1 The dose-related, calcium-dependent, potassium-stimulated release of preloaded 3H]-dopamine from the superfused rat retina has been demonstrated. 2 A high-affinity uptake system for dopamine exists in rat retina in vitro; Km value was calculated as 1.89 μM, Vmax value as 1.4 nmol g-1 tissue h-1. 3 Dopamine (0.8 and 4 mM) inhibited the spontaneous release of 3H]-glycine from retina, and in the case of 0.8 mM dopamine this inhibitory effect was antagonized by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol. 4 The potassium-evoked (25 mM) release of 3H]-glycine from rat retina was similarly inhibited by dopamine (0.4-4 mM) in a dose-related manner when added to the superfusate with the potassium. The effect of 0.8 mM dopamine was antagonized by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol. 5 Dopamine (4 mM) significantly reduced the spontaneous release of 3H]-taurine from rat retina. 6 The potassium-stimulated (25 mM) release of 3H]-taurine occurred after the cessation of the depolarizing stimulus. This delayed release of 3H]-taurine was unaffected if dopamine was applied to the superfusate at the same time as the potassium, but it was significantly reduced if dopamine (0.8 and 4 mM) was applied after the depolarizing stimulus had been removed and during the actual amino acid release phase. 7 The inhibition of K+-stimulated (25 mM) delayed release of 3H]-taurine by applying dopamine (0.8 mM) after the depolarizing stimulus was blocked by 10 μM (+)-butaclamol but not by 10 μM (-)-butaclamol. 8 The results are discussed with respect to the possible neurotransmitter role for dopamine within the rat retina, and its possible interaction with glycine and taurine. |