Role of Metabotropic Glutamate Receptors in the Mechanisms of Experimental Parkinsonism Development
Role of Metabotropic Glutamate Receptors in the Mechanisms of Experimental Parkinsonism Development
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DOI：
10.1007/s10517-012-1790-9
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发表时间：
2012-09-01
影响因子：
0.7
通讯作者：
Sudakov, S. K.
中科院分区：
文献类型：
--
作者：
Bashkatova, V. G.;Sudakov, S. K.
我们研究了代谢型谷氨酸受体5（mGluR 5）拮抗剂6-甲基-2-（苯乙炔基）-吡啶（MPEP）对大鼠在低剂量鱼藤酮（线粒体复合物I抑制剂）长期治疗条件下的僵住症和纹状体中NO生成的影响。在接受单次腹腔注射鱼藤酮（1.5毫克/公斤）的大鼠，在纹状体中的NO浓度没有不同的动物接受向日葵油。在这些术语中，两个动物组均未观察到僵住症体征。结果表明，长期鱼藤酮治疗诱导与大鼠纹状体中NO产生增强相关的僵住症。mGluR 5拮抗剂MPEP减轻了鱼藤酮长期治疗引起的僵住症，并阻止了鱼藤酮诱导的NO生成刺激。
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 sunfl ower 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.