Matsuda H, Hiyama Y, Terasawa K, Watanabe H, Matsumoto K
Department of Japanese Oriental (Kampo) Medicine, Toyama Medical and Pharmaceutical University, Toyama, Japan.
Pharmacol Biochem Behav. 1992 Jun;42(2):213-8. doi: 10.1016/0091-3057(92)90518-k.
To clarify if the enhancement of rotational behavior induced by repeated administration of SKF38393 is mediated by upregulation of D1 and/or D2 receptors in the striatum, we investigated effects of SCH23390 and sulpiride on SKF38393-induced rotational behavior and the changes in striatal dopamine receptors in rats with unilateral nigrostriatal 6-hydroxydopamine lesions (1). Repeated weekly administration of SKF38393 markedly enhanced the number of rotations and shortened the latency of rotational behavior depending on the number of SKF38393 administrations 1 or 6 weeks after the treatment with 6-OHDA (2). A selective D1 antagonist, SCH23390, but not a selective D2 antagonist, sulpiride, suppressed SKF38393-induced rotation and inhibited the enhancement by the repeated administration (3). Repeated administration of SKF38393 did not modify the density and the affinity of either the striatal D1 or D2 receptors in the striatum. These results suggest that the enhancement of SKF38393-induced rotational behavior by the repeated administration is not associated with the upregulation of striatal D1 and D2 receptors.
为了阐明重复给予SKF38393所诱导的旋转行为增强是否由纹状体中D1和/或D2受体的上调介导，我们研究了SCH23390和舒必利对SKF38393诱导的旋转行为的影响以及单侧黑质纹状体6-羟基多巴胺损伤大鼠纹状体多巴胺受体的变化(1)。每周重复给予SKF38393显著增加了旋转次数，并根据6-OHDA治疗后1或6周给予SKF38393的次数缩短了旋转行为的潜伏期(2)。选择性D1拮抗剂SCH23390而非选择性D2拮抗剂舒必利抑制了SKF38393诱导的旋转，并抑制了重复给药所导致的增强作用(3)。重复给予SKF38393并未改变纹状体中D1或D2受体的密度和亲和力。这些结果表明，重复给药增强SKF38393诱导的旋转行为与纹状体D1和D2受体的上调无关。
