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Voltage‐dependent facilitation of a neuronal alpha 1C L‐type calcium channel.
Author(s) -
Bourinet E.,
Charnet P.,
Tomlinson W.J.,
Stea A.,
Snutch T.P.,
Nargeot J.
Publication year - 1994
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1994.tb06832.x
Subject(s) - columbia university , library science , biology , sociology , media studies , computer science
Calcium entry into excitable cells through voltage‐gated calcium channels can be influenced by both the rate and pattern of action potentials. We report here that a cloned neuronal alpha 1C L‐type calcium channel can be facilitated by positive pre‐depolarization. Both calcium and barium were effective as charge carriers in eliciting voltage‐dependent facilitation. The induction of facilitation was shown to be independent of intracellular calcium levels, G‐protein interaction and the level of phosphatase activity. Facilitation was reduced by the injection of inhibitors of protein kinase A and required the coexpression of a calcium channel beta subunit. In contrast, three neuronal non‐L‐type calcium channels, alpha 1A, alpha 1B and alpha 1E, were not subject to voltage‐dependent facilitation when coexpressed with a beta subunit. The results indicate that the mechanism of neuronal L‐type calcium channel facilitation involves the interaction of alpha 1 and beta subunits and is dependent on protein kinase A activity. The selective voltage‐dependent modulation of L‐type calcium channels is likely to play an important role in neuronal physiology and plasticity.