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Abstract:
Iontophoretic application of serotonin on some neurons of Aplysia causes a slow, voltage-dependent inward current. Experimental evidence indicates that the current is carried by calcium ions: the response to serotonin is unaffected by changes in chloride or potassium concentration, slowly attenuated by sodium-free solutions, reduced in some (although not all) preparations by a low-calcium solution, and blocked by calcium channel blockers. The transmitter-induced calcium current has a voltage sensitivity similar to that of calcium currents in other systems. Intracellular application of cyclic AMP also elicits a voltage-dependent inward current. Although cyclic AMP mimics serotonin, pharmacological agents do not have the actions expected if cyclic AMP were mediating the response to serotonin, Phosphodiesterase inhibitors block the responses to both serotonin and cyclic AMP; 5,5'-dithiobis(2-nitrobenzoic acid), and adenylate cyclase inhibitor, and imidazole, a phosphodiesterase activator, do not reduce the serotonin response. Because calcium has many important roles in neuronal activity, including synaptic transmission, the current evoked by serotonin and by cyclic AMP, whether acting independently or as part of the same mechanism, would have important functional consequences.