Effects of catechol-O-methyltransferase inhibition on the rates of uptake and reversibility of 6-fluoro-L-dopa trapping in MPTP-induced Parkinsonism in monkeys
Identifieur interne : 003C61 ( Main/Exploration ); précédent : 003C60; suivant : 003C62Effects of catechol-O-methyltransferase inhibition on the rates of uptake and reversibility of 6-fluoro-L-dopa trapping in MPTP-induced Parkinsonism in monkeys
Auteurs : D. J. Doudet [Canada] ; G. L. Y. Chan [Canada] ; J. E. Holden [États-Unis] ; K. S. Morrison [Canada] ; R. J. Wyatt [États-Unis] ; T. J. Ruth [Canada]Source :
- Neuropharmacology [ 0028-3908 ] ; 1997.
Descripteurs français
- Pascal (Inist)
- Tolcapone, Inhibiteur enzyme, Dopa, Catechol O-methyltransferase, Antiparkinsonien, Parkinson maladie, Animal, Singe, Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro), Voie intrapéritonéale, Association médicamenteuse, Interaction médicamenteuse, Pharmacocinétique, Aminoacide, Traitement, Chimiothérapie.
- Wicri :
- topic : Singe.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Aminoacid, Animal, Animals, Antiparkinson agent, Benzophenones (pharmacology), Catechol O-Methyltransferase (drug effects), Catechol O-methyltransferase, Chemotherapy, Disease Models, Animal, Dopa, Drug combination, Drug interaction, Enzyme Inhibitors (pharmacology), Enzyme inhibitor, Intraperitoneal administration, Levodopa (metabolism), Macaca mulatta, Monkey, Nitrophenols, Parkinson Disease (metabolism), Parkinson disease, Pharmacokinetics, Tolcapone, Treatment.
- MESH :
- chemical , drug effects : Catechol O-Methyltransferase.
- chemical , metabolism : Levodopa.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Benzophenones, Enzyme Inhibitors.
- metabolism : Parkinson Disease.
- Animals, Disease Models, Animal, Macaca mulatta, Nitrophenols.
Abstract
The uptake rate constant and the loss rate constant that expresses the reversibility of the uptake process of 6-[18F]fluoro-L-Dopa (FDOPA) were measured by positron emission tomography in the striatum of normal rhesus monkeys and in monkeys with unilateral lesions of the dopaminergic nigro-striatal pathway, induced by intracarotid injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Each animal was studied twice: with and without pretreatment of the catechol-O-methyltransferase (COMT) inhibitor Ro 40-7592, tolcapone. After pretreatment with tolcapone, there was a very significant increase in plasma FDOPA throughout the course of the study, accompanied by a significant decrease in its main metabolite, 3-O-methylfluorodopa. Tolcapone did not induce a significant change in the uptake rate constant in either the normal or the MPTP-treated striatum. However, after tolcapone pretreatment, there was a significant decrease in the loss rate constant in the MPTP-treated striatum (25%) and a smaller, non-significant decrease in the normal striatum (13%). It is concluded that the COMT inhibitor tolcapone exhibits clear peripheral and central activity. As compared to peripheral COMT inhibitors, this central effect may help preserve and stabilize the synaptic levels of DA and, thus, further improve the effects of L-DOPA therapy in parkinsonian patients.
Affiliations:
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J." last="Doudet">D. J. Doudet</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Neurology and Neurodegenerative Disorders Centre and TRIUMF, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Chan, G L Y" sort="Chan, G L Y" uniqKey="Chan G" first="G. L. Y." last="Chan">G. L. Y. Chan</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Neurology and Neurodegenerative Disorders Centre and TRIUMF, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Holden, J E" sort="Holden, J E" uniqKey="Holden J" first="J. E." last="Holden">J. E. Holden</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Medical Physics, University of Wisconsin</s1><s2>Madison, WI</s2><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Madison, WI</wicri:noRegion></affiliation></author><author><name sortKey="Morrison, K S" sort="Morrison, K S" uniqKey="Morrison K" first="K. S." last="Morrison">K. S. Morrison</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Neurology and Neurodegenerative Disorders Centre and TRIUMF, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Wyatt, R J" sort="Wyatt, R J" uniqKey="Wyatt R" first="R. J." last="Wyatt">R. J. Wyatt</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Neuropsychiatry Branch, National Institute of Mental Health, NIH, IRP</s1><s2>Bethesda, MD</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Bethesda, MD</wicri:noRegion></affiliation></author><author><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T. J." last="Ruth">T. J. Ruth</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Medicine, Division of Neurology and Neurodegenerative Disorders Centre and TRIUMF, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Neuropharmacology</title><title level="j" type="abbreviated">Neuropharmacology</title><idno type="ISSN">0028-3908</idno><imprint><date when="1997">1997</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuropharmacology</title><title level="j" type="abbreviated">Neuropharmacology</title><idno type="ISSN">0028-3908</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology)</term><term>Aminoacid</term><term>Animal</term><term>Animals</term><term>Antiparkinson agent</term><term>Benzophenones (pharmacology)</term><term>Catechol O-Methyltransferase (drug effects)</term><term>Catechol O-methyltransferase</term><term>Chemotherapy</term><term>Disease Models, Animal</term><term>Dopa</term><term>Drug combination</term><term>Drug interaction</term><term>Enzyme Inhibitors (pharmacology)</term><term>Enzyme inhibitor</term><term>Intraperitoneal administration</term><term>Levodopa (metabolism)</term><term>Macaca mulatta</term><term>Monkey</term><term>Nitrophenols</term><term>Parkinson Disease (metabolism)</term><term>Parkinson disease</term><term>Pharmacokinetics</term><term>Tolcapone</term><term>Treatment</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Catechol O-Methyltransferase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Benzophenones</term><term>Enzyme Inhibitors</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Macaca mulatta</term><term>Nitrophenols</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Tolcapone</term><term>Inhibiteur enzyme</term><term>Dopa</term><term>Catechol O-methyltransferase</term><term>Antiparkinsonien</term><term>Parkinson maladie</term><term>Animal</term><term>Singe</term><term>Pyridine(1-méthyl-4-phényl-1,2,3,6-tétrahydro)</term><term>Voie intrapéritonéale</term><term>Association médicamenteuse</term><term>Interaction médicamenteuse</term><term>Pharmacocinétique</term><term>Aminoacide</term><term>Traitement</term><term>Chimiothérapie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The uptake rate constant and the loss rate constant that expresses the reversibility of the uptake process of 6-[<sup>18</sup>F]fluoro-L-Dopa (FDOPA) were measured by positron emission tomography in the striatum of normal rhesus monkeys and in monkeys with unilateral lesions of the dopaminergic nigro-striatal pathway, induced by intracarotid injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Each animal was studied twice: with and without pretreatment of the catechol-O-methyltransferase (COMT) inhibitor Ro 40-7592, tolcapone. After pretreatment with tolcapone, there was a very significant increase in plasma FDOPA throughout the course of the study, accompanied by a significant decrease in its main metabolite, 3-O-methylfluorodopa. Tolcapone did not induce a significant change in the uptake rate constant in either the normal or the MPTP-treated striatum. However, after tolcapone pretreatment, there was a significant decrease in the loss rate constant in the MPTP-treated striatum (25%) and a smaller, non-significant decrease in the normal striatum (13%). It is concluded that the COMT inhibitor tolcapone exhibits clear peripheral and central activity. As compared to peripheral COMT inhibitors, this central effect may help preserve and stabilize the synaptic levels of DA and, thus, further improve the effects of L-DOPA therapy in parkinsonian patients.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Doudet, D J" sort="Doudet, D J" uniqKey="Doudet D" first="D. J." last="Doudet">D. J. Doudet</name></noRegion><name sortKey="Chan, G L Y" sort="Chan, G L Y" uniqKey="Chan G" first="G. L. Y." last="Chan">G. L. Y. Chan</name><name sortKey="Morrison, K S" sort="Morrison, K S" uniqKey="Morrison K" first="K. S." last="Morrison">K. S. Morrison</name><name sortKey="Ruth, T J" sort="Ruth, T J" uniqKey="Ruth T" first="T. J." last="Ruth">T. J. Ruth</name></country><country name="États-Unis"><noRegion><name sortKey="Holden, J E" sort="Holden, J E" uniqKey="Holden J" first="J. E." last="Holden">J. E. Holden</name></noRegion><name sortKey="Wyatt, R J" sort="Wyatt, R J" uniqKey="Wyatt R" first="R. J." last="Wyatt">R. J. Wyatt</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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