Abstract

The effect of Ca 2+/calmodulin-dependent protein phosphorylation on K + channels was examined in snail neurons, using several pharmacological agents, the voltage clamp method and the pressure injection technique. H-7, a general protein kinase inhibitor, reduced the delayed outward K + current ( I KD) which was suppressed by tetraethylammonium. Ca 2+/calmodulin-dependent protein kinase II, when injected into neurons which had been treated with H-7, transiently restored the reduced I KD nearly to the pre-H-7 level. However, this restoration was blocked by W-7, a calmodulin inhibitor. In contrast, the catalytic subunit of cAMP-dependent protein kinase or protein kinase C injected into the H-7-treated neurons had little effect on the current. These findings suggest that Ca 2+/calmodulin-dependent protein phosphorylation is involved in the opening process of K +channels.

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