In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease
Identifieur interne : 003485 ( Main/Exploration ); précédent : 003484; suivant : 003486In vivo positron emission tomographic evidence for compensatory changes in presynaptic dopaminergic nerve terminals in Parkinson's disease
Auteurs : Chong S. Lee [Canada] ; Ali Samii [Canada] ; Vesna Sossi [Canada] ; Thomas J. Ruth [Canada] ; Michael Schulzer [Canada] ; James E. Holden [États-Unis] ; Jess Wudel [Canada] ; Pramod K. Pal [Canada] ; Raul De La Fuente-Fernandez [Canada] ; Donald B. Calne [Canada] ; A. Jon Stoessl [Canada]Source :
- Annals of Neurology [ 0364-5134 ] ; 2000-04.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Aged, Carbon Radioisotopes, Carrier Proteins (metabolism), Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Corpus striatum, Dopamine (metabolism), Dopamine Plasma Membrane Transport Proteins, Dopaminergic neuron, Down-Regulation (physiology), Emission tomography, Exploration, Fluorine Radioisotopes, Homovanillic Acid (metabolism), Human, Humans, In vivo, Membrane Glycoproteins, Membrane Transport Proteins, Middle Aged, Nerve Tissue Proteins, Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Parkinson disease, Positron, Presynaptic Terminals (metabolism), Presynaptic nerve ending, Tetrabenazine (analogs & derivatives), Tomography, Emission-Computed.
- MESH :
- chemical , analogs & derivatives : Tetrabenazine.
- chemical , metabolism : Carrier Proteins, Dopamine, Homovanillic Acid.
- chemical : Carbon Radioisotopes, Dopamine Plasma Membrane Transport Proteins, Fluorine Radioisotopes, Membrane Glycoproteins, Membrane Transport Proteins, Nerve Tissue Proteins.
- diagnostic imaging : Corpus Striatum, Parkinson Disease.
- metabolism : Corpus Striatum, Parkinson Disease, Presynaptic Terminals.
- physiology : Down-Regulation.
- Aged, Humans, Middle Aged, Tomography, Emission-Computed.
Abstract
Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using [11C]dihydrotetrabenazine ([11C]DTBZ; labeling the vesicular monoamine transporter type 2), [11C]methylphenidate (labeling the plasma membrane DA transporter), and [18F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three‐dimensional mode by using each tracer on 35 patients and 16 age‐matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug‐naive and drug‐treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [18F]dopa and [11C]DTBZ, and of [11C]methylphenidate and [11C]DTBZ, were compared between the PD and the normal control subjects. We found that [18F]dopa Ki was reduced less than the binding potential (Bmax/Kd) for [11C]DTBZ in the parkinsonian striatum, whereas the [11C]methylphenidate binding potential was reduced more than [11C]DTBZ binding potential. These observations suggest that the activity of aromatic L‐amino acid decarboxylase is up‐regulated, whereas the plasma membrane DA transporter is down‐regulated in the striatum of patients with PD. Ann Neurol 2000;47:493–503.
Url:
DOI: 10.1002/1531-8249(200004)47:4<493::AID-ANA13>3.0.CO;2-4
Affiliations:
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Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation><affiliation wicri:level="1"><country>Canada</country><wicri:regionArea>Neurodegenerative Disorders Centre, Purdy Pavilion, Vancouver Hospital and Health Sciences Centre, 2221 Wesbrook Mall, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Samii, Ali" sort="Samii, Ali" uniqKey="Samii A" first="Ali" last="Samii">Ali Samii</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Sossi, Vesna" sort="Sossi, Vesna" uniqKey="Sossi V" first="Vesna" last="Sossi">Vesna Sossi</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>TRIUMF, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J." last="Ruth">Thomas J. 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Holden</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Wisconsin</region></placeName><wicri:cityArea>Department of Medical Physics, University of Wisconsin, Madison</wicri:cityArea></affiliation></author><author><name sortKey="Wudel, Jess" sort="Wudel, Jess" uniqKey="Wudel J" first="Jess" last="Wudel">Jess Wudel</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Pal, Pramod K" sort="Pal, Pramod K" uniqKey="Pal P" first="Pramod K." last="Pal">Pramod K. 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Jon Stoessl</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Neurodegenerative Disorders Centre, Vancouver Hospital and Health Sciences Centre, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2000-04">2000-04</date><biblScope unit="volume">47</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="493">493</biblScope><biblScope unit="page" to="503">503</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">DD5F4FDC31B8B85FA9A92FEDD6B1427EB473593F</idno><idno type="DOI">10.1002/1531-8249(200004)47:4<493::AID-ANA13>3.0.CO;2-4</idno><idno type="ArticleID">ANA13</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Carbon Radioisotopes</term><term>Carrier Proteins (metabolism)</term><term>Corpus Striatum (diagnostic imaging)</term><term>Corpus Striatum (metabolism)</term><term>Corpus striatum</term><term>Dopamine (metabolism)</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Dopaminergic neuron</term><term>Down-Regulation (physiology)</term><term>Emission tomography</term><term>Exploration</term><term>Fluorine Radioisotopes</term><term>Homovanillic Acid (metabolism)</term><term>Human</term><term>Humans</term><term>In vivo</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Middle Aged</term><term>Nerve Tissue Proteins</term><term>Parkinson Disease (diagnostic imaging)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson disease</term><term>Positron</term><term>Presynaptic Terminals (metabolism)</term><term>Presynaptic nerve ending</term><term>Tetrabenazine (analogs & derivatives)</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carrier Proteins</term><term>Dopamine</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Carbon Radioisotopes</term><term>Dopamine Plasma Membrane Transport Proteins</term><term>Fluorine Radioisotopes</term><term>Membrane Glycoproteins</term><term>Membrane Transport Proteins</term><term>Nerve Tissue Proteins</term></keywords><keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Presynaptic Terminals</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Down-Regulation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Middle Aged</term><term>Tomography, Emission-Computed</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Corps strié</term><term>Exploration</term><term>Homme</term><term>In vivo</term><term>Neurone dopaminergique</term><term>Parkinson maladie</term><term>Positon</term><term>Terminaison nerveuse présynaptique</term><term>Tomoscintigraphie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clinical symptoms of Parkinson's disease (PD) do not manifest until dopamine (DA) neuronal loss reaches a symptomatic threshold. To explore the mechanisms of functional compensation that occur in presynaptic DA nerve terminals in PD, we compared striatal positron emission tomographic (PET) measurements by using [11C]dihydrotetrabenazine ([11C]DTBZ; labeling the vesicular monoamine transporter type 2), [11C]methylphenidate (labeling the plasma membrane DA transporter), and [18F]dopa (reflecting synthesis and storage of DA). Three consecutive PET scans were performed in three‐dimensional mode by using each tracer on 35 patients and 16 age‐matched, normal controls. PET measurements by the three tracers were compared between subgroups of earlier and later stages of PD, between drug‐naive and drug‐treated subgroups of PD, and between subregions of the parkinsonian striatum. The quantitative relationships of [18F]dopa and [11C]DTBZ, and of [11C]methylphenidate and [11C]DTBZ, were compared between the PD and the normal control subjects. We found that [18F]dopa Ki was reduced less than the binding potential (Bmax/Kd) for [11C]DTBZ in the parkinsonian striatum, whereas the [11C]methylphenidate binding potential was reduced more than [11C]DTBZ binding potential. These observations suggest that the activity of aromatic L‐amino acid decarboxylase is up‐regulated, whereas the plasma membrane DA transporter is down‐regulated in the striatum of patients with PD. Ann Neurol 2000;47:493–503.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Wisconsin</li></region></list><tree><country name="Canada"><noRegion><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S." last="Lee">Chong S. Lee</name></noRegion><name sortKey="Calne, Donald B" sort="Calne, Donald B" uniqKey="Calne D" first="Donald B." last="Calne">Donald B. Calne</name><name sortKey="De La Fuente Ernandez, Raul" sort="De La Fuente Ernandez, Raul" uniqKey="De La Fuente Ernandez R" first="Raul" last="De La Fuente-Fernandez">Raul De La Fuente-Fernandez</name><name sortKey="Lee, Chong S" sort="Lee, Chong S" uniqKey="Lee C" first="Chong S." last="Lee">Chong S. Lee</name><name sortKey="Pal, Pramod K" sort="Pal, Pramod K" uniqKey="Pal P" first="Pramod K." last="Pal">Pramod K. Pal</name><name sortKey="Ruth, Thomas J" sort="Ruth, Thomas J" uniqKey="Ruth T" first="Thomas J." last="Ruth">Thomas J. Ruth</name><name sortKey="Samii, Ali" sort="Samii, Ali" uniqKey="Samii A" first="Ali" last="Samii">Ali Samii</name><name sortKey="Schulzer, Michael" sort="Schulzer, Michael" uniqKey="Schulzer M" first="Michael" last="Schulzer">Michael Schulzer</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><name sortKey="Wudel, Jess" sort="Wudel, Jess" uniqKey="Wudel J" first="Jess" last="Wudel">Jess Wudel</name></country><country name="États-Unis"><region name="Wisconsin"><name sortKey="Holden, James E" sort="Holden, James E" uniqKey="Holden J" first="James E." last="Holden">James E. Holden</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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