Potentiation of transmitter release from NMB human neuroblastoma cells by kappa-opioids is mediated by N-type voltage-dependent calcium channels

The selective kappa-opioid agonist trans-(+/-)-3,4-dichloro-N-methyl-N-[2-( 1-pyrrolidinyl) cyclohexyl] benzenacetamidemethansulfonate (U50,488) potent iates both basal and depolarization-evoked [H-3]dopamine release from NMB c ells. The potentiation of dopamine release by U50,488 is mediated by N-type voltage-dependent calcium channels since it is blocked by omega-conotoxin, and is resistant to pertussis toxin (PTX)-treatment. When the stimulation of release by U50,488 is blocked by the N-channel antagonist omega-conotoxi n, an inhibitory effect on dopamine release is revealed, suggesting that st imulatory and inhibitory effects of U50,488 are exerted in parallel.