Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced dyskinesia
Identifieur interne : 000B90 ( Main/Corpus ); précédent : 000B89; suivant : 000B91Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced dyskinesia
Auteurs : Mahmoud M. Iravani ; Sergio Costa ; Ghassan Al-Bargouthy ; Michael J. Jackson ; Bai-Yun Zeng ; Mikko Kuoppam Ki ; Jose A. Obeso ; Peter JennerSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2005-09.
English descriptors
- KwdEn :
Abstract
Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.
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DOI: 10.1111/j.1460-9568.2005.04308.x
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Iravani</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Costa, Sergio" sort="Costa, Sergio" uniqKey="Costa S" first="Sergio" last="Costa">Sergio Costa</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Al Argouthy, Ghassan" sort="Al Argouthy, Ghassan" uniqKey="Al Argouthy G" first="Ghassan" last="Al-Bargouthy">Ghassan Al-Bargouthy</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Jackson, Michael J" sort="Jackson, Michael J" uniqKey="Jackson M" first="Michael J." last="Jackson">Michael J. 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Obeso</name><affiliation><mods:affiliation>Department of Neurology and Neurosurgery, Neuroscience Centre, Clinica Universitaria and Medical School, University of Navarra and FIMA, Pamplona, Spain</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 Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, 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 Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-09">2005-09</date><biblScope unit="volume">22</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1305">1305</biblScope><biblScope unit="page" to="1318">1318</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">57CA92414D8BA630969BF5B26F0D3B78EE25815C</idno><idno type="DOI">10.1111/j.1460-9568.2005.04308.x</idno><idno type="ArticleID">EJN4308</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</term><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated primates</term><term>dyskinesia</term><term>globus pallidus</term><term>levodopa</term><term>pallidotomy</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mahmoud M. 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Obeso</name><affiliations><json:string>Department of Neurology and Neurosurgery, Neuroscience Centre, Clinica Universitaria and Medical School, University of Navarra and FIMA, Pamplona, Spain</json:string></affiliations></json:item><json:item><name>Peter Jenner</name><affiliations><json:string>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>dyskinesia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>globus pallidus</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated primates</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pallidotomy</value></json:item></subject><articleId><json:string>EJN4308</json:string></articleId><language><json:string>eng</json:string></language><abstract>Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.</abstract><qualityIndicators><score>8.476</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1836</abstractCharCount><pdfWordCount>7123</pdfWordCount><pdfCharCount>44907</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>248</abstractWordCount></qualityIndicators><title>Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced 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UK</affiliation></author><author><persName><forename type="first">Ghassan</forename><surname>Al‐Bargouthy</surname></persName><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">Michael J.</forename><surname>Jackson</surname></persName><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">Bai‐Yun</forename><surname>Zeng</surname></persName><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">Mikko</forename><surname>Kuoppamäki</surname></persName><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">Jose A.</forename><surname>Obeso</surname></persName><affiliation>Department of Neurology and Neurosurgery, Neuroscience Centre, Clinica Universitaria and Medical School, University of Navarra and FIMA, Pamplona, Spain</affiliation></author><author><persName><forename type="first">Peter</forename><surname>Jenner</surname></persName><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</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 Science Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2005-09"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1305">1305</biblScope><biblScope unit="page" to="1318">1318</biblScope></imprint></monogr><idno type="istex">57CA92414D8BA630969BF5B26F0D3B78EE25815C</idno><idno type="DOI">10.1111/j.1460-9568.2005.04308.x</idno><idno type="ArticleID">EJN4308</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>dyskinesia</term></item><item><term>globus pallidus</term></item><item><term>levodopa</term></item><item><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</term></item><item><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated primates</term></item><item><term>pallidotomy</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-09">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/57CA92414D8BA630969BF5B26F0D3B78EE25815C/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 Science 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="09106"><doi origin="wiley">10.1111/ejn.2005.22.issue-6</doi><numberingGroup><numbering type="journalVolume" number="22">22</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2005-09">September 2005</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="5" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2005.04308.x</doi><idGroup><id type="unit" value="EJN4308"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2005-09-27"></event><event type="publishedOnlineFinalForm" date="2005-09-27"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.27 mode:FullText source:FullText result:FullText" date="2010-12-09"></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="1305">1305</numbering><numbering type="pageLast" number="1318">1318</numbering></numberingGroup><correspondenceTo>Professor Peter Jenner, as above.
E‐mail: <email>div.pharm@kcl.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN4308.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 5 April 2005, revised 19 June 2005, accepted 4 July 2005</unparsedEditorialHistory><countGroup><count type="figureTotal" number="10"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="63"></count><count type="wordTotal" number="5542"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced dyskinesia</title><title type="shortAuthors">M. M. Iravani <i>et al.</i></title><title type="short">Pallidotomy in dyskinetic MPTP‐treated primates</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Mahmoud M.</givenNames><familyName>Iravani</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Sergio</givenNames><familyName>Costa</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Ghassan</givenNames><familyName>Al‐Bargouthy</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Michael J.</givenNames><familyName>Jackson</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Bai‐Yun</givenNames><familyName>Zeng</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Mikko</givenNames><familyName>Kuoppamäki</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a2"><personName><givenNames>Jose A.</givenNames><familyName>Obeso</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>Peter</givenNames><familyName>Jenner</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="GB"><unparsedAffiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="ES"><unparsedAffiliation>Department of Neurology and Neurosurgery, Neuroscience Centre, Clinica Universitaria and Medical School, University of Navarra and FIMA, Pamplona, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">dyskinesia</keyword><keyword xml:id="k2">globus pallidus</keyword><keyword xml:id="k3">levodopa</keyword><keyword xml:id="k4">1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</keyword><keyword xml:id="k5">1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated primates</keyword><keyword xml:id="k6">pallidotomy</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced dyskinesia</title></titleInfo><titleInfo type="abbreviated"><title>Pallidotomy in dyskinetic MPTP‐treated primates</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Unilateral pallidotomy in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets exhibiting levodopa‐induced dyskinesia</title></titleInfo><name type="personal"><namePart type="given">Mahmoud M.</namePart><namePart type="family">Iravani</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sergio</namePart><namePart type="family">Costa</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ghassan</namePart><namePart type="family">Al‐Bargouthy</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael J.</namePart><namePart type="family">Jackson</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bai‐Yun</namePart><namePart type="family">Zeng</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mikko</namePart><namePart type="family">Kuoppamäki</namePart><affiliation>Neurodegenerative Disease Research Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose A.</namePart><namePart type="family">Obeso</namePart><affiliation>Department of Neurology and Neurosurgery, Neuroscience Centre, Clinica Universitaria and Medical School, University of Navarra and FIMA, Pamplona, Spain</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 Centre, GKT School of Biomedical Sciences, King's College London, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Science Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2005-09</dateIssued><edition>Received 5 April 2005, revised 19 June 2005, accepted 4 July 2005</edition><copyrightDate encoding="w3cdtf">2005</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">10</extent><extent unit="references">63</extent><extent unit="words">5542</extent></physicalDescription><abstract lang="en">Pallidotomy paradoxically reduces the intensity of levodopa‐induced dyskinesia without worsening motor symptoms. The reasons for this are not clear and no experimental study has investigated this phenomenon. The objective of this investigation was to evaluate the effects of unilateral pallidotomy on locomotor activity, motor disability and levodopa‐induced dyskinesia in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated levodopa‐primed common marmosets. Animals were primed to exhibit dyskinesia by daily administration of levodopa until stable dyskinesia was evoked by each dose. Locomotor activity, motor disability and dyskinesia were assessed weekly at baseline and following an acute levodopa challenge. Prior to pallidotomies, two distinct groups of animals emerged: poor responders to levodopa with mild dyskinesia (Group 1) and those exhibiting a marked increase in motor activity and pronounced dyskinesia (Group 2). Electrolytic lesions were placed in the left internal segment of the globus pallidus. Pallidotomy had no effect on basal or levodopa‐induced motor activity in either group but significantly improved basal motor disability in Group 2. Following pallidotomy, the ability of levodopa to reduce motor disability was significantly increased in both groups. Pallidotomy improved dyskinesia in both Groups 1 and 2 but it was more effective in reducing dystonia compared with chorea. The effect of pallidotomy on dyskinesia in Group 2 was transient, with the intensity of involuntary movements reverting to presurgery levels 4 weeks later. This study shows that in levodopa‐primed, parkinsonian marmosets, placement of discrete globus pallidus lesions can ameliorate levodopa‐induced dyskinesia but not akinesia. This model allows the evaluation of pallidotomy‐induced biochemical changes in dyskinetic primates.</abstract><subject lang="en"><genre>Keywords</genre><topic>dyskinesia</topic><topic>globus pallidus</topic><topic>levodopa</topic><topic>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</topic><topic>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated primates</topic><topic>pallidotomy</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>2005</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>1305</start><end>1318</end><total>14</total></extent></part></relatedItem><identifier type="istex">57CA92414D8BA630969BF5B26F0D3B78EE25815C</identifier><identifier type="DOI">10.1111/j.1460-9568.2005.04308.x</identifier><identifier type="ArticleID">EJN4308</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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