纹状体D1和D2多巴胺受体在大鼠抗精神病性猝厥中的特异性参与。

Polish journal of pharmacology Pub Date : 1995-07-01
J Wardas, M Pietraszek, K Ossowska, S Wolfarth
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引用次数: 0

摘要

由于D1 (SCH 39166)和D2 (raclopride)多巴胺受体的高度特异性拮抗剂最近已经出现,我们决定研究这些受体的纹状体种群在猝死症(一种抗精神病药诱导的人类帕金森病动物模型)中的作用。向纹状体腹吻侧部分注射(2.5、5和10微克/0.5微升)可引起强烈、剂量依赖性和持久的猝倒。胃内注射SCH 39166(1.5和3.6微克/ 0.5微升)也会引起剂量依赖性,但持续时间较短的麻痹。目前的研究结果表明,抗精神病药的副作用特异性依赖于纹状体中D2和D1多巴胺受体的阻断。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Specific involvement of striatal D1 and D2 dopamine receptors in the neuroleptic catalepsy in rats.

Since highly specific antagonists of D1 (SCH 39166) and D2 (raclopride) dopamine receptors have recently become available, we decided to investigate the role of striatal populations of these receptors in catalepsy - an animal model of neuroleptic-induced parkinsonism in humans. Injections of raclopride (2.5, 5 and 10 micrograms/0.5 microliters) into the ventro-rostral part of the striatum induced a strong, dose-dependent and long-lasting catalepsy. Intrastriatal injections of SCH 39166 (1.5 and 3.6 micrograms/ 0.5 microliters) also evoked a dose-dependent, but short-lasting catalepsy. The present results suggest, that neuroleptic side-effects are specifically dependent on the blockade of D2 and D1 dopamine receptors in the striatum.

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