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Spike Ca 2+ influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of K V 7/M channels
Author(s) -
Chen Shmuel,
Yaari Yoel
Publication year - 2008
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.2007.148171
Subject(s) - afterdepolarization , bursting , biophysics , spike (software development) , chemistry , intracellular , repolarization , neuroscience , electrophysiology , biology , biochemistry , computer science , software engineering
In principal brain neurons, activation of Ca 2+ channels during an action potential, or spike, causes Ca 2+ entry into the cytosol within a millisecond. This in turn causes rapid activation of large conductance Ca 2+ ‐gated channels, which enhances repolarization and abbreviates the spike. Here we describe another remarkable consequence of spike Ca 2+ entry: enhancement of the spike afterdepolarization. This action is also mediated by intracellular modulation of a particular class of K + channels, namely by inhibition of K V 7 (KCNQ) channels. These channels generate the subthreshold, non‐inactivating M‐type K + current, whose activation curtails the spike afterdepolarization. Inhibition of K V 7/M by spike Ca 2+ entry allows the spike afterdepolarization to grow and can convert solitary spikes into high‐frequency bursts of action potentials. Through this novel intracellular modulatory action, Ca 2+ spike entry regulates the discharge mode and the signalling capacity of principal brain neurons.