The rate of release of [3H]GABA from intact goldfish retinas was studied using a modified superfusion technique. Small, significant increases in the rate of GABA release were observed when the retinas were exposed to dopamine (DA) (100-1000 microM); however, when free Ca2+ was removed from the medium, the basal rate of GABA release was increased and DA became inhibitory. Forskolin, a non-specific stimulator of adenylate cyclase in intact cells, also inhibited GABA release in the absence of Ca2+. There was no significant effect of forskolin in the presence of Ca2+; however, (+)-butaclamol, a dopamine antagonist, increased basal GABA release under these conditions. L-glutamic acid (L-Glu) (1-10 mM) causes up to a 10-fold increase in GABA release. In the presence of Ca2+, DA did not significantly alter the effects of L-Glu; however, in the absence of Ca2+ a significant inhibition of the effects of L-Glu by DA was observed. Forskolin, on the other hand, inhibited the effects of L-Glu both in the presence and absence of Ca2+. Finally, EGTA (0.3-1 mM) produced a large release of GABA: this release was inhibited by DA, forskolin, theophylline, and 8-bromo cyclic AMP. These results suggest a model wherein DA stimulates Ca2+-dependent GABA release from one site and inhibits Ca2+-independent GABA release from another site via a cyclic AMP-mediated event.