Trifluoperazine and chlorpromazine, blockers of calmodulin action, potentiate slow inward current in molluscan neurons identically to the action of cAMP. The sulfoxide derivative of chloropromazine does not appreciably bind to calmodulin and also fails to enhance the inward current. The likelihood that these effects are mediated by cAMP via inhibition of a Ca2+-calmodulin-activated phosphodiesterase is discussed and related to other data.