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Ca2+-activated I_CAN and synaptic depression promotes network-dependent oscil. (Rubin et al. 2009)
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"... 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. ..."
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  • Rubin JE, Hayes JA, Mendenhall JL, Del Negro CA (2009) Show Other
  • Rubin, Jonathan E [jonrubin at pitt.edu] Show Other
tom.morse@yale.edu
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Revisions: 8
Last Time: 9/13/2017 5:34:14 PM
Reviewer: Tom Morse - MoldelDB admin
Owner: Tom Morse - MoldelDB admin