[Mechanisms of calcium current decay acceleration induced by cyclic AMP].

In isolated snail neurones the level of cyclic AMP was increased either by intracellular injection of cAMP or by extracellular application of dibutyryl-cAMP and the change of high-threshold calcium current (ICa) decay was investigated. In 20 from 38 neurones it was obtained that both fast and slow phases of ICa decay were accelerated 2-2.5 times as affected by cAMP. The effect did not depend on the test-pulse potential and was displayed on the IBa. In the double-pulse experiments it was shown that cAMP enhanced the influence of depolarized prepulses (Vc) on the ICa tested (It). Analysis of the It-Vc curve showed that cAMP enhanced both Ca(2+)-dependent and voltage-dependent inactivation of ICa. The experiments where the intervals between Vc and Vt varied have shown that cAMP slowed down the rate of Ca(2+)-channels recovery from inactivation. The results suggest that cAMP increases the affinity of the Ca(2+)-channel inactivating substrate for Ca(2+)-ions.