Endogenous dopamine release after pharmacological challenges in Parkinson's disease
Identifieur interne : 001812 ( Main/Corpus ); précédent : 001811; suivant : 001813Endogenous dopamine release after pharmacological challenges in Parkinson's disease
Auteurs : Paola Piccini ; Nicola Pavese ; David J. BrooksSource :
- Annals of Neurology [ 0364-5134 ] ; 2003-05.
Abstract
Using 11C‐raclopride positron emission tomography after methamphetamine challenge, we have evaluated regional brain changes in synaptic dopamine (DA) levels in six volunteers and six advanced Parkinson's disease (PD) patients. The pharmacological challenge induced significant release of endogenous DA in putamen not only in the normal subjects, as reflected by a 25.2% reduction in 11C‐raclopride binding potential as compared with placebo, but also in the PD patients (6.8%). In individual PD patients, we found a correlation between putamen DA release and DA storage, as measured by 18F‐dopa uptake. Localization of significant changes in 11C‐raclopride binding after methamphetamine at a voxel level with statistical parametric mapping identified striatal and prefrontal DA release in both cohorts. Statistical comparisons between normal subjects and PD confirmed significantly reduced DA release in striatal areas in PD, but normal levels of prefrontal DA release. In conclusion, significant endogenous DA release can still be induced by pharmacological challenges in the putamen of advanced PD patients, and this release correlates with residual DA storage capacity. Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. Ann Neurol 2003
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DOI: 10.1002/ana.10526
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The pharmacological challenge induced significant release of endogenous DA in putamen not only in the normal subjects, as reflected by a 25.2% reduction in 11C‐raclopride binding potential as compared with placebo, but also in the PD patients (6.8%). In individual PD patients, we found a correlation between putamen DA release and DA storage, as measured by 18F‐dopa uptake. Localization of significant changes in 11C‐raclopride binding after methamphetamine at a voxel level with statistical parametric mapping identified striatal and prefrontal DA release in both cohorts. Statistical comparisons between normal subjects and PD confirmed significantly reduced DA release in striatal areas in PD, but normal levels of prefrontal DA release. In conclusion, significant endogenous DA release can still be induced by pharmacological challenges in the putamen of advanced PD patients, and this release correlates with residual DA storage capacity. Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. Ann Neurol 2003</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Paola Piccini MD</name><affiliations><json:string>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Nicola Pavese MD</name><affiliations><json:string>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>David J. 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In individual PD patients, we found a correlation between putamen DA release and DA storage, as measured by 18F‐dopa uptake. Localization of significant changes in 11C‐raclopride binding after methamphetamine at a voxel level with statistical parametric mapping identified striatal and prefrontal DA release in both cohorts. Statistical comparisons between normal subjects and PD confirmed significantly reduced DA release in striatal areas in PD, but normal levels of prefrontal DA release. In conclusion, significant endogenous DA release can still be induced by pharmacological challenges in the putamen of advanced PD patients, and this release correlates with residual DA storage capacity. Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. 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Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. 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affiliationRef="#af1" corresponding="yes"><personName><givenNames>Paola</givenNames><familyName>Piccini</familyName><degrees>MD</degrees></personName><contactDetails><email>paola.piccini@csc.mrc.ac.uk</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Nicola</givenNames><familyName>Pavese</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>David J.</givenNames><familyName>Brooks</familyName><degrees>MD, DSc, FRCP</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Institute of Neurology, London, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Using <sup>11</sup>C‐raclopride positron emission tomography after methamphetamine challenge, we have evaluated regional brain changes in synaptic dopamine (DA) levels in six volunteers and six advanced Parkinson's disease (PD) patients. The pharmacological challenge induced significant release of endogenous DA in putamen not only in the normal subjects, as reflected by a 25.2% reduction in <sup>11</sup>C‐raclopride binding potential as compared with placebo, but also in the PD patients (6.8%). In individual PD patients, we found a correlation between putamen DA release and DA storage, as measured by <sup>18</sup>F‐dopa uptake. Localization of significant changes in <sup>11</sup>C‐raclopride binding after methamphetamine at a voxel level with statistical parametric mapping identified striatal and prefrontal DA release in both cohorts. Statistical comparisons between normal subjects and PD confirmed significantly reduced DA release in striatal areas in PD, but normal levels of prefrontal DA release. In conclusion, significant endogenous DA release can still be induced by pharmacological challenges in the putamen of advanced PD patients, and this release correlates with residual DA storage capacity. Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. Ann Neurol 2003</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Endogenous dopamine release after pharmacological challenges in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Endogenous Dopamine Release</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Endogenous dopamine release after pharmacological challenges in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Piccini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation><description>Correspondence: MRC Cyclotron Building, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Road W12 0NN, London United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nicola</namePart><namePart type="family">Pavese</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><namePart type="termsOfAddress">MD, DSc, FRCP</namePart><affiliation>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, United Kingdom</affiliation><affiliation>Institute of Neurology, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2003-05</dateIssued><dateCaptured encoding="w3cdtf">2002-08-13</dateCaptured><dateValid encoding="w3cdtf">2002-12-21</dateValid><copyrightDate encoding="w3cdtf">2003</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">3</extent><extent unit="references">40</extent><extent unit="words">5044</extent></physicalDescription><abstract lang="en">Using 11C‐raclopride positron emission tomography after methamphetamine challenge, we have evaluated regional brain changes in synaptic dopamine (DA) levels in six volunteers and six advanced Parkinson's disease (PD) patients. The pharmacological challenge induced significant release of endogenous DA in putamen not only in the normal subjects, as reflected by a 25.2% reduction in 11C‐raclopride binding potential as compared with placebo, but also in the PD patients (6.8%). In individual PD patients, we found a correlation between putamen DA release and DA storage, as measured by 18F‐dopa uptake. Localization of significant changes in 11C‐raclopride binding after methamphetamine at a voxel level with statistical parametric mapping identified striatal and prefrontal DA release in both cohorts. Statistical comparisons between normal subjects and PD confirmed significantly reduced DA release in striatal areas in PD, but normal levels of prefrontal DA release. In conclusion, significant endogenous DA release can still be induced by pharmacological challenges in the putamen of advanced PD patients, and this release correlates with residual DA storage capacity. Our data also show that the capacity to release normal DA levels in prefrontal areas after a pharmacological challenge is preserved in severe stages of the disease. Ann Neurol 2003</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Original Articles</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>647</start><end>653</end><total>7</total></extent></part></relatedItem><identifier type="istex">E5B0FD15A455D9FA4621407A6B07D3D2FA0FA5DB</identifier><identifier type="DOI">10.1002/ana.10526</identifier><identifier type="ArticleID">ANA10526</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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