Dorsal root ganglion (primary somatosensory) neurons (Rho & Prescott 2012)

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Accession:190261
In this paper, we demonstrate how dorsal root ganglion (DRG) neuron excitability can become pathologically altered, as occurs in neuropathic pain. Specifically, we reproduce pathological changes in spiking pattern (from transient to repetitive spiking) and the development of membrane potential oscillations and bursting.
Reference:
1 . Rho YA, Prescott SA (2012) Identification of molecular pathologies sufficient to cause neuropathic excitability in primary somatosensory afferents using dynamical systems theory. PLoS Comput Biol 8:e1002524 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type:
Brain Region(s)/Organism:
Cell Type(s): Abstract Morris-Lecar neuron;
Channel(s):
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: XPP;
Model Concept(s): Action Potential Initiation; Bifurcation; Nociception;
Implementer(s): Prescott, Steven [steve.prescott at sickkids.ca]];
# from Rho and Prescott, PLoS Comput Biol 2012
# to be run in XPP
# standard 2-D model (see Fig 2)
# gna corresponds to gfast; gk corresponds to gslow; gl corresponds to gleak


# DIFFERENTIAL EQUATIONS

dv/dt = (Istim-gna*minf(V)*(V-Vna)-gk*w*(V-VK)-gl*(V-Vl))/cap
dw/dt = phi_w*(winf(V)-w)/tauw(V)

# FUNCTIONS AND PARAMETERS

minf(v)=.5*(1+tanh((v-beta_m)/gamma_m))
winf(v)=.5*(1+tanh((v-beta_w)/gamma_w))

tauw(v)=1/cosh((v-beta_w)/(2*gamma_w))


param Istim=0 
param vna=50,vk=-100,vl=-70
param gk=20,gl=2,gna=20
param beta_m=-1.2,gamma_m=18
param beta_w=-13,gamma_w=10
# beta_w = -21 for transient spiking; beta_w = -13 for repetitive spiking
param phi_w=.15
param cap=2

# INITIAL CONDITIONS
V(0)=-70
w(0)=0.000025

# ALWAYS USE EULER! - Actually this is only true for noise
@ total=10000,dt=.05,xlo=-100,xhi=60,ylo=-.125,yhi=.6,xp=v,yp=w
@ meth=euler
@ MAXSTOR=1000000,bounds=10000

done