Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-20611
EMBO J 1994 Nov 01;1321:5032-9. doi: 10.1002/j.1460-2075.1994.tb06832.x.
Show Gene links Show Anatomy links

Voltage-dependent facilitation of a neuronal alpha 1C L-type calcium channel.

Bourinet E , Charnet P , Tomlinson WJ , Stea A , Snutch TP , Nargeot J .


???displayArticle.abstract???
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.

???displayArticle.pubmedLink??? 7957069
???displayArticle.pmcLink??? PMC395449
???displayArticle.link??? EMBO J



References [+] :
Aniksztejn, Novel form of long-term potentiation produced by a K+ channel blocker in the hippocampus. 1991, Pubmed