Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats
Identifieur interne : 001C07 ( Main/Corpus ); précédent : 001C06; suivant : 001C08Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats
Auteurs : Maria Papathanou ; Sarah Rose ; Andrew Mccreary ; Peter JennerSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2011-06.
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- KwdEn :
Abstract
Dyskinesia induction in Parkinson’s disease (PD) appears less marked with long‐acting dopamine agonists than with short‐acting L‐Dopa, but the relationship to duration of drug action is unknown. It is also unclear whether the duration of drug action affects the expression of established dyskinesia. This study compared the ability of L‐Dopa and four dopamine agonists of different duration of action to induce abnormal involuntary movements (AIMs) in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, and their ability to express established AIMs following prior exposure to L‐Dopa. 6‐OHDA‐lesioned rats were treated with saline, L‐Dopa/benserazide, apomorphine, ropinirole, pramipexole or pergolide once daily for 15 days. Repeated administration of the short‐acting dopamine agonists, apomorphine (duration 80 min) and ropinirole (duration 90 min) induced marked axial, limb and orolingual AIMs at peak effect. L‐Dopa (duration 100 min) produced moderate AIMs at peak effect, while administration of the long‐acting dopamine agonists, pramipexole (duration 150 min) and pergolide (duration 240 min) resulted in mild AIMs. In rats primed to exhibit severe AIMs following repeated L‐Dopa administration, acute administration of apomorphine, ropinirole and L‐Dopa induced severe AIMs. By contrast, pramipexole and pergolide evoked only mild–moderate AIMs. Again, there was a negative correlation between duration of effect and the severity of AIMs expressed. These studies show that both the induction and expression of AIMs in 6‐OHDA‐lesioned rats are related to the duration of action of dopaminergic drugs. These findings suggest that continuous dopaminergic stimulation could be used both to avoid dyskinesia induction and to improve motor function in late‐stage PD when troublesome dyskinesia is evident.
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DOI: 10.1111/j.1460-9568.2011.07704.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats</title><author><name sortKey="Papathanou, Maria" sort="Papathanou, Maria" uniqKey="Papathanou M" first="Maria" last="Papathanou">Maria Papathanou</name><affiliation><mods:affiliation>Ludwig Institute for Cancer Research and Department of Cell and Molecular Biology, Karolinska Institutet, Box 240, Nobels väg 3, SE‐171 77 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Rose, Sarah" sort="Rose, Sarah" uniqKey="Rose S" first="Sarah" last="Rose">Sarah Rose</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</mods:affiliation></affiliation></author><author><name sortKey="Mccreary, Andrew" sort="Mccreary, Andrew" uniqKey="Mccreary A" first="Andrew" last="Mccreary">Andrew Mccreary</name><affiliation><mods:affiliation>Abbott Healthcare B.V, C J Van Houtenlaan 36, Weesp, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:21B15318C543E544E3F3BD8FA645985A299D6FAE</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1460-9568.2011.07704.x</idno><idno type="url">https://api.istex.fr/document/21B15318C543E544E3F3BD8FA645985A299D6FAE/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001C07</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats</title><author><name sortKey="Papathanou, Maria" sort="Papathanou, Maria" uniqKey="Papathanou M" first="Maria" last="Papathanou">Maria Papathanou</name><affiliation><mods:affiliation>Ludwig Institute for Cancer Research and Department of Cell and Molecular Biology, Karolinska Institutet, Box 240, Nobels väg 3, SE‐171 77 Stockholm, Sweden</mods:affiliation></affiliation></author><author><name sortKey="Rose, Sarah" sort="Rose, Sarah" uniqKey="Rose S" first="Sarah" last="Rose">Sarah Rose</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</mods:affiliation></affiliation></author><author><name sortKey="Mccreary, Andrew" sort="Mccreary, Andrew" uniqKey="Mccreary A" first="Andrew" last="Mccreary">Andrew Mccreary</name><affiliation><mods:affiliation>Abbott Healthcare B.V, C J Van Houtenlaan 36, Weesp, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-06">2011-06</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="2247">2247</biblScope><biblScope unit="page" to="2254">2254</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">21B15318C543E544E3F3BD8FA645985A299D6FAE</idno><idno type="DOI">10.1111/j.1460-9568.2011.07704.x</idno><idno type="ArticleID">EJN7704</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>L‐Dopa</term><term>Parkinson’s disease</term><term>abnormal involuntary movements</term><term>continuous dopaminergic stimulation</term><term>dopamine agonists</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dyskinesia induction in Parkinson’s disease (PD) appears less marked with long‐acting dopamine agonists than with short‐acting L‐Dopa, but the relationship to duration of drug action is unknown. It is also unclear whether the duration of drug action affects the expression of established dyskinesia. This study compared the ability of L‐Dopa and four dopamine agonists of different duration of action to induce abnormal involuntary movements (AIMs) in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, and their ability to express established AIMs following prior exposure to L‐Dopa. 6‐OHDA‐lesioned rats were treated with saline, L‐Dopa/benserazide, apomorphine, ropinirole, pramipexole or pergolide once daily for 15 days. Repeated administration of the short‐acting dopamine agonists, apomorphine (duration 80 min) and ropinirole (duration 90 min) induced marked axial, limb and orolingual AIMs at peak effect. L‐Dopa (duration 100 min) produced moderate AIMs at peak effect, while administration of the long‐acting dopamine agonists, pramipexole (duration 150 min) and pergolide (duration 240 min) resulted in mild AIMs. In rats primed to exhibit severe AIMs following repeated L‐Dopa administration, acute administration of apomorphine, ropinirole and L‐Dopa induced severe AIMs. By contrast, pramipexole and pergolide evoked only mild–moderate AIMs. Again, there was a negative correlation between duration of effect and the severity of AIMs expressed. These studies show that both the induction and expression of AIMs in 6‐OHDA‐lesioned rats are related to the duration of action of dopaminergic drugs. 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It is also unclear whether the duration of drug action affects the expression of established dyskinesia. This study compared the ability of L‐Dopa and four dopamine agonists of different duration of action to induce abnormal involuntary movements (AIMs) in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, and their ability to express established AIMs following prior exposure to L‐Dopa. 6‐OHDA‐lesioned rats were treated with saline, L‐Dopa/benserazide, apomorphine, ropinirole, pramipexole or pergolide once daily for 15 days. Repeated administration of the short‐acting dopamine agonists, apomorphine (duration 80 min) and ropinirole (duration 90 min) induced marked axial, limb and orolingual AIMs at peak effect. L‐Dopa (duration 100 min) produced moderate AIMs at peak effect, while administration of the long‐acting dopamine agonists, pramipexole (duration 150 min) and pergolide (duration 240 min) resulted in mild AIMs. In rats primed to exhibit severe AIMs following repeated L‐Dopa administration, acute administration of apomorphine, ropinirole and L‐Dopa induced severe AIMs. By contrast, pramipexole and pergolide evoked only mild–moderate AIMs. Again, there was a negative correlation between duration of effect and the severity of AIMs expressed. These studies show that both the induction and expression of AIMs in 6‐OHDA‐lesioned rats are related to the duration of action of dopaminergic drugs. These findings suggest that continuous dopaminergic stimulation could be used both to avoid dyskinesia induction and to improve motor function in late‐stage PD when troublesome dyskinesia is evident.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>abnormal involuntary movements</term></item><item><term>continuous dopaminergic stimulation</term></item><item><term>dopamine agonists</term></item><item><term>L‐Dopa</term></item><item><term>Parkinson’s disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/21B15318C543E544E3F3BD8FA645985A299D6FAE/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="06112"><doi origin="wiley">10.1111/ejn.2011.33.issue-12</doi><numberingGroup><numbering type="journalVolume" number="33">33</numbering><numbering type="journalIssue" number="12">12</numbering></numberingGroup><coverDate startDate="2011-06">June 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2011.07704.x</doi><idGroup><id type="unit" value="EJN7704"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">NEUROSYSTEMS</title></titleGroup><copyright>© 2011 The Authors. European Journal of Neuroscience © 2011 Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.5 mode:FullText" date="2011-06-20"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-05-25"></event><event type="firstOnline" date="2011-05-25"></event><event type="publishedOnlineFinalForm" date="2011-06-20"></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="2247">2247</numbering><numbering type="pageLast" number="2254">2254</numbering></numberingGroup><correspondenceTo>Professor P. Jenner, as above.
E‐mail: <email>peter.jenner@kcl.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN7704.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 23 January 2011, revised 10 March 2011, accepted 28 March 2011</unparsedEditorialHistory><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats</title><title type="shortAuthors">M. Papathanou <i>et al.</i></title><title type="short">Dopaminergic stimulation in 6‐OHDA‐lesioned rats</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Maria</givenNames><familyName>Papathanou</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Sarah</givenNames><familyName>Rose</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>Andrew</givenNames><familyName>McCreary</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2"><personName><givenNames>Peter</givenNames><familyName>Jenner</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="SE"><unparsedAffiliation>Ludwig Institute for Cancer Research and Department of Cell and Molecular Biology, Karolinska Institutet, Box 240, Nobels väg 3, SE‐171 77 Stockholm, Sweden</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="GB"><unparsedAffiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="NL"><unparsedAffiliation>Abbott Healthcare B.V, C J Van Houtenlaan 36, Weesp, The Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">abnormal involuntary movements</keyword><keyword xml:id="k2">continuous dopaminergic stimulation</keyword><keyword xml:id="k3">dopamine agonists</keyword><keyword xml:id="k4">L‐Dopa</keyword><keyword xml:id="k5">Parkinson’s disease</keyword></keywordGroup><supportingInformation><p>Fig. S1. (A–C) Example of time course of rotational activity in three 6‐OHDA‐lesioned rats following an acute administration of amphetamine (2.5 mg/kg i.p.; dotted line) and apomorphine (0.5 mg/kg s.c.; continuous line) 2 weeks post surgery.</p><p>As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.</p><supportingInfoItem><mediaResource alt="supporting info item" href="urn-x:wiley:0953816X:media:ejn7704:EJN_7704_sm_figureS1"></mediaResource><caption>Supporting info item</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Dyskinesia induction in Parkinson’s disease (PD) appears less marked with long‐acting dopamine agonists than with short‐acting L‐Dopa, but the relationship to duration of drug action is unknown. It is also unclear whether the duration of drug action affects the expression of established dyskinesia. This study compared the ability of L‐Dopa and four dopamine agonists of different duration of action to induce abnormal involuntary movements (AIMs) in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, and their ability to express established AIMs following prior exposure to L‐Dopa. 6‐OHDA‐lesioned rats were treated with saline, L‐Dopa/benserazide, apomorphine, ropinirole, pramipexole or pergolide once daily for 15 days. Repeated administration of the short‐acting dopamine agonists, apomorphine (duration 80 min) and ropinirole (duration 90 min) induced marked axial, limb and orolingual AIMs at peak effect. L‐Dopa (duration 100 min) produced moderate AIMs at peak effect, while administration of the long‐acting dopamine agonists, pramipexole (duration 150 min) and pergolide (duration 240 min) resulted in mild AIMs. In rats primed to exhibit severe AIMs following repeated L‐Dopa administration, acute administration of apomorphine, ropinirole and L‐Dopa induced severe AIMs. By contrast, pramipexole and pergolide evoked only mild–moderate AIMs. Again, there was a negative correlation between duration of effect and the severity of AIMs expressed. These studies show that both the induction and expression of AIMs in 6‐OHDA‐lesioned rats are related to the duration of action of dopaminergic drugs. These findings suggest that continuous dopaminergic stimulation could be used both to avoid dyskinesia induction and to improve motor function in late‐stage PD when troublesome dyskinesia is evident.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats</title></titleInfo><titleInfo type="abbreviated"><title>Dopaminergic stimulation in 6‐OHDA‐lesioned rats</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Induction and expression of abnormal involuntary movements is related to the duration of dopaminergic stimulation in 6‐OHDA‐lesioned rats</title></titleInfo><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">Papathanou</namePart><affiliation>Ludwig Institute for Cancer Research and Department of Cell and Molecular Biology, Karolinska Institutet, Box 240, Nobels väg 3, SE‐171 77 Stockholm, Sweden</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sarah</namePart><namePart type="family">Rose</namePart><affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew</namePart><namePart type="family">McCreary</namePart><affiliation>Abbott Healthcare B.V, C J Van Houtenlaan 36, Weesp, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Jenner</namePart><affiliation>Neurodegenerative Disease Research Group, School of Biomedical Sciences, Kings College, Southwark, London SE1 8UB, UK</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">2011-06</dateIssued><edition>Received 23 January 2011, revised 10 March 2011, accepted 28 March 2011</edition><copyrightDate encoding="w3cdtf">2011</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">5</extent></physicalDescription><abstract lang="en">Dyskinesia induction in Parkinson’s disease (PD) appears less marked with long‐acting dopamine agonists than with short‐acting L‐Dopa, but the relationship to duration of drug action is unknown. It is also unclear whether the duration of drug action affects the expression of established dyskinesia. This study compared the ability of L‐Dopa and four dopamine agonists of different duration of action to induce abnormal involuntary movements (AIMs) in 6‐hydroxydopamine (6‐OHDA)‐lesioned rats, and their ability to express established AIMs following prior exposure to L‐Dopa. 6‐OHDA‐lesioned rats were treated with saline, L‐Dopa/benserazide, apomorphine, ropinirole, pramipexole or pergolide once daily for 15 days. Repeated administration of the short‐acting dopamine agonists, apomorphine (duration 80 min) and ropinirole (duration 90 min) induced marked axial, limb and orolingual AIMs at peak effect. L‐Dopa (duration 100 min) produced moderate AIMs at peak effect, while administration of the long‐acting dopamine agonists, pramipexole (duration 150 min) and pergolide (duration 240 min) resulted in mild AIMs. In rats primed to exhibit severe AIMs following repeated L‐Dopa administration, acute administration of apomorphine, ropinirole and L‐Dopa induced severe AIMs. By contrast, pramipexole and pergolide evoked only mild–moderate AIMs. Again, there was a negative correlation between duration of effect and the severity of AIMs expressed. These studies show that both the induction and expression of AIMs in 6‐OHDA‐lesioned rats are related to the duration of action of dopaminergic drugs. These findings suggest that continuous dopaminergic stimulation could be used both to avoid dyskinesia induction and to improve motor function in late‐stage PD when troublesome dyskinesia is evident.</abstract><subject lang="en"><genre>Keywords</genre><topic>abnormal involuntary movements</topic><topic>continuous dopaminergic stimulation</topic><topic>dopamine agonists</topic><topic>L‐Dopa</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Fig. S1. (A–C) Example of time course of rotational activity in three 6‐OHDA‐lesioned rats following an acute administration of amphetamine (2.5 mg/kg i.p.; dotted line) and apomorphine (0.5 mg/kg s.c.; continuous line) 2 weeks post surgery. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Fig. S1. (A–C) Example of time course of rotational activity in three 6‐OHDA‐lesioned rats following an acute administration of amphetamine (2.5 mg/kg i.p.; dotted line) and apomorphine (0.5 mg/kg s.c.; continuous line) 2 weeks post surgery. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer‐reviewed and may be re‐organized for online delivery, but are not copy‐edited or typeset by Wiley‐Blackwell. Technical support issues arising from supporting information (other than missing files) should be addressed to the authors.Supporting Info Item: Supporting info item - </note><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>2011</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>2247</start><end>2254</end><total>8</total></extent></part></relatedItem><identifier type="istex">21B15318C543E544E3F3BD8FA645985A299D6FAE</identifier><identifier type="DOI">10.1111/j.1460-9568.2011.07704.x</identifier><identifier type="ArticleID">EJN7704</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 The Authors. European Journal of Neuroscience © 2011 Federation of European Neuroscience Societies and Blackwell Publishing Ltd</accessCondition><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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