Presynaptic regulation of electrically evoked dopamine overflow in nucleus accumbens: a pharmacological study using fast cyclic voltammetry in vitro.

Fast cyclic voltammetry has been used to measure electrically evoked dopamine overflow from slices of rat nucleus accumbens in vitro. The substance detected was shown voltammetrically and biochemically to be dopamine of neuronal origin. Enough dopamine was released by a single electrical pulse to be easily detectable, and under these conditions there was no auto-inhibition by the endogenous transmitter (as demonstrated by the failure of dopamine antagonists to increase the amount released). There was no significant inhibition, or enhancement, of release by agonists at the following receptor types: dopamine D1, 5-hydroxytryptamine, cholinoceptors, alpha 1-, alpha 2-, beta-adrenoceptors, cholecystokinin or neurotensin receptors. However, the dopamine D2 receptor agonist, quinpirole, was capable of totally inhibiting the release; this effect was concentration-dependently antagonized by the D2 antagonists haloperidol, sulpiride, metoclopramide and clozapine, with potencies which corresponded to their affinities for D2 receptors in striatal tissue. The results show that the presynaptic receptors on dopaminergic nerve terminals are of the D2 type and apparently identical to those in the corpus striatum.