Dopamine influences the light peak in the perfused mammalian eye.

Dopamine, cis-flupenthixol, and dibutyryl cAMP affected the standing potential and light-evoked responses of the perfused cat eye in vitro. At micromolar concentrations, dopamine, a retinal neurotransmitter, increased the standing potential of the eye. At slightly higher concentrations, dopamine abolished the "light peak," a slow voltage response to light generated by the retinal pigment epithelium. The light peak was depressed by cis-flupenthixol, a dopamine antagonist, at micromolar concentrations. Dibutyryl cAMP produced effects similar to those produced by dopamine. A possible interpretation is that the generation of the light peak involves a catecholamine-stimulated adenylate cyclase in retinal pigment epithelium that is influenced by dopamine released from retinal neurons.