[The mechanisms of the inhibiting action of cyclic adenosine monophosphate on the calcium current of intact mollusk neurons].

Experiments were conducted on isolated unidentified snail neurons using the method of voltage clamp by two-microelectrodes. The intracellular level of cAMP was increased either by intracellular injection of the cAMP or by extracellular application of dcAMP or isobutylmethylxanthine. The inhibitory effect of cAMP on the ICa was investigated as well as on the IBa. Intracellular injection of cGMP into the same neurons through multibarrel microelectrodes enhanced the ICa, while application of the phorbol ester had no effect on the ICa. Intracellular injection of EGTA enhanced the ICa, but the inhibitory effect of cAMP on the ICa was not changed in the presence of EGTA. Tolbutamide and H-8 (to the less degree) reduced the ICa. In 6 from 12 experiments the inhibitory effects of tolbutamide and dcAMP on ICa were not additive. The results suggest that the inhibitory effect of cAMP on the ICa is not due to the activation of cAMP- or cGMP-dependent protein kinase or protein kinase C. The cAMP effect does not depend on the cytoplasmic Ca2(+)-level. The possibility of the direct cAMP interaction with the Ca2(+)-channel is discussed.