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Data
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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
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Rubin, Jonathan E [jonrubin at pitt.edu] Show
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tom.morse@yale.edu
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NeuronetExperimenter demo file Show
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Neuronet Experimenter simulator file Show
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Ca2+ activated etc Rubin et al. 2009 XPP file Show
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