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The role of subunit composition on prepulse facilitation of the cardiac L‐type calcium channel
Author(s) -
Dai Shuiping,
Klugbauer Norbert,
Zong Xiangang,
Seisenberger Claudia,
Hofmann Franz
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)01632-9
Subject(s) - prepulse inhibition , facilitation , l type calcium channel , protein subunit , depolarization , biophysics , calcium channel , chemistry , calcium , endocrinology , medicine , neuroscience , biology , biochemistry , schizophrenia (object oriented programming) , psychiatry , gene
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 α 1C‐a subunit with the cardiac β 2a 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 α 1C‐a subunit which was truncated at residue 1733 removing the cAMP kinase site at Ser‐1928. Facilitation was abolished by coexpression of the α 2 δ‐1 or α 2 δ‐3 subunit. We conclude that the expressed α 1C‐a β 2a complex is sufficient to support prepulse facilitation. Facilitation is prevented by coexpression of the α 2 δ subunit.