Abstract

Systemic administration of the catecholamine uptake inhibitor nomifensine (NOM) in doses of 20–36 mg/kg strongly depressed the discharge rate of dopamine (DA) neurons in the substantia nigra of mice for more than 2–3 h. This effect was fully reverted by the systemically administered DA receptor antagonist haloperidol. Impulse activity of most neurons showed a reduced rhythmicity under the influence of NOM, as assessed by autocorrelograms. It is suggested that the depression of discharge activity of DA neurons by NOM represents an indirect agonist action on the DA receptor, probably via reduced elimination of DA from the extraneuronal space.

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