DOPAMINERGIC REGULATION OF DOPAMINE RELEASE FROM PC12 CELLS VIA A PERTUSSIS TOXIN-SENSITIVE G-PROTEIN

Regulation of dopamine (DA) release from PC12 cells was investigated. Apomorphine and quinpirole, a selective D2 agonist, significantly reduced K+-evoked DA release, and this reduction was reversed by haloperidol. Furthermore, spiroperidol, a selective D2 antagonist, and haloperidol, a nonselective DA antagonist, enhanced the K+-evoked DA release. Pertussis toxin treatment of the cells abolished the quinpirole-induced reduction of K+-evoked DA release. Also, the haloperidol-induced enhancement of K+-evoked DA release was not seen in pertussis toxin treated cells. These results, therefore, suggest the presence of D2 receptors on PC12 cells which result in the modulation of K+-evoked DA release via a pertussis toxin-sensitive G protein.