VMAT2 binding is elevated in dopa-responsive dystonia: visualizing empty vesicles by PET.
Identifieur interne : 001342 ( PubMed/Checkpoint ); précédent : 001341; suivant : 001343VMAT2 binding is elevated in dopa-responsive dystonia: visualizing empty vesicles by PET.
Auteurs : Raúl De La Fuente-Fernández [Canada] ; Sarah Furtado ; Mark Guttman ; Yoshiaki Furukawa ; Chong S. Lee ; Donald B. Calne ; Thomas J. Ruth ; A Jon StoesslSource :
- Synapse (New York, N.Y.) [ 0887-4476 ] ; 2003.
English descriptors
- KwdEn :
- Adolescent, Adult, Carbon Radioisotopes, Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Cytoplasmic Vesicles (metabolism), Cytoplasmic Vesicles (ultrastructure), Dopamine (deficiency), Dopamine (metabolism), Dopamine Agents, Dystonic Disorders (diagnostic imaging), Dystonic Disorders (drug therapy), Dystonic Disorders (genetics), Dystonic Disorders (metabolism), Female, Fluorine Radioisotopes, Humans, Levodopa (therapeutic use), Male, Membrane Glycoproteins (metabolism), Membrane Transport Proteins, Methylphenidate, Middle Aged, Neuropeptides, Parkinson Disease (metabolism), Raclopride, Tetrabenazine (analogs & derivatives), Tomography, Emission-Computed, Vesicular Biogenic Amine Transport Proteins, Vesicular Monoamine Transport Proteins.
- MESH :
- chemical , analogs & derivatives : Tetrabenazine.
- chemical , deficiency : Dopamine.
- chemical , metabolism : Dopamine, Membrane Glycoproteins.
- chemical , therapeutic use : Levodopa.
- chemical : Carbon Radioisotopes, Dopamine Agents, Fluorine Radioisotopes, Membrane Transport Proteins, Methylphenidate, Neuropeptides, Raclopride, Vesicular Biogenic Amine Transport Proteins, Vesicular Monoamine Transport Proteins.
- diagnostic imaging : Corpus Striatum, Dystonic Disorders.
- drug therapy : Dystonic Disorders.
- genetics : Dystonic Disorders.
- metabolism : Corpus Striatum, Cytoplasmic Vesicles, Dystonic Disorders, Parkinson Disease.
- ultrastructure : Cytoplasmic Vesicles.
- Adolescent, Adult, Female, Humans, Male, Middle Aged, Tomography, Emission-Computed.
Abstract
Dopa-responsive dystonia (DRD) is a lifelong disorder in which dopamine deficiency is not associated with neuronal loss and therefore it is an ideal human model for investigating the compensatory changes that occur in response to this biochemical abnormality. Using positron emission tomography (PET), we examined the (+/-)-alpha-[(11)C]dihydrotetrabenazine ([(11)C]DTBZ) binding potential of untreated DRD patients and normal controls. Two other PET markers of presynaptic nigrostriatal function, d-threo-[(11)C]methylphenidate ([(11)C]MP) and 6-[(18)F]fluoro-L-dopa ([(18)F]-dopa), and [(11)C]raclopride were also used in the study. We found increased [(11)C]DTBZ binding potential in the striatum of DRD patients. By contrast, no significant changes were detected in either [(11)C]MP binding potential or [(18)F]-dopa uptake rate constant. In addition, we found evidence for increased dopamine turnover in one DRD patient by examining changes in [(11)C]raclopride binding potential in relation to levodopa treatment. We propose that the increase in [(11)C]DTBZ binding likely reflects the dramatic decrease in the intravesicular concentration of dopamine that occurs in DRD; upregulation of vesicular monoamine transporter type 2 (VMAT2) expression may also contribute. Our findings suggest that the striatal expression of VMAT2 (as estimated by [(11)C]DTBZ binding) is not coregulated with dopamine synthesis. This is in keeping with a role for VMAT2 in other cellular processes (i.e., sequestration and release from the cell of potential toxic products), in addition to its importance for the quantal release of monoamines.
DOI: 10.1002/syn.10199
PubMed: 12710012
Affiliations:
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pubmed:12710012Le document en format XML
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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">Synapse (New York, N.Y.)</title><idno type="ISSN">0887-4476</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Carbon Radioisotopes</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Cytoplasmic Vesicles (metabolism)</term><term>Cytoplasmic Vesicles (ultrastructure)</term><term>Dopamine (deficiency)</term><term>Dopamine (metabolism)</term><term>Dopamine Agents</term><term>Dystonic Disorders (diagnostic imaging)</term><term>Dystonic Disorders (drug therapy)</term><term>Dystonic Disorders (genetics)</term><term>Dystonic Disorders (metabolism)</term><term>Female</term><term>Fluorine Radioisotopes</term><term>Humans</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Membrane Glycoproteins (metabolism)</term><term>Membrane Transport Proteins</term><term>Methylphenidate</term><term>Middle Aged</term><term>Neuropeptides</term><term>Parkinson Disease (metabolism)</term><term>Raclopride</term><term>Tetrabenazine (analogs & derivatives)</term><term>Tomography, Emission-Computed</term><term>Vesicular Biogenic Amine Transport Proteins</term><term>Vesicular Monoamine Transport Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Membrane Glycoproteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Carbon Radioisotopes</term><term>Dopamine Agents</term><term>Fluorine Radioisotopes</term><term>Membrane Transport Proteins</term><term>Methylphenidate</term><term>Neuropeptides</term><term>Raclopride</term><term>Vesicular Biogenic Amine Transport Proteins</term><term>Vesicular Monoamine Transport Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Cytoplasmic Vesicles</term><term>Dystonic Disorders</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Cytoplasmic Vesicles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Tomography, Emission-Computed</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Dopa-responsive dystonia (DRD) is a lifelong disorder in which dopamine deficiency is not associated with neuronal loss and therefore it is an ideal human model for investigating the compensatory changes that occur in response to this biochemical abnormality. Using positron emission tomography (PET), we examined the (+/-)-alpha-[(11)C]dihydrotetrabenazine ([(11)C]DTBZ) binding potential of untreated DRD patients and normal controls. Two other PET markers of presynaptic nigrostriatal function, d-threo-[(11)C]methylphenidate ([(11)C]MP) and 6-[(18)F]fluoro-L-dopa ([(18)F]-dopa), and [(11)C]raclopride were also used in the study. We found increased [(11)C]DTBZ binding potential in the striatum of DRD patients. By contrast, no significant changes were detected in either [(11)C]MP binding potential or [(18)F]-dopa uptake rate constant. In addition, we found evidence for increased dopamine turnover in one DRD patient by examining changes in [(11)C]raclopride binding potential in relation to levodopa treatment. We propose that the increase in [(11)C]DTBZ binding likely reflects the dramatic decrease in the intravesicular concentration of dopamine that occurs in DRD; upregulation of vesicular monoamine transporter type 2 (VMAT2) expression may also contribute. Our findings suggest that the striatal expression of VMAT2 (as estimated by [(11)C]DTBZ binding) is not coregulated with dopamine synthesis. This is in keeping with a role for VMAT2 in other cellular processes (i.e., sequestration and release from the cell of potential toxic products), in addition to its importance for the quantal release of monoamines.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12710012</PMID><DateCreated><Year>2003</Year><Month>04</Month><Day>23</Day></DateCreated><DateCompleted><Year>2003</Year><Month>07</Month><Day>17</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0887-4476</ISSN><JournalIssue CitedMedium="Print"><Volume>49</Volume><Issue>1</Issue><PubDate><Year>2003</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Synapse (New York, N.Y.)</Title><ISOAbbreviation>Synapse</ISOAbbreviation></Journal><ArticleTitle>VMAT2 binding is elevated in dopa-responsive dystonia: visualizing empty vesicles by PET.</ArticleTitle><Pagination><MedlinePgn>20-8</MedlinePgn></Pagination><Abstract><AbstractText>Dopa-responsive dystonia (DRD) is a lifelong disorder in which dopamine deficiency is not associated with neuronal loss and therefore it is an ideal human model for investigating the compensatory changes that occur in response to this biochemical abnormality. Using positron emission tomography (PET), we examined the (+/-)-alpha-[(11)C]dihydrotetrabenazine ([(11)C]DTBZ) binding potential of untreated DRD patients and normal controls. Two other PET markers of presynaptic nigrostriatal function, d-threo-[(11)C]methylphenidate ([(11)C]MP) and 6-[(18)F]fluoro-L-dopa ([(18)F]-dopa), and [(11)C]raclopride were also used in the study. We found increased [(11)C]DTBZ binding potential in the striatum of DRD patients. By contrast, no significant changes were detected in either [(11)C]MP binding potential or [(18)F]-dopa uptake rate constant. In addition, we found evidence for increased dopamine turnover in one DRD patient by examining changes in [(11)C]raclopride binding potential in relation to levodopa treatment. We propose that the increase in [(11)C]DTBZ binding likely reflects the dramatic decrease in the intravesicular concentration of dopamine that occurs in DRD; upregulation of vesicular monoamine transporter type 2 (VMAT2) expression may also contribute. Our findings suggest that the striatal expression of VMAT2 (as estimated by [(11)C]DTBZ binding) is not coregulated with dopamine synthesis. This is in keeping with a role for VMAT2 in other cellular processes (i.e., sequestration and release from the cell of potential toxic products), in addition to its importance for the quantal release of monoamines.</AbstractText><CopyrightInformation>Copyright 2003 Wiley-Liss, Inc.</CopyrightInformation></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, B.C., Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Furtado</LastName><ForeName>Sarah</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Guttman</LastName><ForeName>Mark</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Furukawa</LastName><ForeName>Yoshiaki</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Chong S</ForeName><Initials>CS</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="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Synapse</MedlineTA><NlmUniqueID>8806914</NlmUniqueID><ISSNLinking>0887-4476</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002250">Carbon Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015259">Dopamine Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005462">Fluorine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009479">Neuropeptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493452">SLC18A2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050492">Vesicular Biogenic Amine Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050493">Vesicular Monoamine Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>207ZZ9QZ49</RegistryNumber><NameOfSubstance UI="D008774">Methylphenidate</NameOfSubstance></Chemical><Chemical><RegistryNumber>3466-75-9</RegistryNumber><NameOfSubstance UI="C032811">dihydrotetrabenazine</NameOfSubstance></Chemical><Chemical><RegistryNumber>430K3SOZ7G</RegistryNumber><NameOfSubstance UI="D020891">Raclopride</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>Z9O08YRN8O</RegistryNumber><NameOfSubstance UI="D013747">Tetrabenazine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002250" MajorTopicYN="N">Carbon Radioisotopes</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="D022162" MajorTopicYN="N">Cytoplasmic Vesicles</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015259" MajorTopicYN="N">Dopamine Agents</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020821" MajorTopicYN="N">Dystonic Disorders</DescriptorName><QualifierName UI="Q000000981" MajorTopicYN="N">diagnostic imaging</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005462" MajorTopicYN="N">Fluorine Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008562" MajorTopicYN="N">Membrane Glycoproteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="Y">Membrane Transport Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008774" MajorTopicYN="N">Methylphenidate</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009479" MajorTopicYN="Y">Neuropeptides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020891" 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Calne</name><name sortKey="Furtado, Sarah" sort="Furtado, Sarah" uniqKey="Furtado S" first="Sarah" last="Furtado">Sarah Furtado</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="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S" last="Lee">Chong S. Lee</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J" last="Ruth">Thomas J. Ruth</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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