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神经节苷脂GM1可抵消亚急性甲苯暴露对阿扑吗啡诱导的运动活动的增强作用。

Ganglioside GM1 counteracts the enhancing effects of subacute toluene exposure on apomorphine-induced locomotor activity.

作者信息

von Euler G, Ogren S O, Fuxe K, Gustafsson J A

机构信息

Department of Histology and Neurobiology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Toxicol Lett. 1992 Nov;63(2):165-9. doi: 10.1016/0378-4274(92)90008-8.

Abstract

Previous studies indicate that subacute toluene exposure enhances the effects of postsynaptic doses of apomorphine on locomotor activity in the rat. We have now studied the effects of the ganglioside GM1 on toluene-affected apomorphine-induced (1 mg/kg, s.c.) locomotion, motility, and rearing. Treatment with GM1 (10 mg/kg, i.p., 1 h before exposure) was found to counteract or even reverse the enhancing effect of toluene on apomorphine-induced locomotion and rearing, but had similarly to toluene no significant effects on apomorphine-induced motility or on spontaneous locomotor activity. The antagonistic effects of GM1 may be due to its ability to block toluene-induced changes in D2 receptor binding.

摘要

先前的研究表明,亚急性甲苯暴露会增强突触后剂量的阿扑吗啡对大鼠运动活性的影响。我们现在研究了神经节苷脂GM1对受甲苯影响的阿扑吗啡诱导(1毫克/千克,皮下注射)的运动、活动和竖毛行为的影响。发现用GM1(10毫克/千克,腹腔注射,暴露前1小时)治疗可抵消甚至逆转甲苯对阿扑吗啡诱导的运动和竖毛行为的增强作用,但与甲苯类似,对阿扑吗啡诱导的活动或自发运动活性没有显著影响。GM1的拮抗作用可能是由于其能够阻断甲苯诱导的D2受体结合变化。

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