Spike Ca2+ influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of KV7/M channels
- 29 February 2008
- journal article
- Published by Wiley in The Journal of Physiology
- Vol. 586 (5), 1351-1363
- https://doi.org/10.1113/jphysiol.2007.148171
Abstract
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.This publication has 87 references indexed in Scilit:
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