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

"... 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. ..."

Model Type: Realistic Network; Neuron or other electrically excitable cell

Cell Type(s): PreBotzinger complex neuron

Currents: I CAN

Receptors: AMPA; mGluR

Model Concept(s): Bursting; Oscillations

Simulation Environment: C or C++ program (web link to model); XPP (web link to model); NeuronetExperimenter (web link to model)

Implementer(s): Rubin, Jonathan E [jonrubin at pitt.edu]

References:

Rubin JE, Hayes JA, Mendenhall JL, Del Negro CA. (2009). Calcium-activated nonspecific cation current and synaptic depression promote network-dependent burst oscillations. Proceedings of the National Academy of Sciences of the United States of America. 106 [PubMed]