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- W2169381921 endingPage "1363" @default.
- W2169381921 startingPage "1351" @default.
- W2169381921 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." @default.
- W2169381921 created "2016-06-24" @default.
- W2169381921 creator A5034037462 @default.
- W2169381921 creator A5045000426 @default.
- W2169381921 date "2008-02-29" @default.
- W2169381921 modified "2023-10-18" @default.
- W2169381921 title "Spike Ca<sup>2+</sup> influx upmodulates the spike afterdepolarization and bursting via intracellular inhibition of K<sub>V</sub>7/M channels" @default.
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- W2169381921 doi "https://doi.org/10.1113/jphysiol.2007.148171" @default.
- W2169381921 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2375679" @default.
- W2169381921 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18187471" @default.
- W2169381921 hasPublicationYear "2008" @default.
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