Dopaminergic regulation of GABA release from the intact goldfish retina

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 μM); 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 conditios. 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 cyclic AMP-mediated event.