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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 |
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container_title | CNS neuroscience & therapeutics |
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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 |
format | article |
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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.</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 & 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 & therapeutics, 2017-01, Vol.23 (1), p.23-32</ispartof><rights>2016 John Wiley & Sons Ltd</rights><rights>2016 John Wiley & Sons Ltd.</rights><rights>Copyright © 2017 John Wiley & 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 & 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.
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><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Basal ganglia circuit</subject><subject>Chromatography, High Pressure Liquid</subject><subject>Corpus Striatum - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Electroacupuncture</subject><subject>Excitatory Amino Acid Agents - pharmacology</subject><subject>Gene Expression Regulation - physiology</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Male</subject><subject>mGluR</subject><subject>Motor Activity - physiology</subject><subject>Original</subject><subject>Oxidopamine - toxicity</subject><subject>Parkinson's disease</subject><subject>Parkinsonian Disorders - chemically induced</subject><subject>Parkinsonian Disorders - pathology</subject><subject>Parkinsonian Disorders - physiopathology</subject><subject>Parkinsonian Disorders - therapy</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Metabotropic Glutamate - genetics</subject><subject>Receptors, Metabotropic Glutamate - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Sympatholytics - toxicity</subject><subject>Time Factors</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><issn>1755-5930</issn><issn>1755-5949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqNkU9vFCEYhydGY2v14BcwJF7sYVtgZoC5mJhNu27SqmnXM2GYdyx1Bqb8aVM_vYxbN9bERC5AeN6HF35F8ZrgI5LHsbbhiNBa8CfFPuF1vaibqnm6W5d4r3gRwjXGjIpGPC_2KK8IpQzvFz82V4Au3ADI9WjlXZrQeo3OIarWRe8mo9FqSFGNKmYONEzR-YCMRTEXXkZvVEzjvD8ZQOcKpdOUrI7JA9p4UHEEG2f5F-W_GxucNcqiCxXDy-JZr4YArx7mg-Lr6clm-XFx9nm1Xn44W-iKM76odU8r3oq-bqgqSUm7rumAln0nWqC854pR3RIuGmhIx7igdYdZruhYQymF8qB4v_VOqR2h07kfrwY5eTMqfy-dMvLxiTVX8pu7laxqaHZkwbsHgXc3CUKUowkahkFZcClIIub_5kTw_0Ap45TUtM7o27_Qa5e8zT8xCzEWmJH57sMtpb0LwUO_65tgOYcvc_jyV_iZffPnQ3fk77QzcLwF7swA9_82yeWny63yJ98TujU</recordid><startdate>201701</startdate><enddate>201701</enddate><creator>Jia, Yan‐Jun</creator><creator>Deng, Jia‐Hui</creator><creator>Zhang, Wen‐Zhong</creator><creator>Sun, Zuo‐Li</creator><creator>Yang, Jian</creator><creator>Yu, Yan</creator><creator>Gong, Xiao‐Li</creator><creator>Jia, Jun</creator><creator>Wang, Xiao‐Min</creator><general>John Wiley & 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 & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience & 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 & 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 & 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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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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