Abstract

Pretreatment with the monoamine oxidase inhibitor pargyline or the catecholamine uptake blocker nomifensine both protected central catecholamine neurons against MPTP-induced neurotoxicity as monitored by analyzing catecholamine levels and [ 3H]mazindol binding. Post-treatment with the inhibitors showed that the administration of nomifensine could be delayed longer than that of pargyline in order to achieve a protective effect. The results are compatible with the view that the monoamine oxidase-catalyzed conversion of MPTP to a toxic metabolite MPP + occurs mainly extraneuronally. MPP + is subsequently taken up and accumulated selectively in catecholamine neurons, initiating degeneration.

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