The effect of dopamine on depolarization-induced Ca2+ influx was studied using the fluorescent Ca2+ indicator fura-2 in synaptic terminals of bipolar neurons from gold-fish retina. Dopamine reversibly enhanced the rise in intracellular Ca2+ elicited by elevated external potassium. The enhancement was slowly reversible. The effect of dopamine was mimicked by forskolin and CPT-cAMP, a membrane-permeant analog of cAMP. However, 1,9-dideoxyforskolin, a forskolin analog that does not activate adenylyl cyclase, was ineffective. This suggests that dopamine, via cAMP, regulates the rise in presynaptic Ca2+ concentration in response to depolarization, potentially enhancing transmitter release.