POSSIBLE INVOLVEMENT OF PROTEIN-KINASE-C IN NEUROTENSIN-INDUCED POTENTIATION OF DOPAMINE RELEASE FROM THE RAT RETINA

A possible role of protein kinase C in the neurotensin (NT)-induced potentiation of endogenous dopamine (DA) release was studied in the isolated rat retina. NT and sulpiride potentiated the release of endogenous DA induced by electrical stimulation as reported in our previous study. 12-O-Tetradecanoyl-phorbol-13-acetate (TPA) (10(-9)-10(-5)M) was also effective in potentiating this electrical stimulation-induced release of DA. Polymyxin B (10(-6)M) decreased the electrical stimulation-induced release of DA, without affecting its spontaneous release. In the presence of polymyxin B, both the effects of TPA (10(-6)M) and NT (10(-6)M) in potentiating the electrical stimulation-induced release of DA were completely abolished. On the other hand, sulpiride (10(-8) and 10(-7)M)-induced potentiation of DA release was not affected either by pretreatment with polymyxin B (10(-6)M) nor by simultaneous application of TPA (10(-6)M). These results suggest that protein kinase C is probably involved in the NT-induced, but not sulpiride-induced potentiation of DA release from the rat retinal preparations.