Boireau A, Miquet J M, Olivier V
Rhône-Poulenc Rorer SA, Centre de recherche de Vitry-Alfortville, Vitry-sur-Seine, France.
Fundam Clin Pharmacol. 1993;7(2):109-14. doi: 10.1111/j.1472-8206.1993.tb00224.x.
We have studied the effects of neurotensin (NT) on the release of [3H]dopamine ([3H]DA) evoked by terminal depolarization with either K+, veratridine or 4-aminopyridine (4-AP). NT (1-1000 nM) induced a net potentiation (up to 170%) of the K+ (25 mM)-evoked release of [3H]DA. The capacity of NT to potentiate the effect of K+ ions decreased as the K+ concentration rose from 25 to 50 mM and totally disappeared at this high K+ concentration. NT (100 nM; 1,000 nM) had no significant effect on the veratridine (1.5; 5 microM) or 4-AP (20 microM) -evoked release of [3H]DA. The relevance of these experimental models of DA release to physiological transmitter release remains to be established. Those data highlight the complexity of the modulation of evoked neurotransmitter release by pharmacological agents.