High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute l‐3,4‐dihydroxyphenylalanine in dopaminergic denervated rats
Identifieur interne : 001A47 ( Main/Corpus ); précédent : 001A46; suivant : 001A48High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute l‐3,4‐dihydroxyphenylalanine in dopaminergic denervated rats
Auteurs : Emilie Lacombe ; Carole Carcenac ; Sabrina Boulet ; Claude Feuerstein ; Anne Bertrand ; Annie Poupard ; Marc SavastaSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2007-09.
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- KwdEn :
Abstract
High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) is a powerful approach for treating the motor symptoms of Parkinson's disease (PD). It results in clinical improvement in patients with PD, further reducing the l‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.
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DOI: 10.1111/j.1460-9568.2007.05747.x
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It results in clinical improvement in patients with PD, further reducing the l‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Emilie Lacombe</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string></affiliations></json:item><json:item><name>Carole Carcenac</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string></affiliations></json:item><json:item><name>Sabrina Boulet</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string></affiliations></json:item><json:item><name>Claude Feuerstein</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string><json:string>Centre Hospitalier Universitaire de Grenoble, Grenoble, France</json:string></affiliations></json:item><json:item><name>Anne Bertrand</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string></affiliations></json:item><json:item><name>Annie Poupard</name><affiliations><json:string>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</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, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</json:string><json:string>Université Joseph Fourier and</json:string><json:string>Centre Hospitalier Universitaire de Grenoble, Grenoble, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dopamine</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>L‐3, 4‐dihydroxyphenylalanine treatment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>subthalamic nucleus</value></json:item></subject><articleId><json:string>EJN5747</json:string></articleId><language><json:string>eng</json:string></language><abstract>High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) is a powerful approach for treating the motor symptoms of Parkinson's disease (PD). It results in clinical improvement in patients with PD, further reducing the l‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.</abstract><qualityIndicators><score>7.832</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1700</abstractCharCount><pdfWordCount>9549</pdfWordCount><pdfCharCount>60531</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>236</abstractWordCount></qualityIndicators><title>High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute l‐3,4‐dihydroxyphenylalanine in dopaminergic denervated 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type="first">Carole</forename><surname>Carcenac</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation></author><author><persName><forename type="first">Sabrina</forename><surname>Boulet</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation></author><author><persName><forename type="first">Claude</forename><surname>Feuerstein</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><affiliation>Centre Hospitalier Universitaire de Grenoble, Grenoble, France</affiliation></author><author><persName><forename type="first">Anne</forename><surname>Bertrand</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation></author><author><persName><forename type="first">Annie</forename><surname>Poupard</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation></author><author><persName><forename type="first">Marc</forename><surname>Savasta</surname></persName><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><affiliation>Centre Hospitalier Universitaire de Grenoble, Grenoble, 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="2007-09"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1670">1670</biblScope><biblScope unit="page" to="1680">1680</biblScope></imprint></monogr><idno type="istex">E9089923F3EF1906FF4AD539ED2F26EFCE5872EE</idno><idno type="DOI">10.1111/j.1460-9568.2007.05747.x</idno><idno type="ArticleID">EJN5747</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) is a powerful approach for treating the motor symptoms of Parkinson's disease (PD). It results in clinical improvement in patients with PD, further reducing the l‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>dopamine</term></item><item><term>high‐frequency stimulation</term></item><item><term>L‐3, 4‐dihydroxyphenylalanine treatment</term></item><item><term>Parkinson's disease</term></item><item><term>subthalamic nucleus</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E9089923F3EF1906FF4AD539ED2F26EFCE5872EE/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="09006"><doi origin="wiley">10.1111/ejn.2007.26.issue-6</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2007-09">September 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="25" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2007.05747.x</doi><idGroup><id type="unit" value="EJN5747"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2007-09-06"></event><event type="publishedOnlineFinalForm" date="2007-09-06"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.16 mode:FullText" date="2010-08-27"></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="1670">1670</numbering><numbering type="pageLast" number="1680">1680</numbering></numberingGroup><correspondenceTo>Dr Marc Savasta, Dynamique des Réseaux Neuroneaux du Mouvement, Institut National de la Santé et de la Recherche Médicale, Unité 836 (ex Unité 704), Université Joseph Fourier, Domaine Universitaire, 2280 rue de la Piscine, BP 53, 38041 Grenoble Cedex 09, France.
E‐mail: <email normalForm="marc.savasta@ujf-grenoble.fr">marc.savasta@ujf‐grenoble.fr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN5747.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 23 February 2007, revised 30 June 2007, accepted 9 July 2007</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="99"></count><count type="wordTotal" number="6516"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute <sc>l</sc>‐3,4‐dihydroxyphenylalanine in dopaminergic denervated rats</title><title type="shortAuthors">E. Lacombe <i>et al.</i></title><title type="short">STN‐HFS and L‐DOPA effects on striatal dopamine contents</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>Emilie</givenNames><familyName>Lacombe</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2"><personName><givenNames>Carole</givenNames><familyName>Carcenac</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2"><personName><givenNames>Sabrina</givenNames><familyName>Boulet</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Claude</givenNames><familyName>Feuerstein</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a2"><personName><givenNames>Anne</givenNames><familyName>Bertrand</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1 #a2"><personName><givenNames>Annie</givenNames><familyName>Poupard</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Marc</givenNames><familyName>Savasta</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Université Joseph Fourier and</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="FR"><unparsedAffiliation>Centre Hospitalier Universitaire de Grenoble, Grenoble, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dopamine</keyword><keyword xml:id="k2">high‐frequency stimulation</keyword><keyword xml:id="k3"><sc>L</sc>‐3, 4‐dihydroxyphenylalanine treatment</keyword><keyword xml:id="k4">Parkinson's disease</keyword><keyword xml:id="k5">subthalamic nucleus </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) is a powerful approach for treating the motor symptoms of Parkinson's disease (PD). It results in clinical improvement in patients with PD, further reducing the <sc>l</sc>‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute l‐3,4‐dihydroxyphenylalanine in dopaminergic denervated rats</title></titleInfo><titleInfo type="abbreviated"><title>STN‐HFS and L‐DOPA effects on striatal dopamine contents</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>High‐frequency stimulation of the subthalamic nucleus prolongs the increase in striatal dopamine induced by acute</title></titleInfo><name type="personal"><namePart type="given">Emilie</namePart><namePart type="family">Lacombe</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carole</namePart><namePart type="family">Carcenac</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sabrina</namePart><namePart type="family">Boulet</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Claude</namePart><namePart type="family">Feuerstein</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><affiliation>Centre Hospitalier Universitaire de Grenoble, Grenoble, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anne</namePart><namePart type="family">Bertrand</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Annie</namePart><namePart type="family">Poupard</namePart><affiliation>Institut National de la Santé et de la Recherche Médicale, Unité 836, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</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, Grenoble Institut des Neurosciences, Equipe Dynamique des Réseaux Neuronaux du Mouvement,</affiliation><affiliation>Université Joseph Fourier and</affiliation><affiliation>Centre Hospitalier Universitaire de Grenoble, Grenoble, 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">2007-09</dateIssued><edition>Received 23 February 2007, revised 30 June 2007, accepted 9 July 2007</edition><copyrightDate encoding="w3cdtf">2007</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">2</extent><extent unit="tables">2</extent><extent unit="references">99</extent><extent unit="words">6516</extent></physicalDescription><abstract lang="en">High‐frequency stimulation of the subthalamic nucleus (STN‐HFS) is a powerful approach for treating the motor symptoms of Parkinson's disease (PD). It results in clinical improvement in patients with PD, further reducing the l‐3,4‐dihydroxyphenylalanine (L‐DOPA) requirement and thus L‐DOPA‐induced dyskinesia. However, it remains unclear how STN‐HFS modifies the response to L‐DOPA. We investigated the effect of STN‐HFS on striatal extracellular concentrations of dopamine and its metabolites following acute L‐DOPA administration in intact or partially dopaminergic denervated (DA‐PL) rats. L‐DOPA treatment significantly increased striatal dopamine levels in intact and DA‐PL animals, with the maximal effect observed 1 h after L‐DOPA injection. This increase was more pronounced in DA‐PL rats (ipsilateral to the lesion) than in intact animals. It remained fairly stable 1 h after the maximal effect of L‐DOPA and then decreased towards basal values. STN‐HFS in intact rats had no effect on the maximal L‐DOPA‐induced increase in striatal extracellular dopamine concentration or the return to basal values, the profiles observed being similar to those for non‐stimulated intact animals. Conversely, STN‐HFS amplified the L‐DOPA‐induced increase in striatal dopamine levels during the stimulation period (1 h) in DA‐PL rats and this increase was sustained throughout the post‐stimulation period (2.5 h), without the return to basal levels observed in stimulated intact and non‐stimulated rats. These new neurochemical data suggest that STN‐HFS interferes with L‐DOPA effects, probably synergically, by stabilizing dopamine levels in the striatum and shed light on the mechanisms of STN‐HFS in PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>dopamine</topic><topic>high‐frequency stimulation</topic><topic>L‐3, 4‐dihydroxyphenylalanine treatment</topic><topic>Parkinson's disease</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>2007</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1670</start><end>1680</end><total>11</total></extent></part></relatedItem><identifier type="istex">E9089923F3EF1906FF4AD539ED2F26EFCE5872EE</identifier><identifier type="DOI">10.1111/j.1460-9568.2007.05747.x</identifier><identifier type="ArticleID">EJN5747</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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