Open AccessThe Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats
Author(s) -
Jia YanJun,
Deng JiaHui,
Zhang WenZhong,
Sun ZuoLi,
Yang Jian,
Yu Yan,
Gong XiaoLi,
Jia Jun,
Wang XiaoMin
Publication year - 2017
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12587
Subject(s) - metabotropic glutamate receptor , metabotropic glutamate receptor 2 , glutamatergic , striatum , glutamate receptor , electroacupuncture , neuroscience , metabotropic receptor , metabotropic glutamate receptor 5 , chemistry , dopamine , medicine , pharmacology , endocrinology , psychology , receptor , acupuncture , pathology , alternative medicine
Summary Aims Glutamatergic transmission may play a critical role in the pathogenesis of Parkinson's disease (PD). Electroacupuncture (EA) has been demonstrated to effectively alleviate PD symptoms. In this study, a potential glutamate‐dependent mechanism underlying the therapeutic action of EA was investigated. Methods The effects of EA stimulation on motor behaviors, dopamine contents, glutamate release, and group II metabotropic glutamate receptor (mGluR2/3) expression in unilateral 6‐hydroxydopamine (6‐OHDA)‐lesioned rats were examined. Results Unilateral 6‐OHDA lesions of the nigrostriatal system caused a marked increase in glutamate content in the ipsilateral cortex and striatum. mGluR2/3 protein expression and mGluR3 mRNA expression were reduced in the striatum. Noticeably, prolonged EA stimulation at 100 Hz significantly reversed these changes in the striatal glutamate system. Behaviorally, EA improved the motor deficits induced by 6‐OHDA lesions. Intrastriatal infusion of an mGluR2/3 antagonist APICA blocked the improving effect of EA. Conclusions These data collectively demonstrate that the group II mGluR‐mediated glutamatergic transmission in the striatum is sensitive to dopamine depletion and may serve as a substrate of EA for mediating the therapeutic effect of EA in a rat model of PD.