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The role of subunit composition on prepulse facilitation of the cardiac L-type calcium channel.


PMID 9923607

Abstract

Facilitation of calcium current by depolarizing prepulses has been observed in many cells including cardiac muscle. The mechanism underlying prepulse facilitation is controversial with respect to the requirements of channel subunits and cAMP kinase. We found that coexpression of the cardiac alpha1C-a subunit with the cardiac beta2a subunit significantly promotes the facilitation of I(Ba) by strong depolarizing prepulses. The magnitude of I(Ba) facilitation depended on the voltage potential of the prepulse and the interval duration between prepulse and test pulse. Prepulse facilitation was not affected by coexpression of AKAP79 and conditions favoring cAMP-dependent phosphorylation. Prepulse facilitation was also observed in cells expressing an alpha1C-a subunit which was truncated at residue 1733 removing the cAMP kinase site at Ser-1928. Facilitation was abolished by coexpression of the alpha2delta-1 or alpha2delta-3 subunit. We conclude that the expressed alpha1C-a beta2a complex is sufficient to support prepulse facilitation. Facilitation is prevented by coexpression of the alpha2delta subunit.

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