Newly synthesized dopamine in the nucleus accumbens is regulated by β-adrenergic, but not α-adrenergic, receptors

Abstract

Previous microdialysis studies have led to the hypothesis that activation of mesolimbic α-adrenoceptors inhibits the release of mesolimbic dopamine from α-methyl- p-tyrosine-resistant, reserpine-sensitive pools, and that activation of mesolimbic β-adrenoceptors stimulates the release of mesolimbic dopamine from α-methyl- p-tyrosine-sensitive, reserpine-resistant pools. In the present study we analysed the ability of mesolimbic α- and β-adrenoceptors to modulate the release of dopamine from α-methyl- p-tyrosine-sensitive pools in the nucleus accumbens of high and low responders to novelty. Under non-challenged conditions, α-methyl- p-tyrosine (10 −4 M, 40 min) produced a decrease in dopamine release that did not differ between high and low responders to novelty. The continuous infusion of 10 −6 M isoproterenol (β-adrenoceptor agonist) diminished the α-methyl- p-tyrosine-induced decrease in dopamine, whereas the continuous infusion of 10 −5 M phenylephrine (α-adrenoceptor agonist) remained ineffective. It is concluded that the release of mesolimbic dopamine from α-methyl- p-tyrosine-sensitive, reserpine-resistant pools is under excitatory control of β-adrenergic, but not α-adrenergic, receptors in both high and low responders to novelty. In general, this study implies that mesolimbic dopamine that is derived from different pools is regulated via different noradrenergic receptors.