX cad2
	USEION ca READ ica, cai WRITE cai
	RANGE ica, channel_flow, depth, B
	GLOBAL cai, tau, cainf
}

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

CONSTANT {
        FARADAY = 96154 (coul)
	:FARADAY = 93149 (coul)		: moles do not appear in units
					: note this value is chosen to fit with
					: Genesis
}

PARAMETER {
	dt (ms)
	depth = 1 	(um)		: shell within which cai is calculated
					        : to match Bhalla and Bower 1993 set
					        : depth = diam/4 for each compartment
	tau = 800 	(ms)		: cai decay constant
	cainf = 1e-5	(mM)	: baseline calcium concentration
	ica		(mA/cm2)
	f = 1.0    : warmen
}

STATE {
	cai		(mM)
}

INITIAL {
	cai = cainf
}

ASSIGNED {
	channel_flow	(mM/ms)
	B		(mM cm2/ms/mA)
}

BREAKPOINT {
	SOLVE state METHOD cnexp
}

DERIVATIVE state {
	B = -f*(1e4)/(2*FARADAY*depth)
	channel_flow = B*ica
	if (channel_flow <= 0.0 ) { channel_flow = 0.0 }	: one way flow in channel
	cai' = channel_flow  - (cai - cainf)/tau
}
	






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