Breese G R, Mueller R A
Eur J Pharmacol. 1985 Jul 11;113(1):109-14. doi: 10.1016/0014-2999(85)90349-8.
SCH-23390, a selective D-1 dopamine antagonist, was found to antagonize the locomotor stimulation induced by LY-171555, an action similar to that for haloperidol in control animals. However, this action of SCH-23390 was prevented in rats treated with 6-hydroxydopamine (6-OHDA) or with reserpine plus alpha-methyl-tyrosine pretreatment. These results indicate that the action of SCH-23390 to antagonize D-2 dopamine receptor actions is dependent upon functional catecholamine-containing neurons. In contrast to the lack of action of SCH-23390 to antagonize LY-171555 in 6-OHDA-treated rats, SCH-23390 blocked the locomotor stimulation induced by SKF-39393, a D-1 dopamine agonist, after this treatment. Thus, D-1 dopamine receptors are distinct from D-2 receptor sites and can exhibit a behavior similar to that observed when D-2 receptors are stimulated. These data suggest that D-1 receptor sites modulate D-2 dopamine receptor function through a mechanism dependent upon functionally intact catecholamine-containing neurons.
SCH-23390是一种选择性D-1多巴胺拮抗剂,研究发现它能拮抗LY-171555诱导的运动兴奋,这一作用与对照动物中氟哌啶醇的作用相似。然而,在用6-羟基多巴胺(6-OHDA)处理或用利血平加α-甲基酪氨酸预处理的大鼠中,SCH-23390的这一作用受到了抑制。这些结果表明,SCH-23390拮抗D-2多巴胺受体作用的行为依赖于含功能正常的儿茶酚胺能神经元。与SCH-23390在6-OHDA处理的大鼠中对LY-171555缺乏拮抗作用相反,在该处理后,SCH-23390能阻断D-1多巴胺激动剂SKF-39393诱导的运动兴奋。因此,D-1多巴胺受体与D-2受体位点不同,并且能表现出与刺激D-2受体时观察到的行为相似的行为。这些数据表明,D-1受体位点通过一种依赖于功能完整的含儿茶酚胺能神经元的机制来调节D-2多巴胺受体功能。