Abstract

Release of [3H]dopamine ([3H]DA) from striatal synaptosomes is evoked most commonly by elevating potassium levels in the presence of calcium. However, it has been difficult to show that DA agonists or antagonists can modify K+-evoked release of [3H]DA. DA. In this study [3H]DA release evoked by exposure of synaptosomes (isolated and superfused previously with 0.0 mM Ca++ and 0.1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid) to 1.25 mM Ca++ can be modulated by the DA (D2) agonists apomorphine, pergolide and quinpirole and antagonists l-sulpiride and domperidone. The release was evoked under low potassium (6 mM or less) concentrations and the potassium concentration in the superfusion medium was not elevated before or during Ca++ exposure. Analysis of the superfusates obtained during Ca++ exposure revealed that approximately 80% of the tritium released was [3H]DA. The ability of DA (D2) agonists to inhibit the Ca++-evoked release from synaptosomes superfused with 9 mM K+ was greatly reduced. Therefore, prolonged depolarization may block DA (D2) regulation of [3H]DA release from synaptosomes. The Ca++-evoked release of [3H]DA was reduced greatly when 1 microM tetrodotoxin was present indicating sodium channels play a role in triggering the processes involved in Ca++-evoked [3H]DA release.