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代谢型谷氨酸受体在实验性帕金森病发生机制中的作用

Role of metabotropic glutamate receptors in the mechanisms of experimental parkinsonism development.

作者信息

Bashkatova V G, Sudakov S K

机构信息

PK Anokhin Institute of Normal Physiology, Russian Academy of Medical Sciences, Moscow, Russia.

出版信息

Bull Exp Biol Med. 2012 Sep;153(5):655-7. doi: 10.1007/s10517-012-1790-9.

Abstract

We studied the effects of metabotropic glutamate receptor 5 (mGluR5) antagonist 6-methyl-2-(phenylethynyl)-pyridine (MPEP) on the development of catalepsy and NO generation in the striatum of rats under conditions of long-term treatment with low doses of rotenone, a mitochondrial complex I inhibitor. In rats receiving single intraperitoneal injection of rotenone (1.5 mg/kg), NO concentration in the striatum did not differ from that in animals receiving sunflower oil. No signs of catalepsy were observed at these terms in both animal groups. It was demonstrated that long-term rotenone treatment induced catalepsy associated with enhanced NO production in the rat striatum. mGluR5 antagonist MPEP alleviated catalepsy caused by long-term rotenone treatment and prevented rotenone-induced stimulation of NO generation.

摘要

我们研究了代谢型谷氨酸受体5(mGluR5)拮抗剂6-甲基-2-(苯乙炔基)-吡啶(MPEP)对长期低剂量给予线粒体复合体I抑制剂鱼藤酮的大鼠纹状体中僵住症发展及一氧化氮(NO)生成的影响。在单次腹腔注射鱼藤酮(1.5毫克/千克)的大鼠中,纹状体中的NO浓度与接受葵花籽油注射的动物相比无差异。在这些时间点,两个动物组均未观察到僵住症迹象。结果表明,长期给予鱼藤酮可诱导大鼠纹状体中与NO生成增加相关的僵住症。mGluR5拮抗剂MPEP减轻了长期鱼藤酮治疗所致的僵住症,并阻止了鱼藤酮诱导的NO生成增加。

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