Targeting β-arrestin2 in the treatment of l-DOPA–induced dyskinesia in Parkinson’s disease
Identifieur interne : 001694 ( Ncbi/Curation ); précédent : 001693; suivant : 001695Targeting β-arrestin2 in the treatment of l-DOPA–induced dyskinesia in Parkinson’s disease
Auteurs : Nikhil M. Urs ; Simone Bido [France] ; Sean M. Peterson ; Tanya L. Daigle ; Caroline E. Bass ; Raul R. Gainetdinov [Russie] ; Erwan Bezard [France] ; Marc G. CaronSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2015.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (chemistry), Animals, Arrestins (genetics), Arrestins (metabolism), Behavior, Animal, Disease Models, Animal, Dopamine (metabolism), Dyskinesia, Drug-Induced (metabolism), Dyskinesias (metabolism), Gene Deletion, Levodopa (chemistry), Macaca, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Neurons (metabolism), Oxidopamine (chemistry), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Rats, Rats, Sprague-Dawley, Signal Transduction, Up-Regulation, beta-Arrestins.
- MESH :
- chemical , chemistry : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Levodopa, Oxidopamine.
- chemical , genetics : Arrestins.
- chemical , metabolism : Arrestins, Dopamine.
- drug therapy : Parkinson Disease.
- metabolism : Dyskinesia, Drug-Induced, Dyskinesias, Neurons, Parkinson Disease.
- Animals, Behavior, Animal, Disease Models, Animal, Gene Deletion, Macaca, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Rats, Sprague-Dawley, Signal Transduction, Up-Regulation, beta-Arrestins.
Abstract
β-Arrestins are unique proteins that have multiple cellular functions such as G protein-coupled receptor signal desensitization, protein trafficking and signaling molecule scaffolding. Treatment of Parkinson’s disease (PD) motor symptoms by
Url:
DOI: 10.1073/pnas.1502740112
PubMed: 25918399
PubMed Central: 4434696
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PMC:4434696Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Targeting β-arrestin2 in the treatment of <sc>l</sc>
-DOPA–induced dyskinesia in Parkinson’s disease</title>
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<country xml:lang="fr">France</country>
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<affiliation wicri:level="1"><nlm:aff id="aff5">Institut des Maladies Neurodégénératives, UMR 5293,<institution>CNRS</institution>
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, The State Uiversity of New York, Buffalo,<addr-line>NY</addr-line>
14260</nlm:aff>
</affiliation>
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<author><name sortKey="Gainetdinov, Raul R" sort="Gainetdinov, Raul R" uniqKey="Gainetdinov R" first="Raul R." last="Gainetdinov">Raul R. Gainetdinov</name>
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, St. Petersburg, 199034,<country>Russia</country>
</nlm:aff>
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, 33000 Bordeaux,<country>France</country>
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, 33000 Bordeaux,<country>France</country>
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</affiliation>
<affiliation><nlm:aff id="aff3">Neurobiology,<institution>Duke University Medical Center</institution>
, Durham<addr-line>NC</addr-line>
27710;</nlm:aff>
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<term>Animals</term>
<term>Arrestins (genetics)</term>
<term>Arrestins (metabolism)</term>
<term>Behavior, Animal</term>
<term>Disease Models, Animal</term>
<term>Dopamine (metabolism)</term>
<term>Dyskinesia, Drug-Induced (metabolism)</term>
<term>Dyskinesias (metabolism)</term>
<term>Gene Deletion</term>
<term>Levodopa (chemistry)</term>
<term>Macaca</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Neurons (metabolism)</term>
<term>Oxidopamine (chemistry)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Signal Transduction</term>
<term>Up-Regulation</term>
<term>beta-Arrestins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term>
<term>Levodopa</term>
<term>Oxidopamine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Arrestins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Arrestins</term>
<term>Dopamine</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>Dyskinesia, Drug-Induced</term>
<term>Dyskinesias</term>
<term>Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Behavior, Animal</term>
<term>Disease Models, Animal</term>
<term>Gene Deletion</term>
<term>Macaca</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Signal Transduction</term>
<term>Up-Regulation</term>
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<front><div type="abstract" xml:lang="en"><title>Significance</title>
<p>β-Arrestins are unique proteins that have multiple cellular functions such as G protein-coupled receptor signal desensitization, protein trafficking and signaling molecule scaffolding. Treatment of Parkinson’s disease (PD) motor symptoms by <sc>l</sc>
-3,4-dihydroxyphenylalanine (<sc>l</sc>
-DOPA) has been hampered by abnormal involuntary movements or dyskinetic side effects. The cause of these dyskinesias has been attributed to receptor supersensitivity and uncontrolled neuronal excitability. Here we demonstrate in multiple preclinical models of <sc>l</sc>
-DOPA–induced dyskinesias and PD that expression levels of β-arrestin2 can alter manifestation of these dyskinesias by reducing receptor supersensitivity while maintaining the therapeutic effect of <sc>l</sc>
-DOPA. Thus novel drugs that increase β-arrestin–dependent function at dopamine receptors may be useful in ameliorating PD motor symptoms without inducing dyskinesias.</p>
</div>
</front>
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