Dynamic, adaptive changes in MAO-A binding after alterations in substrate availability: an in vivo [11C]-harmine positron emission tomography study
Identifieur interne : 001680 ( Main/Exploration ); précédent : 001679; suivant : 001681Dynamic, adaptive changes in MAO-A binding after alterations in substrate availability: an in vivo [11C]-harmine positron emission tomography study
Auteurs : Julia Sacher [Canada, Allemagne] ; Eugenii A. Rabiner [Canada] ; Michael Clark [Canada] ; Pablo Rusjan [Canada] ; Alexandra Soliman [Canada] ; Rada Boskovic [Canada] ; Stephen J. Kish [Canada] ; Alan A. Wilson [Canada] ; Sylvain Houle [Canada] ; Jeffrey H. Meyer [Canada]Source :
- Journal of Cerebral Blood Flow & Metabolism [ 0271-678X ] ; 2011.
English descriptors
- KwdEn :
- Carbidopa (administration & dosage), Carbidopa (blood), Carbidopa (pharmacology), Carbon Radioisotopes, Corpus Striatum (enzymology), Corpus Striatum (metabolism), Dopamine (metabolism), Dopamine Agonists (administration & dosage), Dopamine Agonists (blood), Dopamine Agonists (pharmacology), Drug Combinations, Harmine (metabolism), Humans, Levodopa (administration & dosage), Levodopa (blood), Levodopa (pharmacology), Monoamine Oxidase (metabolism), Parkinson Disease (enzymology), Positron-Emission Tomography, Prefrontal Cortex (enzymology), Prefrontal Cortex (metabolism), Protein Binding, Serotonin (metabolism), Substrate Specificity, Time Factors, Tryptophan (blood).
- MESH :
- chemical , administration & dosage : Carbidopa, Dopamine Agonists, Levodopa.
- chemical , blood : Carbidopa, Dopamine Agonists, Levodopa, Tryptophan.
- chemical , metabolism : Dopamine, Harmine, Monoamine Oxidase, Serotonin.
- chemical , pharmacology : Carbidopa, Dopamine Agonists, Levodopa.
- chemical : Carbon Radioisotopes, Drug Combinations.
- enzymology : Corpus Striatum, Parkinson Disease, Prefrontal Cortex.
- metabolism : Corpus Striatum, Prefrontal Cortex.
- Humans, Positron-Emission Tomography, Protein Binding, Substrate Specificity, Time Factors.
Abstract
Monoamine oxidase A (MAO-A) is an important target in the pathophysiology and therapeutics of major depressive disorder, aggression, and neurodegenerative conditions. We measured the effect of changes in MAO-A substrate on MAO-A binding in regions implicated in affective and neurodegenerative disease with [11C]-harmine positron emission tomography in healthy volunteers. Monoamine oxidase A VT, an index of MAO-A density, was decreased (mean: 14%±9%) following tryptophan depletion in prefrontal cortex (
Url:
DOI: 10.1038/jcbfm.2011.184
PubMed: 22186668
PubMed Central: 3293124
Affiliations:
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Le document en format XML
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[<sup>11</sup>
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</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Boskovic, Rada" sort="Boskovic, Rada" uniqKey="Boskovic R" first="Rada" last="Boskovic">Rada Boskovic</name>
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</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<affiliation wicri:level="1"><nlm:aff id="aff5"><institution>The Clinical Pharmacology and Toxicology Division, The Hospital for Sick Children, University of Toronto</institution>
, Toronto,<country>Canada</country>
</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J" last="Kish">Stephen J. Kish</name>
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</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<author><name sortKey="Meyer, Jeffrey H" sort="Meyer, Jeffrey H" uniqKey="Meyer J" first="Jeffrey H" last="Meyer">Jeffrey H. Meyer</name>
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</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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<term>Carbidopa (blood)</term>
<term>Carbidopa (pharmacology)</term>
<term>Carbon Radioisotopes</term>
<term>Corpus Striatum (enzymology)</term>
<term>Corpus Striatum (metabolism)</term>
<term>Dopamine (metabolism)</term>
<term>Dopamine Agonists (administration & dosage)</term>
<term>Dopamine Agonists (blood)</term>
<term>Dopamine Agonists (pharmacology)</term>
<term>Drug Combinations</term>
<term>Harmine (metabolism)</term>
<term>Humans</term>
<term>Levodopa (administration & dosage)</term>
<term>Levodopa (blood)</term>
<term>Levodopa (pharmacology)</term>
<term>Monoamine Oxidase (metabolism)</term>
<term>Parkinson Disease (enzymology)</term>
<term>Positron-Emission Tomography</term>
<term>Prefrontal Cortex (enzymology)</term>
<term>Prefrontal Cortex (metabolism)</term>
<term>Protein Binding</term>
<term>Serotonin (metabolism)</term>
<term>Substrate Specificity</term>
<term>Time Factors</term>
<term>Tryptophan (blood)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Carbidopa</term>
<term>Dopamine Agonists</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Carbidopa</term>
<term>Dopamine Agonists</term>
<term>Levodopa</term>
<term>Tryptophan</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
<term>Harmine</term>
<term>Monoamine Oxidase</term>
<term>Serotonin</term>
</keywords>
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<term>Parkinson Disease</term>
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<term>Prefrontal Cortex</term>
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<front><div type="abstract" xml:lang="en"><p>Monoamine oxidase A (MAO-A) is an important target in the pathophysiology and therapeutics of major depressive disorder, aggression, and neurodegenerative conditions. We measured the effect of changes in MAO-A substrate on MAO-A binding in regions implicated in affective and neurodegenerative disease with [<sup>11</sup>
C]-harmine positron emission tomography in healthy volunteers. Monoamine oxidase A V<sub>T</sub>
, an index of MAO-A density, was decreased (mean: 14%±9%) following tryptophan depletion in prefrontal cortex (<italic>P</italic>
<0.031), and elevated (mean: 17%±11%) in striatum following carbidopa–levodopa administration (<italic>P</italic>
<0.007). These findings suggest an adaptive role for MAO-A in maintaining monoamine neurotransmitter homeostasis by rapidly compensating fluctuating monoamine levels.</p>
</div>
</front>
<back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Alia Klein, N" uniqKey="Alia Klein N">N Alia-Klein</name>
</author>
<author><name sortKey="Goldstein, Rz" uniqKey="Goldstein R">RZ Goldstein</name>
</author>
<author><name sortKey="Kriplani, A" uniqKey="Kriplani A">A Kriplani</name>
</author>
<author><name sortKey="Logan, J" uniqKey="Logan J">J Logan</name>
</author>
<author><name sortKey="Tomasi, D" uniqKey="Tomasi D">D Tomasi</name>
</author>
<author><name sortKey="Williams, B" uniqKey="Williams B">B Williams</name>
</author>
<author><name sortKey="Telang, F" uniqKey="Telang F">F Telang</name>
</author>
<author><name sortKey="Shumay, E" uniqKey="Shumay E">E Shumay</name>
</author>
<author><name sortKey="Biegon, A" uniqKey="Biegon A">A Biegon</name>
</author>
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