Spike Ca2+ influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of KV7/M channels

The Journal of Physiology
Shmuel Chen, Yoel Yaari

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.

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Citations

May 7, 2010·Journal of Molecular Neuroscience : MN·David A Brown
Feb 7, 2009·Nature Nanotechnology·Gabriel A Silva
Aug 21, 2012·PloS One·Guillaume DrionRodolphe Sepulchre
Oct 5, 2010·Progress in Biophysics and Molecular Biology·Jakub NowackiKrasimira Tsaneva-Atanasova
Feb 16, 2019·PloS One·Natalia Z BielczykUrszula Foryś
Mar 21, 2009·British Journal of Pharmacology·David A Brown, Gayle M Passmore
Sep 20, 2008·The Journal of Physiology·Victoria F SafiulinaEnrico Cherubini
Aug 11, 2016·The Journal of Physiology·Arik TzourAlexander M Binshtok
Apr 9, 2020·Journal of Neurophysiology·Hanna YousufJames R Moyer
Jun 17, 2016·PLoS Computational Biology·Dominik ThalmeierRaoul-Martin Memmesheimer
Jun 21, 2021·The Journal of Physiology·Sandesh MohanYoel Yaari
Mar 27, 2021·Brain : a Journal of Neurology·Isamu Aiba, Jeffrey L Noebels

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