[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.
Solntseva
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EI
D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects*; D000242:Cyclic AMP / Q000494:pharmacology*; D006372:Helix, Snails; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects
D015220:Calcium Channels; D003994:Bucladesine; D000242:Cyclic AMP
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