Decreased binding of the D3 dopamine receptor-preferring ligand [11C]-(+)-PHNO in drug-naive Parkinson's disease.
Identifieur interne : 000A18 ( Ncbi/Merge ); précédent : 000A17; suivant : 000A19Decreased binding of the D3 dopamine receptor-preferring ligand [11C]-(+)-PHNO in drug-naive Parkinson's disease.
Auteurs : Isabelle Boileau [Canada] ; Mark Guttman ; Pablo Rusjan ; John R. Adams ; Sylvain Houle ; Junchao Tong ; Oleh Hornykiewicz ; Yoshiaki Furukawa ; Alan A. Wilson ; Shitij Kapur ; Stephen J. KishSource :
- Brain : a journal of neurology [ 1460-2156 ] ; 2009.
English descriptors
- KwdEn :
- Aged, Binding, Competitive, Carbon Radioisotopes (metabolism), Case-Control Studies, Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Dopamine (metabolism), Dopamine Antagonists (metabolism), Dopamine Antagonists (therapeutic use), Female, Globus Pallidus (diagnostic imaging), Globus Pallidus (metabolism), Humans, Male, Middle Aged, Oxazines (metabolism), Parkinson Disease (diagnostic imaging), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Positron-Emission Tomography, Raclopride (metabolism), Raclopride (therapeutic use), Receptors, Dopamine D3 (metabolism), Statistics, Nonparametric.
- MESH :
- chemical , metabolism : Carbon Radioisotopes, Dopamine, Dopamine Antagonists, Oxazines, Raclopride, Receptors, Dopamine D3.
- diagnostic imaging : Corpus Striatum, Globus Pallidus, Parkinson Disease.
- drug therapy : Parkinson Disease.
- metabolism : Corpus Striatum, Globus Pallidus, Parkinson Disease.
- chemical , therapeutic use : Dopamine Antagonists, Raclopride.
- Aged, Binding, Competitive, Case-Control Studies, Female, Humans, Male, Middle Aged, Positron-Emission Tomography, Statistics, Nonparametric.
Abstract
The D(3) dopamine (DA) receptor is a member of the D(2)-like DA receptor family. While the D(2) receptor is abundant especially in motor-regions of the striatum, the D(3) receptor shows a relative abundance in limbic regions and globus pallidus. This receptor is of current interest in neurology because of its potential involvement in psychiatric and motor complications in Parkinson's disease and the possibility that dopamine D(3)-preferring agonist therapy might delay progression of the disorder. Preclinical data indicate that striatal levels of the D(3) (but not the D(2)) DA receptor are decreased following lesion of nigrostriatal DA neurons; at present, there are no in vivo data on this receptor subtype in Parkinson's disease. The objective of this positron emission tomography study was to compare [(11)C]-(+)-PHNO (D(3) versus D(2) preferring) and [(11)C]raclopride (D(3) = D(2)) binding in brain of non-depressed, non-demented, dopaminergic drug-naïve patients with early-stage Parkinson's disease (n = 10), relative to matched-controls (n = 9). Parkinson's disease was associated with a trend for bilaterally decreased [(11)C]-(+)-PHNO (but not [(11)C]raclopride) binding in the D(3)-rich ventral striatum (-11%, P = 0.07) and significantly decreased binding in globus pallidus (-42%, P = 0.02). In contrast, in the primarily D(2)-populated putamen, both [(11)C]-(+)-PHNO (25%, P = 0.02) and [(11)C]raclopride (25%, P < 0.01) binding were similarly increased, especially on the side contra-lateral to the symptoms. In the midbrain, presumably containing D(3) receptors localized to the substantia nigra, [(11)C]-(+)-PHNO binding was normal. Decreased [(11)C]-(+)-PHNO to [(11)C]raclopride ratio correlated with motor deficits and lowered-mood (P < 0.02). Our imaging data suggest that brain DA neuron loss in the human causes region-specific differential changes in DA D(2) and D(3) receptors with D(3) receptor 'downregulation' possibly related to some motor and mood problems in Parkinson disease. D(3) receptor levels might be a determinant vulnerability factor underlying side-effects associated with treatment; hence, these initial findings provide valuable baseline information to understand the role of D(3) receptors in response to Parkinson's disease medication.
DOI: 10.1093/brain/awn337
PubMed: 19153147
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pubmed:19153147Le document en format XML
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Adams</name></author><author><name sortKey="Houle, Sylvain" sort="Houle, Sylvain" uniqKey="Houle S" first="Sylvain" last="Houle">Sylvain Houle</name></author><author><name sortKey="Tong, Junchao" sort="Tong, Junchao" uniqKey="Tong J" first="Junchao" last="Tong">Junchao Tong</name></author><author><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name></author><author><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name></author><author><name sortKey="Wilson, Alan A" sort="Wilson, Alan A" uniqKey="Wilson A" first="Alan A" last="Wilson">Alan A. Wilson</name></author><author><name sortKey="Kapur, Shitij" sort="Kapur, Shitij" uniqKey="Kapur S" first="Shitij" last="Kapur">Shitij Kapur</name></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J" last="Kish">Stephen J. Kish</name></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="eISSN">1460-2156</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Binding, Competitive</term><term>Carbon Radioisotopes (metabolism)</term><term>Case-Control Studies</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Dopamine (metabolism)</term><term>Dopamine Antagonists (metabolism)</term><term>Dopamine Antagonists (therapeutic use)</term><term>Female</term><term>Globus Pallidus (diagnostic imaging)</term><term>Globus Pallidus (metabolism)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Oxazines (metabolism)</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Positron-Emission Tomography</term><term>Raclopride (metabolism)</term><term>Raclopride (therapeutic use)</term><term>Receptors, Dopamine D3 (metabolism)</term><term>Statistics, Nonparametric</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carbon Radioisotopes</term><term>Dopamine</term><term>Dopamine Antagonists</term><term>Oxazines</term><term>Raclopride</term><term>Receptors, Dopamine D3</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Globus Pallidus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Globus Pallidus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Dopamine Antagonists</term><term>Raclopride</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Binding, Competitive</term><term>Case-Control Studies</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term><term>Statistics, Nonparametric</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The D(3) dopamine (DA) receptor is a member of the D(2)-like DA receptor family. While the D(2) receptor is abundant especially in motor-regions of the striatum, the D(3) receptor shows a relative abundance in limbic regions and globus pallidus. This receptor is of current interest in neurology because of its potential involvement in psychiatric and motor complications in Parkinson's disease and the possibility that dopamine D(3)-preferring agonist therapy might delay progression of the disorder. Preclinical data indicate that striatal levels of the D(3) (but not the D(2)) DA receptor are decreased following lesion of nigrostriatal DA neurons; at present, there are no in vivo data on this receptor subtype in Parkinson's disease. The objective of this positron emission tomography study was to compare [(11)C]-(+)-PHNO (D(3) versus D(2) preferring) and [(11)C]raclopride (D(3) = D(2)) binding in brain of non-depressed, non-demented, dopaminergic drug-naïve patients with early-stage Parkinson's disease (n = 10), relative to matched-controls (n = 9). Parkinson's disease was associated with a trend for bilaterally decreased [(11)C]-(+)-PHNO (but not [(11)C]raclopride) binding in the D(3)-rich ventral striatum (-11%, P = 0.07) and significantly decreased binding in globus pallidus (-42%, P = 0.02). In contrast, in the primarily D(2)-populated putamen, both [(11)C]-(+)-PHNO (25%, P = 0.02) and [(11)C]raclopride (25%, P < 0.01) binding were similarly increased, especially on the side contra-lateral to the symptoms. In the midbrain, presumably containing D(3) receptors localized to the substantia nigra, [(11)C]-(+)-PHNO binding was normal. Decreased [(11)C]-(+)-PHNO to [(11)C]raclopride ratio correlated with motor deficits and lowered-mood (P < 0.02). Our imaging data suggest that brain DA neuron loss in the human causes region-specific differential changes in DA D(2) and D(3) receptors with D(3) receptor 'downregulation' possibly related to some motor and mood problems in Parkinson disease. D(3) receptor levels might be a determinant vulnerability factor underlying side-effects associated with treatment; hence, these initial findings provide valuable baseline information to understand the role of D(3) receptors in response to Parkinson's disease medication.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19153147</PMID><DateCreated><Year>2009</Year><Month>05</Month><Day>07</Day></DateCreated><DateCompleted><Year>2009</Year><Month>06</Month><Day>24</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1460-2156</ISSN><JournalIssue CitedMedium="Internet"><Volume>132</Volume><Issue>Pt 5</Issue><PubDate><Year>2009</Year><Month>May</Month></PubDate></JournalIssue><Title>Brain : a journal of neurology</Title><ISOAbbreviation>Brain</ISOAbbreviation></Journal><ArticleTitle>Decreased binding of the D3 dopamine receptor-preferring ligand [11C]-(+)-PHNO in drug-naive Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>1366-75</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1093/brain/awn337</ELocationID><Abstract><AbstractText>The D(3) dopamine (DA) receptor is a member of the D(2)-like DA receptor family. While the D(2) receptor is abundant especially in motor-regions of the striatum, the D(3) receptor shows a relative abundance in limbic regions and globus pallidus. This receptor is of current interest in neurology because of its potential involvement in psychiatric and motor complications in Parkinson's disease and the possibility that dopamine D(3)-preferring agonist therapy might delay progression of the disorder. Preclinical data indicate that striatal levels of the D(3) (but not the D(2)) DA receptor are decreased following lesion of nigrostriatal DA neurons; at present, there are no in vivo data on this receptor subtype in Parkinson's disease. The objective of this positron emission tomography study was to compare [(11)C]-(+)-PHNO (D(3) versus D(2) preferring) and [(11)C]raclopride (D(3) = D(2)) binding in brain of non-depressed, non-demented, dopaminergic drug-naïve patients with early-stage Parkinson's disease (n = 10), relative to matched-controls (n = 9). Parkinson's disease was associated with a trend for bilaterally decreased [(11)C]-(+)-PHNO (but not [(11)C]raclopride) binding in the D(3)-rich ventral striatum (-11%, P = 0.07) and significantly decreased binding in globus pallidus (-42%, P = 0.02). In contrast, in the primarily D(2)-populated putamen, both [(11)C]-(+)-PHNO (25%, P = 0.02) and [(11)C]raclopride (25%, P < 0.01) binding were similarly increased, especially on the side contra-lateral to the symptoms. In the midbrain, presumably containing D(3) receptors localized to the substantia nigra, [(11)C]-(+)-PHNO binding was normal. Decreased [(11)C]-(+)-PHNO to [(11)C]raclopride ratio correlated with motor deficits and lowered-mood (P < 0.02). Our imaging data suggest that brain DA neuron loss in the human causes region-specific differential changes in DA D(2) and D(3) receptors with D(3) receptor 'downregulation' possibly related to some motor and mood problems in Parkinson disease. D(3) receptor levels might be a determinant vulnerability factor underlying side-effects associated with treatment; hence, these initial findings provide valuable baseline information to understand the role of D(3) receptors in response to Parkinson's disease medication.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Boileau</LastName><ForeName>Isabelle</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Human Neurochemical Pathology Laboratory, University of Toronto, Toronto, Ontario, Canada. isabelle_boileau@CAMH.net</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guttman</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Rusjan</LastName><ForeName>Pablo</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Adams</LastName><ForeName>John R</ForeName><Initials>JR</Initials></Author><Author ValidYN="Y"><LastName>Houle</LastName><ForeName>Sylvain</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Tong</LastName><ForeName>Junchao</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Hornykiewicz</LastName><ForeName>Oleh</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Furukawa</LastName><ForeName>Yoshiaki</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Wilson</LastName><ForeName>Alan A</ForeName><Initials>AA</Initials></Author><Author ValidYN="Y"><LastName>Kapur</LastName><ForeName>Shitij</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kish</LastName><ForeName>Stephen J</ForeName><Initials>SJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>01</Month><Day>19</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="D002250">Carbon Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018492">Dopamine Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010078">Oxazines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050637">Receptors, Dopamine D3</NameOfSubstance></Chemical><Chemical><RegistryNumber>22Z7E0X6OF</RegistryNumber><NameOfSubstance UI="C042631">naxagolide</NameOfSubstance></Chemical><Chemical><RegistryNumber>430K3SOZ7G</RegistryNumber><NameOfSubstance UI="D020891">Raclopride</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="D001667" MajorTopicYN="N">Binding, Competitive</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002250" MajorTopicYN="N">Carbon Radioisotopes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018492" MajorTopicYN="N">Dopamine Antagonists</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005917" MajorTopicYN="N">Globus Pallidus</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010078" MajorTopicYN="N">Oxazines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></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="D020891" MajorTopicYN="N">Raclopride</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050637" MajorTopicYN="N">Receptors, Dopamine D3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018709" MajorTopicYN="N">Statistics, Nonparametric</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>1</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>1</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>6</Month><Day>25</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19153147</ArticleId><ArticleId IdType="pii">awn337</ArticleId><ArticleId IdType="doi">10.1093/brain/awn337</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><noCountry><name sortKey="Adams, John R" sort="Adams, John R" uniqKey="Adams J" first="John R" last="Adams">John R. Adams</name><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name><name sortKey="Hornykiewicz, Oleh" sort="Hornykiewicz, Oleh" uniqKey="Hornykiewicz O" first="Oleh" last="Hornykiewicz">Oleh Hornykiewicz</name><name sortKey="Houle, Sylvain" sort="Houle, Sylvain" uniqKey="Houle S" first="Sylvain" last="Houle">Sylvain Houle</name><name sortKey="Kapur, Shitij" sort="Kapur, Shitij" uniqKey="Kapur S" first="Shitij" last="Kapur">Shitij Kapur</name><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J" last="Kish">Stephen J. Kish</name><name sortKey="Rusjan, Pablo" sort="Rusjan, Pablo" uniqKey="Rusjan P" first="Pablo" last="Rusjan">Pablo Rusjan</name><name sortKey="Tong, Junchao" sort="Tong, Junchao" uniqKey="Tong J" first="Junchao" last="Tong">Junchao Tong</name><name sortKey="Wilson, Alan A" sort="Wilson, Alan A" uniqKey="Wilson A" first="Alan A" last="Wilson">Alan A. Wilson</name></noCountry><country name="Canada"><region name="Ontario"><name sortKey="Boileau, Isabelle" sort="Boileau, Isabelle" uniqKey="Boileau I" first="Isabelle" last="Boileau">Isabelle Boileau</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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HfdIndexSelect -h $EXPLOR_AREA/Data/Ncbi/Merge/RBID.i -Sk "pubmed:19153147" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Ncbi/Merge/biblio.hfd \
| NlmPubMed2Wicri -a ParkinsonCanadaV1
| This area was generated with Dilib version V0.6.29. |  |