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The Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats

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...

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Published in:CNS neuroscience & therapeutics 2017-01, Vol.23 (1), p.23-32
Main Authors: Jia, Yan‐Jun, Deng, Jia‐Hui, Zhang, Wen‐Zhong, Sun, Zuo‐Li, Yang, Jian, Yu, Yan, Gong, Xiao‐Li, Jia, Jun, Wang, Xiao‐Min
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cited_by cdi_FETCH-LOGICAL-c4767-5cf247b8f592a3132dd9de23fd8be27f7a62cb1789e91d67825d0647bd69222e3
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container_issue 1
container_start_page 23
container_title CNS neuroscience & therapeutics
container_volume 23
creator Jia, Yan‐Jun
Deng, Jia‐Hui
Zhang, Wen‐Zhong
Sun, Zuo‐Li
Yang, Jian
Yu, Yan
Gong, Xiao‐Li
Jia, Jun
Wang, Xiao‐Min
description 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.
doi_str_mv 10.1111/cns.12587
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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.</description><identifier>ISSN: 1755-5930</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.12587</identifier><identifier>PMID: 27412260</identifier><language>eng</language><publisher>England: John Wiley &amp; Sons, Inc</publisher><subject>Analysis of Variance ; Animals ; Basal ganglia circuit ; Chromatography, High Pressure Liquid ; Corpus Striatum - metabolism ; Disease Models, Animal ; Dopamine ; Electroacupuncture ; Excitatory Amino Acid Agents - pharmacology ; Gene Expression Regulation - physiology ; Glutamate ; Glutamic Acid - metabolism ; Male ; mGluR ; Motor Activity - physiology ; Original ; Oxidopamine - toxicity ; Parkinson's disease ; Parkinsonian Disorders - chemically induced ; Parkinsonian Disorders - pathology ; Parkinsonian Disorders - physiopathology ; Parkinsonian Disorders - therapy ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate - genetics ; Receptors, Metabotropic Glutamate - metabolism ; RNA, Messenger - metabolism ; Rodents ; Sympatholytics - toxicity ; Time Factors ; Tyrosine 3-Monooxygenase - metabolism</subject><ispartof>CNS neuroscience &amp; therapeutics, 2017-01, Vol.23 (1), p.23-32</ispartof><rights>2016 John Wiley &amp; Sons Ltd</rights><rights>2016 John Wiley &amp; Sons Ltd.</rights><rights>Copyright © 2017 John Wiley &amp; Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4767-5cf247b8f592a3132dd9de23fd8be27f7a62cb1789e91d67825d0647bd69222e3</citedby><cites>FETCH-LOGICAL-c4767-5cf247b8f592a3132dd9de23fd8be27f7a62cb1789e91d67825d0647bd69222e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6492692/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6492692/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,27924,27925,46052,46476,53791,53793</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcns.12587$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27412260$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jia, Yan‐Jun</creatorcontrib><creatorcontrib>Deng, Jia‐Hui</creatorcontrib><creatorcontrib>Zhang, Wen‐Zhong</creatorcontrib><creatorcontrib>Sun, Zuo‐Li</creatorcontrib><creatorcontrib>Yang, Jian</creatorcontrib><creatorcontrib>Yu, Yan</creatorcontrib><creatorcontrib>Gong, Xiao‐Li</creatorcontrib><creatorcontrib>Jia, Jun</creatorcontrib><creatorcontrib>Wang, Xiao‐Min</creatorcontrib><title>The Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats</title><title>CNS neuroscience &amp; therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>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. 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Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201701</creationdate><title>The Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats</title><author>Jia, Yan‐Jun ; Deng, Jia‐Hui ; Zhang, Wen‐Zhong ; Sun, Zuo‐Li ; Yang, Jian ; Yu, Yan ; Gong, Xiao‐Li ; Jia, Jun ; Wang, Xiao‐Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4767-5cf247b8f592a3132dd9de23fd8be27f7a62cb1789e91d67825d0647bd69222e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Basal ganglia circuit</topic><topic>Chromatography, High Pressure Liquid</topic><topic>Corpus Striatum - metabolism</topic><topic>Disease Models, Animal</topic><topic>Dopamine</topic><topic>Electroacupuncture</topic><topic>Excitatory Amino Acid Agents - pharmacology</topic><topic>Gene Expression Regulation - physiology</topic><topic>Glutamate</topic><topic>Glutamic Acid - metabolism</topic><topic>Male</topic><topic>mGluR</topic><topic>Motor Activity - physiology</topic><topic>Original</topic><topic>Oxidopamine - toxicity</topic><topic>Parkinson's disease</topic><topic>Parkinsonian Disorders - chemically induced</topic><topic>Parkinsonian Disorders - pathology</topic><topic>Parkinsonian Disorders - physiopathology</topic><topic>Parkinsonian Disorders - therapy</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Metabotropic Glutamate - genetics</topic><topic>Receptors, Metabotropic Glutamate - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Sympatholytics - toxicity</topic><topic>Time Factors</topic><topic>Tyrosine 3-Monooxygenase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jia, Yan‐Jun</creatorcontrib><creatorcontrib>Deng, Jia‐Hui</creatorcontrib><creatorcontrib>Zhang, Wen‐Zhong</creatorcontrib><creatorcontrib>Sun, Zuo‐Li</creatorcontrib><creatorcontrib>Yang, Jian</creatorcontrib><creatorcontrib>Yu, Yan</creatorcontrib><creatorcontrib>Gong, Xiao‐Li</creatorcontrib><creatorcontrib>Jia, Jun</creatorcontrib><creatorcontrib>Wang, Xiao‐Min</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience &amp; therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Jia, Yan‐Jun</au><au>Deng, Jia‐Hui</au><au>Zhang, Wen‐Zhong</au><au>Sun, Zuo‐Li</au><au>Yang, Jian</au><au>Yu, Yan</au><au>Gong, Xiao‐Li</au><au>Jia, Jun</au><au>Wang, Xiao‐Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats</atitle><jtitle>CNS neuroscience &amp; therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2017-01</date><risdate>2017</risdate><volume>23</volume><issue>1</issue><spage>23</spage><epage>32</epage><pages>23-32</pages><issn>1755-5930</issn><eissn>1755-5949</eissn><abstract>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.</abstract><cop>England</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>27412260</pmid><doi>10.1111/cns.12587</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record>
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source Wiley Open Access
subjects Analysis of Variance
Animals
Basal ganglia circuit
Chromatography, High Pressure Liquid
Corpus Striatum - metabolism
Disease Models, Animal
Dopamine
Electroacupuncture
Excitatory Amino Acid Agents - pharmacology
Gene Expression Regulation - physiology
Glutamate
Glutamic Acid - metabolism
Male
mGluR
Motor Activity - physiology
Original
Oxidopamine - toxicity
Parkinson's disease
Parkinsonian Disorders - chemically induced
Parkinsonian Disorders - pathology
Parkinsonian Disorders - physiopathology
Parkinsonian Disorders - therapy
Rats
Rats, Sprague-Dawley
Receptors, Metabotropic Glutamate - genetics
Receptors, Metabotropic Glutamate - metabolism
RNA, Messenger - metabolism
Rodents
Sympatholytics - toxicity
Time Factors
Tyrosine 3-Monooxygenase - metabolism
title The Role of Group II Metabotropic Glutamate Receptors in the Striatum in Electroacupuncture Treatment of Parkinsonian Rats
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