Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors
Identifieur interne : 001419 ( Istex/Corpus ); précédent : 001418; suivant : 001420Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors
Auteurs : Adrien Quintana ; Christophe Melon ; Lydia Kerkerian-Le Goff ; Pascal Salin ; Marc Savasta ; Véronique Sgambato-FaureSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2010-08.
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- KwdEn :
Abstract
Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.
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DOI: 10.1111/j.1460-9568.2010.07290.x
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by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title><author><name sortKey="Quintana, Adrien" sort="Quintana, Adrien" uniqKey="Quintana A" first="Adrien" last="Quintana">Adrien Quintana</name><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Joseph Fourier, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Melon, Christophe" sort="Melon, Christophe" uniqKey="Melon C" first="Christophe" last="Melon">Christophe Melon</name><affiliation><mods:affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</mods:affiliation></affiliation></author><author><name sortKey="Goff, Lydia Kerkerian E" sort="Goff, Lydia Kerkerian E" uniqKey="Goff L" first="Lydia Kerkerian-Le" last="Goff">Lydia Kerkerian-Le Goff</name><affiliation><mods:affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</mods:affiliation></affiliation></author><author><name sortKey="Salin, Pascal" sort="Salin, Pascal" uniqKey="Salin P" first="Pascal" last="Salin">Pascal Salin</name><affiliation><mods:affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</mods:affiliation></affiliation></author><author><name sortKey="Savasta, Marc" sort="Savasta, Marc" uniqKey="Savasta M" first="Marc" last="Savasta">Marc Savasta</name><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Joseph Fourier, Grenoble, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</mods:affiliation></affiliation></author><author><name sortKey="Sgambato Aure, Veronique" sort="Sgambato Aure, Veronique" uniqKey="Sgambato Aure V" first="Véronique" last="Sgambato-Faure">Véronique Sgambato-Faure</name><affiliation><mods:affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</mods:affiliation></affiliation><affiliation><mods:affiliation>Université Joseph 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type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>106</term><term>CP‐101</term><term>glutamate</term><term>high frequency stimulation</term><term>rat</term><term>subthalamic nucleus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Adrien Quintana</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</json:string><json:string>Université Joseph Fourier, Grenoble, France</json:string></affiliations></json:item><json:item><name>Christophe Melon</name><affiliations><json:string>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</json:string></affiliations></json:item><json:item><name>Lydia Kerkerian‐Le Goff</name><affiliations><json:string>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</json:string></affiliations></json:item><json:item><name>Pascal Salin</name><affiliations><json:string>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</json:string></affiliations></json:item><json:item><name>Marc Savasta</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</json:string><json:string>Université Joseph Fourier, Grenoble, France</json:string><json:string>Centre Hospitalier Universitaire, BP217, Grenoble, France</json:string></affiliations></json:item><json:item><name>Véronique Sgambato‐Faure</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</json:string><json:string>Université Joseph Fourier, Grenoble, France</json:string><json:string>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>106</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CP‐101</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>glutamate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>high frequency stimulation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>rat</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic nucleus</value></json:item></subject><articleId><json:string>EJN7290</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. 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Neurosci.</title></host><title>Pallidal origin of GABA release within the substantia nigra pars reticulata during high‐frequency stimulation of the subthalamic nucleus</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>32</volume><publisherId><json:string>EJN</json:string></publisherId><pages><total>12</total><last>434</last><first>423</first></pages><issn><json:string>0953-816X</json:string></issn><issue>3</issue><genre><json:string>journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><categories><wos><json:string>science</json:string><json:string>neurosciences</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & neurosurgery</json:string></scienceMetrix></categories><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1111/j.1460-9568.2010.07290.x</json:string></doi><id>C5ED975075D7B5200F59AC81AC748AEB9163B0E8</id><score>0.15188804</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/C5ED975075D7B5200F59AC81AC748AEB9163B0E8/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/C5ED975075D7B5200F59AC81AC748AEB9163B0E8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C5ED975075D7B5200F59AC81AC748AEB9163B0E8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>© The Authors (2010). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</p></availability><date>2010</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title><author xml:id="author-1"><persName><forename type="first">Adrien</forename><surname>Quintana</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation></author><author xml:id="author-2"><persName><forename type="first">Christophe</forename><surname>Melon</surname></persName><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">Lydia Kerkerian‐Le</forename><surname>Goff</surname></persName><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation></author><author xml:id="author-4"><persName><forename type="first">Pascal</forename><surname>Salin</surname></persName><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Marc</forename><surname>Savasta</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation><affiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</affiliation></author><author xml:id="author-6"><persName><forename type="first">Véronique</forename><surname>Sgambato‐Faure</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation><affiliation>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-08"></date><biblScope unit="volume">32</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="423">423</biblScope><biblScope unit="page" to="434">434</biblScope></imprint></monogr><idno type="istex">C5ED975075D7B5200F59AC81AC748AEB9163B0E8</idno><idno type="DOI">10.1111/j.1460-9568.2010.07290.x</idno><idno type="ArticleID">EJN7290</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>keywords</head><item><term>106</term></item><item><term>CP‐101</term></item><item><term>glutamate</term></item><item><term>high frequency stimulation</term></item><item><term>rat</term></item><item><term>subthalamic nucleus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/C5ED975075D7B5200F59AC81AC748AEB9163B0E8/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="08103"><doi origin="wiley">10.1111/ejn.2010.32.issue-3</doi><numberingGroup><numbering type="journalVolume" number="32">32</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2010-08">August 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="12" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2010.07290.x</doi><idGroup><id type="unit" value="EJN7290"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">NEUROSYSTEMS</title><title type="tocHeading2"> </title></titleGroup><copyright>© The Authors (2010). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2010-07-28"></event><event type="publishedOnlineFinalForm" date="2010-08-02"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-07-28"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.27 mode:FullText source:FullText result:FullText" date="2010-11-22"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="423">423</numbering><numbering type="pageLast" number="434">434</numbering></numberingGroup><correspondenceTo>Dr Marc Savasta, <sup>1</sup>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), as above.
E‐mail: <email normalForm="marc.savasta@ujf-grenoble.fr">marc.savasta@ujf‐grenoble.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN7290.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 22 February 2010, revised 14 April 2010, accepted 20 April 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of <i>N</i>‐methyl‐<sc>d</sc>‐aspartate receptors</title><title type="shortAuthors">A. Quintana <i>et al.</i></title><title type="short">STN‐HFS‐induced forelimb dyskinesia</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>Adrien</givenNames><familyName>Quintana</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a3"><personName><givenNames>Christophe</givenNames><familyName>Melon</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>Lydia Kerkerian‐Le</givenNames><familyName>Goff</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>Pascal</givenNames><familyName>Salin</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a2 #a4"><personName><givenNames>Marc</givenNames><familyName>Savasta</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2 #a5"><personName><givenNames>Véronique</givenNames><familyName>Sgambato‐Faure</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Université Joseph Fourier, Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="FR"><unparsedAffiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="FR"><unparsedAffiliation>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">106</keyword><keyword xml:id="k2">CP‐101</keyword><keyword xml:id="k3">glutamate</keyword><keyword xml:id="k4">high frequency stimulation</keyword><keyword xml:id="k5">rat</keyword><keyword xml:id="k6">subthalamic nucleus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Dyskinesia is a major side‐effect of chronic <sc>l</sc>‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the <sc>l</sc>‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for <sc>l</sc>‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing <i>N</i>‐methyl‐<sc>d</sc>‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr<sup>1472</sup>) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective <i>N</i>‐methyl‐<sc>d</sc>‐aspartate receptor antagonist, MK‐801.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>STN‐HFS‐induced forelimb dyskinesia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Forelimb dyskinesia mediated by high‐frequency stimulation of the subthalamic nucleus is linked to rapid activation of the NR2B subunit of N‐methyl‐d‐aspartate receptors</title></titleInfo><name type="personal"><namePart type="given">Adrien</namePart><namePart type="family">Quintana</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christophe</namePart><namePart type="family">Melon</namePart><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lydia Kerkerian‐Le</namePart><namePart type="family">Goff</namePart><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pascal</namePart><namePart type="family">Salin</namePart><affiliation>Institut de Biologie du Développement de Marseille‐Luminy, UMR 6216 CNRS, Université de la Méditerranée, Marseille, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Savasta</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation><affiliation>Centre Hospitalier Universitaire, BP217, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Véronique</namePart><namePart type="family">Sgambato‐Faure</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836 (INSERM U386), Grenoble Institut des Neurosciences, Dynamique des Réseaux Neuronaux du Mouvement, Université Joseph Fourier, Site Santé La Tronche, BP 170, Grenoble F‐38042, Cedex 09, France</affiliation><affiliation>Université Joseph Fourier, Grenoble, France</affiliation><affiliation>Centre de Neuroscience Cognitive, Centre National de la Recherche Scientifique, UMR 5229, Université de Lyon I, Bron, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-08</dateIssued><edition>Received 22 February 2010, revised 14 April 2010, accepted 20 April 2010</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">6</extent></physicalDescription><abstract lang="en">Dyskinesia is a major side‐effect of chronic l‐DOPA administration, the reference treatment for Parkinson’s disease. High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) alleviates parkinsonian motor symptoms and indirectly improves dyskinesia by decreasing the l‐DOPA requirement. However, inappropriate stimulation can also trigger dyskinetic movements, in both human and rodents. We investigated whether STN‐HFS‐evoked forelimb dyskinesia involved changes in glutamatergic neurotransmission as previously reported for l‐DOPA‐induced dyskinesias, focusing on the role of NR2B‐containing N‐methyl‐d‐aspartate receptors (NR2B/NMDARs). We applied STN‐HFS in normal rats at intensities above and below the threshold for triggering forelimb dyskinesia. Dyskinesiogenic STN‐HFS induced the activation of NR2B (as assessed by immunodetection of the phosphorylated residue Tyr1472) in neurons of the subthalamic nucleus, entopeduncular nucleus, motor thalamus and forelimb motor cortex. The severity of STN‐HFS‐induced forelimb dyskinesia was decreased in a dose‐dependent manner by systemic injections of CP‐101,606, a selective blocker of NR2B/NMDARs, but was either unaffected or increased by the non‐selective N‐methyl‐d‐aspartate receptor antagonist, MK‐801.</abstract><subject lang="en"><genre>keywords</genre><topic>106</topic><topic>CP‐101</topic><topic>glutamate</topic><topic>high frequency stimulation</topic><topic>rat</topic><topic>subthalamic nucleus</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>32</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>423</start><end>434</end><total>12</total></extent></part></relatedItem><identifier type="istex">C5ED975075D7B5200F59AC81AC748AEB9163B0E8</identifier><identifier type="DOI">10.1111/j.1460-9568.2010.07290.x</identifier><identifier type="ArticleID">EJN7290</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Authors (2010). 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