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Distinct roles for I T and I H in controlling the frequency and timing of rebound spike responses
Author(s) -
Engbers Jordan D. T.,
Anderson Dustin,
Tadayonnejad Reza,
Mehaffey W. Hamish,
Molineux Michael L.,
Turner Ray W.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.215632
Subject(s) - hyperpolarization (physics) , hcn channel , neuroscience , electrophysiology , biophysics , ion channel , chemistry , latency (audio) , membrane potential , biology , biochemistry , stereochemistry , computer science , nuclear magnetic resonance spectroscopy , telecommunications , receptor
Non‐Technical Summary The property of excitability is conferred to specific cell types through the action of a host of ion channels. Two classes of ion channels which play crucial roles in cellular excitability are T‐type calcium and hyperpolarization‐activated cyclic‐nucleotide (HCN) channels. Given that T‐type and HCN channel availability is increased upon hyperpolarization, T‐type‐ and HCN‐mediated currents are critical determinants of rebound depolarizations in many cell types. Rebound responses have long been documented in deep cerebellar nuclear (DCN) neurons; however, the extent to which T‐type‐ and HCN‐mediated currents contribute to rebound depolarizations following physiological input has not been established. Using a combination of in vitro electrophysiological and in silico techniques, we define the roles of T‐type‐ and HCN‐mediated currents in controlling the frequency and latency of DCN rebound spike output. Our study demonstrates that T‐type and HCN channels become sufficiently available during physiological levels of hyperpolarization to make distinct contributions to the frequency and latency of rebound responses.