Ichikawa J, Meltzer H Y
Laboratory of Biological Psychiatry, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
Brain Res. 1990 Jan 15;507(1):138-42. doi: 10.1016/0006-8993(90)90532-g.
Chronic administration of haloperidol (2 mg/kg x 21 days) in drinking water decreased basal dopamine (DA) release and metabolism in rat striatum and nucleus accumbens in awake, freely moving rats. In contrast with previous in vivo voltammetric studies in chloral hydrate-anesthetized rats, DA release and metabolism decreased in both regions following administration of (-)apomorphine (50 micrograms/kg, i.v.). These results demonstrate that stimulation of pre- or postsynaptic DA receptors by apomorphine in rats chronically treated with haloperidol further diminishes the release of DA and decreases DA metabolism. These results are difficult to reconcile with current concepts of neuroleptic-induced depolarization inactivation which predict increased release of DA following DA agonist administration.
在清醒、自由活动的大鼠中，通过饮水长期给予氟哌啶醇（2毫克/千克×21天）可降低大鼠纹状体和伏隔核中的基础多巴胺（DA）释放及代谢。与之前在水合氯醛麻醉大鼠中进行的体内伏安法研究不同，给予（-）阿扑吗啡（50微克/千克，静脉注射）后，两个区域的DA释放及代谢均降低。这些结果表明，在长期接受氟哌啶醇治疗的大鼠中，阿扑吗啡对突触前或突触后DA受体的刺激会进一步减少DA的释放并降低DA代谢。这些结果难以与目前关于抗精神病药物诱导的去极化失活的概念相协调，后者预测给予DA激动剂后DA释放会增加。
