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Volume 17, Number 7, Issue of April 1, 1997 pp. 2267-2272
Copyright ©1997 Society for Neuroscience

Monoamine Oxidase Inhibition Causes a Long-Term Prolongation of the Dopamine-Induced Responses in Rat Midbrain Dopaminergic Cells

Received Dec. 6, 1996; revised Jan. 6, 1997; accepted Jan. 13, 1997.

Nicola B. Mercuri, Mariangela Scarponi, Antonello Bonci, Antonio Siniscalchi, and Giorgio Bernardi

Clinica Neurologica, Dipartimento Sanitá Pubblica, Universitá di Roma Tor Vergata and Istituto Ricerca e Cura a Carattere Scientifico Ospedale Santa Lucia, Roma, Italy

The way monoamine oxidase (MAO) modulates the depression of the firing rate and the hyperpolarization of the membrane caused by dopamine (DA) on rat midbrain dopaminergic cells was investigated by means of intracellular recordings in vitro. The cellular responses to DA, attributable to the activation of somatodendritic D2/3 autoreceptors, were prolonged and did not completely wash out after pharmacological blockade of both types (A and B) of MAO. On the contrary, depression of the firing rate and membrane hyperpolarization induced by quinpirole (a direct D2 receptor agonist) were not affected by MAO inhibition. Furthermore, although the inhibition of DA reuptake by cocaine and nomifensine caused a short-term prolongation of DA responses, the combined inhibition of MAO A and B enzymes caused a long-term prolongation of DA effects. Moreover, the effects of DA were not largely prolonged during the simultaneous inhibition of MAO and the DA reuptake system. Interestingly, the actions of amphetamine were not clearly augmented by MAO inhibition.

From the present data it is concluded that the termination of DA action in the brain is controlled mainly by MAO enzymes. This long-term prolongation of the dopaminergic responses suggests a substitutive therapeutic approach that uses MAO inhibitors and DA precursors in DA-deficient disorders in which continuous stimulation of the dopaminergic receptors is preferable.

Key words: pargyline; cocaine; nomifensine; intracellular recordings; substantia nigra; ventral tegmental area

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