Criticality,degeneracy in injury-induced changes in primary afferent excitability (Ratte et al 2014)

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Accession:256627
"Neuropathic pain remains notoriously difficult to treat despite numerous drug targets. Here, we offer a novel explanation for this intractability. Computer simulations predicted that qualitative changes in primary afferent excitability linked to neuropathic pain arise through a switch in spike initiation dynamics when molecular pathologies reach a tipping point (criticality), and that this tipping point can be reached via several different molecular pathologies (degeneracy). ..."
Reference:
1 . Ratté S, Zhu Y, Lee KY, Prescott SA (2014) Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain. Elife 3:e02370 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Abstract Morris-Lecar neuron; Dorsal Root Ganglion (DRG) cell;
Channel(s): I Na,t; I K;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: XPP;
Model Concept(s): Action Potential Initiation; Pathophysiology;
Implementer(s):
Search NeuronDB for information about:  I Na,t; I K;
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RatteEtAl2014
readme.txt
eLIFE_model.ode
                            
This is the XPP model associated with the paper:

Ratté S, Zhu Y, Lee KY, Prescott SA (2014) Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain. Elife 3:e02370

This ModelDB entry contains the authors original code as downloaded from the authors web site:
http://prescottlab.ca/code-for-models
on 20190510.