Beschreibung:
<jats:p>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<jats:sub>1C‐a</jats:sub> subunit with the cardiac β<jats:sub>2a</jats:sub> subunit significantly promotes the facilitation of <jats:italic>I</jats:italic>
<jats:sub>Ba</jats:sub> by strong depolarizing prepulses. The magnitude of <jats:italic>I</jats:italic>
<jats:sub>Ba</jats:sub> 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<jats:sub>1C‐a</jats:sub> subunit which was truncated at residue 1733 removing the cAMP kinase site at Ser‐1928. Facilitation was abolished by coexpression of the α<jats:sub>2</jats:sub>δ‐1 or α<jats:sub>2</jats:sub>δ‐3 subunit. We conclude that the expressed α<jats:sub>1C‐a</jats:sub> β<jats:sub>2a</jats:sub> complex is sufficient to support prepulse facilitation. Facilitation is prevented by coexpression of the α<jats:sub>2</jats:sub>δ subunit.</jats:p>