Levodopa-induced changes in synaptic dopamine levels increase with progression of Parkinson's disease: implications for dyskinesias.
Identifieur interne : 001304 ( PubMed/Checkpoint ); précédent : 001303; suivant : 001305Levodopa-induced changes in synaptic dopamine levels increase with progression of Parkinson's disease: implications for dyskinesias.
Auteurs : Raúl De La Fuente-Fernández [Canada] ; Vesna Sossi ; Zhigao Huang ; Sarah Furtado ; Jian-Qiang Lu ; Donald B. Calne ; Thomas J. Ruth ; A Jon StoesslSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2004.
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Antiparkinson Agents (adverse effects), Antiparkinson Agents (pharmacokinetics), Caudate Nucleus (diagnostic imaging), Caudate Nucleus (metabolism), Disease Progression, Dopamine (metabolism), Dyskinesia, Drug-Induced (diagnostic imaging), Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (metabolism), Female, Humans, Levodopa (adverse effects), Levodopa (pharmacokinetics), Male, Middle Aged, Parkinson Disease (diagnostic imaging), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Positron-Emission Tomography, Putamen (diagnostic imaging), Putamen (metabolism), Synapses (metabolism).
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , metabolism : Dopamine.
- chemical , pharmacokinetics : Antiparkinson Agents, Levodopa.
- diagnostic imaging : Caudate Nucleus, Dyskinesia, Drug-Induced, Parkinson Disease, Putamen.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- metabolism : Caudate Nucleus, Dyskinesia, Drug-Induced, Parkinson Disease, Putamen, Synapses.
- Aged, Analysis of Variance, Disease Progression, Female, Humans, Male, Middle Aged, Positron-Emission Tomography.
Abstract
Peak-dose dyskinesias are abnormal movements that usually occur 1 h after oral administration of levodopa, and often complicate chronic treatment of Parkinson's disease. We investigated by PET with [11C]raclopride whether Parkinson's disease progression modifies the striatal changes in synaptic dopamine levels induced by levodopa administration, and whether this modification, if present, could have an impact on the emergence of dyskinesias. We found that, 1 h after oral administration of standard-release 250/25 mg of levodopa/carbidopa, levodopa-induced increases in synaptic dopamine levels (as estimated by striatal changes in [11C]raclopride binding potential) correlated positively with duration of Parkinson's disease symptoms (for the caudate nucleus, r = 0.79, P < 0.001; for the putamen, r = 0.88, P < 0.0001). Patients with peak-dose dyskinesias had larger 1-h increases in synaptic dopamine levels than stable responders, but there were no between-group differences in [11C]raclopride binding 4 h post-levodopa. The corresponding (time x group) interaction term in the repeated measures analysis of covariance was significant, even after adjusting for between-group differences in duration of Parkinson's disease symptoms (for the caudate nucleus, P = 0.030; for the putamen, P = 0.021). Our results indicate that, at the synaptic level, an identical dose of levodopa induces increasingly larger 1-h changes in dopamine levels as Parkinson's disease progresses. Large levodopa-induced increases in synaptic dopamine concentration can lead to dramatic changes in receptor occupancy, which may be responsible for the emergence of peak-dose dyskinesias in Parkinson's disease.
DOI: 10.1093/brain/awh290
PubMed: 15329355
Affiliations:
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Calne</name></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name></author><author><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (pharmacokinetics)</term><term>Caudate Nucleus (diagnostic imaging)</term><term>Caudate Nucleus (metabolism)</term><term>Disease Progression</term><term>Dopamine (metabolism)</term><term>Dyskinesia, Drug-Induced (diagnostic imaging)</term><term>Dyskinesia, Drug-Induced (etiology)</term><term>Dyskinesia, Drug-Induced (metabolism)</term><term>Female</term><term>Humans</term><term>Levodopa (adverse effects)</term><term>Levodopa (pharmacokinetics)</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Positron-Emission Tomography</term><term>Putamen (diagnostic imaging)</term><term>Putamen (metabolism)</term><term>Synapses (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Caudate Nucleus</term><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Caudate Nucleus</term><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term><term>Putamen</term><term>Synapses</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Peak-dose dyskinesias are abnormal movements that usually occur 1 h after oral administration of levodopa, and often complicate chronic treatment of Parkinson's disease. We investigated by PET with [11C]raclopride whether Parkinson's disease progression modifies the striatal changes in synaptic dopamine levels induced by levodopa administration, and whether this modification, if present, could have an impact on the emergence of dyskinesias. We found that, 1 h after oral administration of standard-release 250/25 mg of levodopa/carbidopa, levodopa-induced increases in synaptic dopamine levels (as estimated by striatal changes in [11C]raclopride binding potential) correlated positively with duration of Parkinson's disease symptoms (for the caudate nucleus, r = 0.79, P < 0.001; for the putamen, r = 0.88, P < 0.0001). Patients with peak-dose dyskinesias had larger 1-h increases in synaptic dopamine levels than stable responders, but there were no between-group differences in [11C]raclopride binding 4 h post-levodopa. The corresponding (time x group) interaction term in the repeated measures analysis of covariance was significant, even after adjusting for between-group differences in duration of Parkinson's disease symptoms (for the caudate nucleus, P = 0.030; for the putamen, P = 0.021). Our results indicate that, at the synaptic level, an identical dose of levodopa induces increasingly larger 1-h changes in dopamine levels as Parkinson's disease progresses. Large levodopa-induced increases in synaptic dopamine concentration can lead to dramatic changes in receptor occupancy, which may be responsible for the emergence of peak-dose dyskinesias in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15329355</PMID><DateCreated><Year>2004</Year><Month>11</Month><Day>24</Day></DateCreated><DateCompleted><Year>2005</Year><Month>01</Month><Day>19</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>127</Volume><Issue>Pt 12</Issue><PubDate><Year>2004</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Levodopa-induced changes in synaptic dopamine levels increase with progression of Parkinson's disease: implications for dyskinesias.</ArticleTitle><Pagination><MedlinePgn>2747-54</MedlinePgn></Pagination><Abstract><AbstractText>Peak-dose dyskinesias are abnormal movements that usually occur 1 h after oral administration of levodopa, and often complicate chronic treatment of Parkinson's disease. We investigated by PET with [11C]raclopride whether Parkinson's disease progression modifies the striatal changes in synaptic dopamine levels induced by levodopa administration, and whether this modification, if present, could have an impact on the emergence of dyskinesias. We found that, 1 h after oral administration of standard-release 250/25 mg of levodopa/carbidopa, levodopa-induced increases in synaptic dopamine levels (as estimated by striatal changes in [11C]raclopride binding potential) correlated positively with duration of Parkinson's disease symptoms (for the caudate nucleus, r = 0.79, P < 0.001; for the putamen, r = 0.88, P < 0.0001). Patients with peak-dose dyskinesias had larger 1-h increases in synaptic dopamine levels than stable responders, but there were no between-group differences in [11C]raclopride binding 4 h post-levodopa. The corresponding (time x group) interaction term in the repeated measures analysis of covariance was significant, even after adjusting for between-group differences in duration of Parkinson's disease symptoms (for the caudate nucleus, P = 0.030; for the putamen, P = 0.021). Our results indicate that, at the synaptic level, an identical dose of levodopa induces increasingly larger 1-h changes in dopamine levels as Parkinson's disease progresses. Large levodopa-induced increases in synaptic dopamine concentration can lead to dramatic changes in receptor occupancy, which may be responsible for the emergence of peak-dose dyskinesias in Parkinson's disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>de la Fuente-Fernández</LastName><ForeName>Raúl</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sossi</LastName><ForeName>Vesna</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Zhigao</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Furtado</LastName><ForeName>Sarah</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Lu</LastName><ForeName>Jian-Qiang</ForeName><Initials>JQ</Initials></Author><Author ValidYN="Y"><LastName>Calne</LastName><ForeName>Donald B</ForeName><Initials>DB</Initials></Author><Author ValidYN="Y"><LastName>Ruth</LastName><ForeName>Thomas J</ForeName><Initials>TJ</Initials></Author><Author ValidYN="Y"><LastName>Stoessl</LastName><ForeName>A Jon</ForeName><Initials>AJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2004</Year><Month>08</Month><Day>25</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Brain</MedlineTA><NlmUniqueID>0372537</NlmUniqueID><ISSNLinking>0006-8950</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000493" MajorTopicYN="Y">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002421" MajorTopicYN="N">Caudate Nucleus</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName><QualifierName UI="Q000493" MajorTopicYN="Y">pharmacokinetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049268" MajorTopicYN="N">Positron-Emission Tomography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011699" MajorTopicYN="N">Putamen</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013569" MajorTopicYN="N">Synapses</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>8</Month><Day>27</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>1</Month><Day>20</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>8</Month><Day>27</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15329355</ArticleId><ArticleId IdType="doi">10.1093/brain/awh290</ArticleId><ArticleId IdType="pii">awh290</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B" last="Calne">Donald B. Calne</name><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</name><name sortKey="Huang, Zhigao" sort="Huang, Zhigao" uniqKey="Huang Z" first="Zhigao" last="Huang">Zhigao Huang</name><name sortKey="Lu, Jian Qiang" sort="Lu, Jian Qiang" uniqKey="Lu J" first="Jian-Qiang" last="Lu">Jian-Qiang Lu</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</name><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><name sortKey="Stoessl, A Jon" sort="Stoessl, A Jon" uniqKey="Stoessl A" first="A Jon" last="Stoessl">A Jon Stoessl</name></noCountry><country name="Canada"><noRegion><name sortKey="De La Fuente Fernandez, Raul" sort="De La Fuente Fernandez, Raul" uniqKey="De La Fuente Fernandez R" first="Raúl" last="De La Fuente-Fernández">Raúl De La Fuente-Fernández</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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