ClC-2 channels regulate neuronal excitability, not intracellular Cl- levels (Ratte & Prescott 2011)

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Accession:142993
"The model is for a generic, single compartment neuron with multiple ion currents. The most notable mechanisms include ClC-2 (a rectifying chloride-leak channel) and KCC2 (potassium chloride co-transporter 2). A significant feature of the model is that it tracks intracellular chloride concentration. Moreover, the GABA-A receptor is modeled as passing both chloride and bicarbonate ions, which is important for proper calculation of the GABA reversal potential. Ornstein-Unlenbeck processes to simulate synaptic inhibition and excitation are also included."
Reference:
1 . Ratté S, Prescott SA (2011) ClC-2 channels regulate neuronal excitability, not intracellular chloride levels. J Neurosci 31:15838-43 [PubMed]
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):
Channel(s): I Cl, leak;
Gap Junctions:
Receptor(s):
Gene(s): CLC-2 CLCN2;
Transmitter(s):
Simulation Environment: XPP;
Model Concept(s): Chloride regulation;
Implementer(s): Prescott, Steven [steve.prescott at sickkids.ca]];
Search NeuronDB for information about:  I Cl, leak;
 
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RattePrescott2011
readme.txt
ClC2-IClamp-Prescott.ode
ClC2-VClamp-Prescott.ode
                            
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