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Modulation of Kv3.4 channel N‐type inactivation by protein kinase C shapes the action potential in dorsal root ganglion neurons
Author(s) -
Ritter David M.,
Ho Cojen,
O’Leary Michael E.,
Covarrubias Manuel
Publication year - 2012
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.2011.218560
Subject(s) - repolarization , dorsal root ganglion , protein kinase a , ion channel , potassium channel , neuroscience , chemistry , biophysics , voltage gated potassium channel , electrophysiology , microbiology and biotechnology , phosphorylation , biology , biochemistry , receptor , spinal cord
Non‐technical summary The orchestrated activity of an ensemble of voltage‐gated ion channels determines the initiation, shape and duration of the action potential in excitable cells. In primary pain‐sensing neurons, this ensemble includes a high voltage‐activated potassium channel. However, its molecular identity, function and modulation were unknown. Here, we show that the rapidly inactivating Kv3.4 channel underlying the high voltage‐activated potassium current is a major determinant of action potential repolarization. Furthermore, we found that physiological activation of protein kinase C dramatically slows Kv3.4 channel inactivation, which enhances the channel's ability to influence action potential repolarization. Based on these results and earlier work, we conclude that phosphorylation of the Kv3.4 channel inactivation gate is a mechanism by which pain‐sensing neurons shape action potential repolarization. This modulation will influence Ca 2+ ‐dependent processes that play vital roles in nociception and might become deregulated in chronic pain.