| Abstract: | Abstract— (–)-Sulpiride (10 Nm -10 μm ) in the superfusate, dose-dependently increased the electrically-evoked release of dopamine from rat striatal slices. (+)-Sulpiride had little effect on evoked release of dopamine up to 10 μm . Apomorphine inhibited electrically evoked release of dopamine, and this effect of apomorphine was antagonized by (–)-sulpiride. SCH23390 and forskolin had no effect on the (–)-sulpiride-induced increase in evoked release of dopamine. Treatment with the irreversible dopamine-receptor antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline caused a significant increase in evoked release of dopamine and prevented the (–)-sulpiride-induced increase in the evoked release of dopamine. These results indicate that the (–)-sulpiride-induced increase in evoked release of dopamine is due to antagonism of the activation of dopamine autoreceptors by endogenously released dopamine. |
