Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study
Identifieur interne : 002D73 ( Main/Corpus ); précédent : 002D72; suivant : 002D74Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study
Auteurs : Ines K. Goerendt ; Cristina Messa ; Andrew D. Lawrence ; Paul M. Grasby ; Paola Piccini ; David J. BrooksSource :
- Brain [ 0006-8950 ] ; 2003-02.
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Abstract
Parkinson’s disease is associated with slowness, especially of sequential movements, and is characterized pathologically by degeneration of dopaminergic neurons, particularly targeting nigrostriatal projections. In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate in vivo, with [11C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [11C]raclopride binding reflects dopamine D2 receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre‐learned sequence of finger movements, a significant reduction in binding potential (BP) of [11C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [11C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. These findings confirm that striatal dopamine release is a component of movement sequencing and show that dopamine release can be detected in early Parkinson’s disease during a behavioural manipulation.
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DOI: 10.1093/brain/awg035
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ISTEX:843AD076B8B7851E2994DD8E23B6FBBAF8338EDFLe document en format XML
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In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate in vivo, with [11C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [11C]raclopride binding reflects dopamine D2 receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre‐learned sequence of finger movements, a significant reduction in binding potential (BP) of [11C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [11C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. 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In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate in vivo, with [11C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [11C]raclopride binding reflects dopamine D2 receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre‐learned sequence of finger movements, a significant reduction in binding potential (BP) of [11C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [11C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. These findings confirm that striatal dopamine release is a component of movement sequencing and show that dopamine release can be detected in early Parkinson’s disease during a behavioural manipulation.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Keywords: Parkinson’s disease; dopamine; [11C]raclopride PET; sequential movement; fMRI</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>Abbreviations: BP = binding potential; DA = dopamine; RAC = [11C]raclopride; ROI = region of interest; SED = standard error of the difference of the means; SMA = supplementary motor area</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-02">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-15">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/843AD076B8B7851E2994DD8E23B6FBBAF8338EDF/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="research-article"><front><journal-meta><journal-id journal-id-type="hwp">brain</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="publisher-id">brainj</journal-id><journal-title>Brain</journal-title><abbrev-journal-title abbrev-type="publisher">Brain</abbrev-journal-title><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">awg035</article-id><article-id pub-id-type="doi">10.1093/brain/awg035</article-id><title-group><article-title>Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Goerendt</surname><given-names>Ines K.</given-names></name><xref rid="AWG035A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Messa</surname><given-names>Cristina</given-names></name><xref rid="AWG035A1">1</xref><xref rid="AWG035A3">3</xref><xref rid="AWG035A4">4</xref><xref rid="AWG035A5">5</xref></contrib><contrib contrib-type="author"><name><surname>Lawrence</surname><given-names>Andrew D.</given-names></name><xref rid="AWG035A1">1</xref><xref rid="AWG035A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Grasby</surname><given-names>Paul M.</given-names></name><xref rid="AWG035A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Piccini</surname><given-names>Paola</given-names></name><xref rid="AWG035A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Brooks</surname><given-names>David J.</given-names></name><xref rid="AWG035A1">1</xref></contrib><aff id="AWG035A1"><label>1</label>MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, </aff><aff id="AWG035A2"><label>2</label>MRC Cognition and Brain Sciences Unit, Cambridge, UK, </aff><aff id="AWG035A3"><label>3</label>INB‐CNR, </aff><aff id="AWG035A4"><label>4</label>University of Milano Bicocca and </aff><aff id="AWG035A5"><label>5</label>S. Raffaele Institute Milano, Italy.</aff><aff>Corresponding author: Andrew Lawrence, MRC Cognition and Brain Sciences Unit, 15 Chaucer Road, Cambridge CB2 2EF, UK E‐mail: <ext-link xlink:href="andrew.lawrence@mrc-cbu.cam.ac.uk" ext-link-type="email">andrew.lawrence@mrc‐cbu.cam.ac.uk</ext-link></aff></contrib-group><pub-date pub-type="ppub"><month>02</month><year>2003</year></pub-date><volume>126</volume><issue>2</issue><fpage>312</fpage><lpage>325</lpage><history><date date-type="accepted"><day>10</day><month>09</month><year>2002</year></date><date date-type="received"><day>03</day><month>04</month><year>2002</year></date><date date-type="rev-recd"><day>01</day><month>07</month><year>2002</year></date></history><copyright-year>2003</copyright-year><abstract xml:lang="en"><p>Parkinson’s disease is associated with slowness, especially of sequential movements, and is characterized pathologically by degeneration of dopaminergic neurons, particularly targeting nigrostriatal projections. In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate <italic>in vivo</italic>, with [<sup>11</sup>C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [<sup>11</sup>C]raclopride binding reflects dopamine D<sub>2</sub> receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre‐learned sequence of finger movements, a significant reduction in binding potential (BP) of [<sup>11</sup>C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [<sup>11</sup>C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. These findings confirm that striatal dopamine release is a component of movement sequencing and show that dopamine release can be detected in early Parkinson’s disease during a behavioural manipulation.</p></abstract><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd><bold>Keywords</bold>: Parkinson’s disease; dopamine; [<sup>11</sup>C]raclopride PET; sequential movement; fMRI</kwd></kwd-group><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd><bold>Abbreviations</bold>: BP = binding potential; DA = dopamine; RAC = [<sup>11</sup>C]raclopride; ROI = region of interest; SED = standard error of the difference of the means; SMA = supplementary motor area</kwd></kwd-group><custom-meta-wrap><custom-meta><meta-name>hwp-legacy-fpage</meta-name><meta-value>312</meta-value></custom-meta><custom-meta><meta-name>hwp-legacy-dochead</meta-name><meta-value>Article</meta-value></custom-meta></custom-meta-wrap></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Dopamine release during sequential finger movements in health and Parkinson’s disease: a PET study</title></titleInfo><name type="personal"><namePart type="given">Ines K.</namePart><namePart type="family">Goerendt</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cristina</namePart><namePart type="family">Messa</namePart><affiliation></affiliation><affiliation></affiliation><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew D.</namePart><namePart type="family">Lawrence</namePart><affiliation></affiliation><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul M.</namePart><namePart type="family">Grasby</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paola</namePart><namePart type="family">Piccini</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David J.</namePart><namePart type="family">Brooks</namePart><affiliation></affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article"></genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2003-02</dateIssued><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Parkinson’s disease is associated with slowness, especially of sequential movements, and is characterized pathologically by degeneration of dopaminergic neurons, particularly targeting nigrostriatal projections. In turn, nigrostriatal dopamine has been suggested to be critical for the execution of sequential movements. The objective of this study was to investigate in vivo, with [11C]raclopride, PET changes in regional brain levels of dopamine in healthy volunteers and Parkinson’s disease patients during the execution of paced, stereotyped sequential finger movements. Striatal [11C]raclopride binding reflects dopamine D2 receptor availability and is influenced by synaptic levels of endogenous dopamine. During execution of a pre‐learned sequence of finger movements, a significant reduction in binding potential (BP) of [11C]raclopride was seen in both caudate and putamen in healthy volunteers compared with a resting baseline, consistent with release of endogenous dopamine. Parkinson’s disease patients also showed attenuated [11C]raclopride BP reductions during the same motor paradigm in striatal areas less affected by the disease process. These findings confirm that striatal dopamine release is a component of movement sequencing and show that dopamine release can be detected in early Parkinson’s disease during a behavioural manipulation.</abstract><subject lang="en"><genre>KWD</genre><topic>Keywords: Parkinson’s disease; dopamine; [11C]raclopride PET; sequential movement; fMRI</topic></subject><subject lang="en"><genre>ABR</genre><topic>Abbreviations: BP = binding potential; DA = dopamine; RAC = [11C]raclopride; ROI = region of interest; SED = standard error of the difference of the means; SMA = supplementary motor area</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><titleInfo type="abbreviated"><title>Brain</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><identifier type="PublisherID-nlm-ta">Brain</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>126</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>312</start><end>325</end></extent></part></relatedItem><identifier type="istex">843AD076B8B7851E2994DD8E23B6FBBAF8338EDF</identifier><identifier type="DOI">10.1093/brain/awg035</identifier><identifier type="local">awg035</identifier><recordInfo><recordContentSource>OUP</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/843AD076B8B7851E2994DD8E23B6FBBAF8338EDF/annexes/jpeg</uri></json:item><json:item><original>true</original><mimetype>image/gif</mimetype><extension>gif</extension><uri>https://api.istex.fr/document/843AD076B8B7851E2994DD8E23B6FBBAF8338EDF/annexes/gif</uri></json:item></annexes><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/843AD076B8B7851E2994DD8E23B6FBBAF8338EDF/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">CLINICAL NEUROLOGY</classCode><classCode scheme="WOS">NEUROSCIENCES</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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