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将阿扑吗啡和(±)-3-(3-羟苯基)-N-正丙基哌啶注射到大鼠纹状体内对其尾状核纺锤波的影响。

Effects of apomorphine and (+/-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine, injected into the striatum, on the caudate spindle in the rat.

作者信息

Hashimoto S, Okuyama S, Aihara H

出版信息

Neuropharmacology. 1987 Jul;26(7A):663-7. doi: 10.1016/0028-3908(87)90226-7.

DOI:10.1016/0028-3908(87)90226-7
PMID:2888038
Abstract

The caudate spindle in rats was observed following bilateral application of apomorphine (1.5-50 micrograms) and (+/-)-3-(3-hydroxyphenyl)-N-n-propylpiperidine (3-PPP, 0.3-3 micrograms) into the striatum. The smallest dose (1.5 micrograms) of apomorphine enhanced the spindle whereas with a larger dose (50 micrograms), suppression occurred. The preferential dopamine (DA) autoreceptor (inhibitory-receptor) agonist, (+/-)-3-PPP, enhanced the spindle, in a dose-dependent manner. The enhancing effect of apomorphine (1.5 micrograms) and (+/-)-3-PPP (3 micrograms) was prevented by neuroleptics, such as haloperidol (20 micrograms/kg, i.v.) and sulpiride (2 mg/kg, i.v.) at doses which, per se, did not affect the spindle. Small doses of neuroleptics are thought to block DA autoreceptors, suggesting that the enhancing effects of the DA agonists are mediated by autoreceptors. These results lend further support to the assumption that the development of the caudate spindle involves activation or DA receptors. Enhancement of the spindle, induced by injections of apomorphine into the striatum (small dose) and (+/-)-3-PPP, may be mediated by DA autoreceptors (inhibitory-receptors) located at presynaptic elements of the nigro-striatal DA system, while suppression may be due to stimulation of the postsynaptic DA receptors.

摘要

在大鼠纹状体内双侧注射阿扑吗啡(1.5 - 50微克)和(±)-3-(3-羟苯基)-N-正丙基哌啶(3-PPP,0.3 - 3微克)后,观察尾状核纺锤波。阿扑吗啡最小剂量(1.5微克)增强纺锤波,而大剂量(50微克)则产生抑制作用。优先性多巴胺(DA)自身受体(抑制性受体)激动剂(±)-3-PPP以剂量依赖性方式增强纺锤波。阿扑吗啡(1.5微克)和(±)-3-PPP(3微克)的增强作用可被氟哌啶醇(20微克/千克,静脉注射)和舒必利(2毫克/千克,静脉注射)等抗精神病药物阻断,这些药物本身并不影响纺锤波。小剂量抗精神病药物被认为可阻断DA自身受体,这表明DA激动剂的增强作用是由自身受体介导的。这些结果进一步支持了尾状核纺锤波的产生涉及DA受体激活的假设。向纹状体内注射阿扑吗啡(小剂量)和(±)-3-PPP所诱导的纺锤波增强可能由黑质 - 纹状体DA系统突触前元件处的DA自身受体(抑制性受体)介导,而抑制作用可能是由于对突触后DA受体的刺激所致。

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