Ca2+-activated I_CAN and synaptic depression promotes network-dependent oscil. (Rubin et al. 2009)


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Accession:125649
"... the preBotzinger complex... we present and analyze a mathematical model demonstrating an unconventional mechanism of rhythm generation in which glutamatergic synapses and the short-term depression of excitatory transmission play key rhythmogenic roles. Recurrent synaptic excitation triggers postsynaptic Ca2+- activated nonspecific cation current (ICAN) to initiate a network-wide burst. Robust depolarization due to ICAN also causes voltage-dependent spike inactivation, which diminishes recurrent excitation and thus attenuates postsynaptic Ca2+ accumulation. ..."
Reference:
1 . Rubin JE, Hayes JA, Mendenhall JL, Del Negro CA (2009) Calcium-activated nonspecific cation current and synaptic depression promote network-dependent burst oscillations. Proc Natl Acad Sci U S A 106:2939-44 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network; Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): PreBotzinger complex neuron;
Channel(s): I CAN;
Gap Junctions:
Receptor(s): AMPA; mGluR;
Gene(s):
Transmitter(s):
Simulation Environment: C or C++ program (web link to model); XPP (web link to model); NeuronetExperimenter (web link to model);
Model Concept(s): Bursting; Oscillations;
Implementer(s): Rubin, Jonathan E [jonrubin at pitt.edu];
Search NeuronDB for information about:  AMPA; mGluR; I CAN;
(located via links below)
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