Targeting β-arrestin2 in the treatment of L-DOPA-induced dyskinesia in Parkinson's disease.
Identifieur interne : 000261 ( PubMed/Checkpoint ); précédent : 000260; suivant : 000262Targeting β-arrestin2 in the treatment of L-DOPA-induced dyskinesia in Parkinson's disease.
Auteurs : Nikhil M. Urs [États-Unis] ; Simone Bido [France] ; Sean M. Peterson ; Tanya L. Daigle ; Caroline E. Bass [États-Unis] ; Raul R. Gainetdinov [Russie] ; Erwan Bezard [France] ; Marc G. Caron [États-Unis]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 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
Parkinson's disease (PD) is characterized by severe locomotor deficits and is commonly treated with the dopamine (DA) precursor l-3,4-dihydroxyphenylalanine (L-DOPA), but its prolonged use causes dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs). Recent studies in animal models of PD have suggested that dyskinesias are associated with the overactivation of G protein-mediated signaling through DA receptors. β-Arrestins desensitize G protein signaling at DA receptors (D1R and D2R) in addition to activating their own G protein-independent signaling events, which have been shown to mediate locomotion. Therefore, targeting β-arrestins in PD L-DOPA therapy might prove to be a desirable approach. Here we show in a bilateral DA-depletion mouse model of Parkinson's symptoms that genetic deletion of β-arrestin2 significantly limits the beneficial locomotor effects while markedly enhancing the dyskinesia-like effects of acute or chronic L-DOPA treatment. Viral rescue or overexpression of β-arrestin2 in knockout or control mice either reverses or protects against LIDs and its key biochemical markers. In other more conventional animal models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated nonhuman primates, β-arrestin2 overexpression significantly reduced dyskinesias while maintaining the therapeutic effect of L-DOPA. Considerable efforts are being spent in the pharmaceutical industry to identify therapeutic approaches to block LIDs in patients with PD. Our results point to a potential therapeutic approach, whereby development of either a genetic or pharmacological intervention to enhance β-arrestin2- or limit G protein-dependent D1/D2R signaling could represent a more mechanistically informed strategy.
DOI: 10.1073/pnas.1502740112
PubMed: 25918399
Affiliations:
- France, Russie, États-Unis
- Aquitaine, Nouvelle-Aquitaine, État de New York
- Bordeaux
- Université de Bordeaux
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pubmed:25918399Le document en format XML
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Caron</name><affiliation wicri:level="1"><nlm:affiliation>Departments of Cell Biology, Medicine, and Neurobiology, Duke University Medical Center, Durham NC 27710; marc.caron@dm.duke.edu nikhil.urs@duke.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Departments of Cell Biology, Medicine, and Neurobiology, Duke University Medical Center</wicri:regionArea><wicri:noRegion>Duke University Medical Center</wicri:noRegion></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (chemistry)</term><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><term>beta-Arrestins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by severe locomotor deficits and is commonly treated with the dopamine (DA) precursor l-3,4-dihydroxyphenylalanine (L-DOPA), but its prolonged use causes dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs). Recent studies in animal models of PD have suggested that dyskinesias are associated with the overactivation of G protein-mediated signaling through DA receptors. β-Arrestins desensitize G protein signaling at DA receptors (D1R and D2R) in addition to activating their own G protein-independent signaling events, which have been shown to mediate locomotion. Therefore, targeting β-arrestins in PD L-DOPA therapy might prove to be a desirable approach. Here we show in a bilateral DA-depletion mouse model of Parkinson's symptoms that genetic deletion of β-arrestin2 significantly limits the beneficial locomotor effects while markedly enhancing the dyskinesia-like effects of acute or chronic L-DOPA treatment. Viral rescue or overexpression of β-arrestin2 in knockout or control mice either reverses or protects against LIDs and its key biochemical markers. In other more conventional animal models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated nonhuman primates, β-arrestin2 overexpression significantly reduced dyskinesias while maintaining the therapeutic effect of L-DOPA. Considerable efforts are being spent in the pharmaceutical industry to identify therapeutic approaches to block LIDs in patients with PD. Our results point to a potential therapeutic approach, whereby development of either a genetic or pharmacological intervention to enhance β-arrestin2- or limit G protein-dependent D1/D2R signaling could represent a more mechanistically informed strategy.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25918399</PMID><DateCreated><Year>2015</Year><Month>05</Month><Day>13</Day></DateCreated><DateCompleted><Year>2015</Year><Month>12</Month><Day>14</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>112</Volume><Issue>19</Issue><PubDate><Year>2015</Year><Month>May</Month><Day>12</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>Targeting β-arrestin2 in the treatment of L-DOPA-induced dyskinesia in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>E2517-26</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.1502740112</ELocationID><Abstract><AbstractText>Parkinson's disease (PD) is characterized by severe locomotor deficits and is commonly treated with the dopamine (DA) precursor l-3,4-dihydroxyphenylalanine (L-DOPA), but its prolonged use causes dyskinesias referred to as L-DOPA-induced dyskinesias (LIDs). Recent studies in animal models of PD have suggested that dyskinesias are associated with the overactivation of G protein-mediated signaling through DA receptors. β-Arrestins desensitize G protein signaling at DA receptors (D1R and D2R) in addition to activating their own G protein-independent signaling events, which have been shown to mediate locomotion. Therefore, targeting β-arrestins in PD L-DOPA therapy might prove to be a desirable approach. Here we show in a bilateral DA-depletion mouse model of Parkinson's symptoms that genetic deletion of β-arrestin2 significantly limits the beneficial locomotor effects while markedly enhancing the dyskinesia-like effects of acute or chronic L-DOPA treatment. Viral rescue or overexpression of β-arrestin2 in knockout or control mice either reverses or protects against LIDs and its key biochemical markers. In other more conventional animal models of DA neuron loss and PD, such as 6-hydroxydopamine-treated mice or rats and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated nonhuman primates, β-arrestin2 overexpression significantly reduced dyskinesias while maintaining the therapeutic effect of L-DOPA. Considerable efforts are being spent in the pharmaceutical industry to identify therapeutic approaches to block LIDs in patients with PD. Our results point to a potential therapeutic approach, whereby development of either a genetic or pharmacological intervention to enhance β-arrestin2- or limit G protein-dependent D1/D2R signaling could represent a more mechanistically informed strategy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Urs</LastName><ForeName>Nikhil M</ForeName><Initials>NM</Initials><AffiliationInfo><Affiliation>Departments of Cell Biology, marc.caron@dm.duke.edu nikhil.urs@duke.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bido</LastName><ForeName>Simone</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institut des Maladies Neurodégénératives, UMR 5293, Université de Bordeaux, 33000 Bordeaux, France; Institut des Maladies Neurodégénératives, UMR 5293, CNRS, 33000 Bordeaux, France;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Peterson</LastName><ForeName>Sean M</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Departments of Cell Biology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Daigle</LastName><ForeName>Tanya L</ForeName><Initials>TL</Initials><AffiliationInfo><Affiliation>Departments of Cell Biology.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bass</LastName><ForeName>Caroline E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University at Buffalo, The State Uiversity of New York, Buffalo, NY 14260; and.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gainetdinov</LastName><ForeName>Raul R</ForeName><Initials>RR</Initials><AffiliationInfo><Affiliation>Departments of Cell Biology, Institute of Translational Biomedicine, St. Petersburg State University, St. Petersburg, 199034, Russia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bezard</LastName><ForeName>Erwan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institut des Maladies Neurodégénératives, UMR 5293, Université de Bordeaux, 33000 Bordeaux, France; Institut des Maladies Neurodégénératives, UMR 5293, CNRS, 33000 Bordeaux, France;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caron</LastName><ForeName>Marc G</ForeName><Initials>MG</Initials><AffiliationInfo><Affiliation>Departments of Cell Biology, Medicine, and Neurobiology, Duke University Medical Center, Durham NC 27710; marc.caron@dm.duke.edu nikhil.urs@duke.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>K01 DA024763</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R37 MH073853</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>5R37MH073853</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K01DA024763</GrantID><Acronym>DA</Acronym><Agency>NIDA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>04</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019390">Arrestins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071557">beta-Arrestins</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Physiol Rev. 1998 Jan;78(1):189-225</RefSource><PMID Version="1">9457173</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Virol. 1998 Mar;72(3):2224-32</RefSource><PMID Version="1">9499080</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 1998 May;50(5):1323-6</RefSource><PMID Version="1">9595981</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1999 Jan 29;283(5402):655-61</RefSource><PMID Version="1">9924018</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 1998 Aug;10(8):2694-706</RefSource><PMID Version="1">9767399</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3712-7</RefSource><PMID Version="1">10097102</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Psychiatr Nervenkr Z Gesamte Neurol Psychiatr. 1962;203:560-74</RefSource><PMID Version="1">13971142</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2005 Jan;57(1):17-26</RefSource><PMID Version="1">15514976</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2005 Feb;191(2):243-50</RefSource><PMID Version="1">15649479</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2005 Mar;18(2):323-35</RefSource><PMID Version="1">15686961</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1448-53</RefSource><PMID Version="1">15671180</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2005 Feb 23;25(8):2157-65</RefSource><PMID Version="1">15728856</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropharmacology. 2005 Mar;48(4):503-16</RefSource><PMID Version="1">15755478</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2005 Apr 22;308(5721):512-7</RefSource><PMID Version="1">15845844</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2005 Jul;194(1):66-75</RefSource><PMID Version="1">15899244</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cell. 2005 Jul 29;122(2):261-73</RefSource><PMID Version="1">16051150</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS Biol. 2005 Aug;3(8):e271</RefSource><PMID Version="1">16050778</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biol Psychiatry. 2006 Jan 1;59(1):64-74</RefSource><PMID Version="1">16139809</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2006 Oct 10;67(7 Suppl 2):S12-7</RefSource><PMID Version="1">17030735</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2006 Oct 27;281(43):32072-80</RefSource><PMID Version="1">16954211</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2006 Oct 31;103(44):16284-9</RefSource><PMID Version="1">17060617</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2007 Jan 24;27(4):881-5</RefSource><PMID Version="1">17251429</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Trends Pharmacol Sci. 2007 Apr;28(4):166-72</RefSource><PMID Version="1">17349698</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2007 Jun 27;27(26):6995-7005</RefSource><PMID Version="1">17596448</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12011-6</RefSource><PMID Version="1">17620599</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2007 Dec 26;27(52):14338-48</RefSource><PMID Version="1">18160641</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2008 Apr 23;28(17):4311-6</RefSource><PMID Version="1">18434508</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2008 Jul 9;28(28):7113-20</RefSource><PMID Version="1">18614680</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Neurosci. 2008 Sep;9(9):665-77</RefSource><PMID Version="1">18714325</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biol Psychiatry. 2009 Mar 15;65(6):518-26</RefSource><PMID Version="1">18947822</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2009 Apr 15;29(15):4829-35</RefSource><PMID Version="1">19369551</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9649-54</RefSource><PMID Version="1">19497875</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Sci Signal. 2009;2(80):ra36</RefSource><PMID Version="1">19622833</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Synapse. 2010 Feb;64(2):177-80</RefSource><PMID Version="1">19852073</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Sci Transl Med. 2010 Apr 21;2(28):28ra28</RefSource><PMID Version="1">20410529</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2010 Sep;39(3):352-61</RefSource><PMID Version="1">20452425</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2010 Jul 29;466(7306):622-6</RefSource><PMID Version="1">20613723</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2010 Jul 30;25(10):1437-43</RefSource><PMID Version="1">20629136</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurochem. 2010 Sep 1;114(5):1344-52</RefSource><PMID Version="1">20534006</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14845-50</RefSource><PMID Version="1">20682746</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2014 Jan 28;82(4):300-7</RefSource><PMID Version="1">24371304</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Parkinsonism Relat Disord. 2014 Sep;20(9):947-56</RefSource><PMID Version="1">24951359</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1999 Dec 24;286(5449):2495-8</RefSource><PMID Version="1">10617462</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Rev Neurosci. 2001 Aug;2(8):577-88</RefSource><PMID Version="1">11484001</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2001 Sep 1;21(17):6853-61</RefSource><PMID Version="1">11517273</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2001 Nov 2;294(5544):1024-30</RefSource><PMID Version="1">11691979</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Neurosci. 2002 Jan;15(1):120-32</RefSource><PMID Version="1">11860512</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Neurosci. 2003 May;6(5):501-6</RefSource><PMID Version="1">12665799</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Med. 2003 Jun;9(6):762-7</RefSource><PMID Version="1">12740572</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Exp Neurol. 2003 Nov;184(1):285-94</RefSource><PMID Version="1">14637099</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):5099-104</RefSource><PMID Version="1">15044694</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2004 Jun;16(1):110-23</RefSource><PMID Version="1">15207268</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Annu Rev Neurosci. 2004;27:107-44</RefSource><PMID Version="1">15217328</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 1986 Jan;6(1):274-80</RefSource><PMID Version="1">2868077</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 1986 May;83(9):2797-801</RefSource><PMID Version="1">2871555</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Eur J Pharmacol. 1987 Mar 3;135(1):101-5</RefSource><PMID Version="1">3494620</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1990 Jun 22;248(4962):1547-50</RefSource><PMID Version="1">2163110</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Can J Neurol Sci. 1992 Feb;19(1 Suppl):147-52</RefSource><PMID Version="1">1349263</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 1992 Sep 5;267(25):17882-90</RefSource><PMID Version="1">1517224</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1996 Jan 19;271(5247):363-6</RefSource><PMID Version="1">8553074</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1996 Feb 15;379(6566):606-12</RefSource><PMID Version="1">8628395</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 1996 Oct 3;383(6599):447-50</RefSource><PMID Version="1">8837779</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2010;5(8):e12322</RefSource><PMID Version="1">20808799</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>PLoS One. 2010;5(11):e14020</RefSource><PMID Version="1">21103359</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):840-5</RefSource><PMID Version="1">21187382</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychopharmacology. 2011 Feb;36(3):551-8</RefSource><PMID Version="1">20980993</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21824-9</RefSource><PMID Version="1">21115823</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 2011 Aug;134(Pt 8):2321-38</RefSource><PMID Version="1">21742735</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Int Rev Neurobiol. 2011;98:95-122</RefSource><PMID Version="1">21907084</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2012 Sep 15;27(11):1373-8</RefSource><PMID Version="1">22976821</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2012 Nov;122(11):3977-89</RefSource><PMID Version="1">23041629</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>CNS Drugs. 2012 Dec;26(12):1017-32</RefSource><PMID Version="1">23114872</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20732-7</RefSource><PMID Version="1">23188793</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurobiol Dis. 2013 Jun;54:339-48</RefSource><PMID Version="1">23328768</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mov Disord. 2013 Nov;28(13):1838-46</RefSource><PMID Version="1">23853029</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019390" 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IdType="pmc">PMC4434696</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>France</li><li>Russie</li><li>États-Unis</li></country><region><li>Aquitaine</li><li>Nouvelle-Aquitaine</li><li>État de New York</li></region><settlement><li>Bordeaux</li></settlement><orgName><li>Université de Bordeaux</li></orgName></list><tree><noCountry><name sortKey="Daigle, Tanya L" sort="Daigle, Tanya L" uniqKey="Daigle T" first="Tanya L" last="Daigle">Tanya L. Daigle</name><name sortKey="Peterson, Sean M" sort="Peterson, Sean M" uniqKey="Peterson S" first="Sean M" last="Peterson">Sean M. Peterson</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Urs, Nikhil M" sort="Urs, Nikhil M" uniqKey="Urs N" first="Nikhil M" last="Urs">Nikhil M. Urs</name></noRegion><name sortKey="Bass, Caroline E" sort="Bass, Caroline E" uniqKey="Bass C" first="Caroline E" last="Bass">Caroline E. Bass</name><name sortKey="Caron, Marc G" sort="Caron, Marc G" uniqKey="Caron M" first="Marc G" last="Caron">Marc G. Caron</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bido, Simone" sort="Bido, Simone" uniqKey="Bido S" first="Simone" last="Bido">Simone Bido</name></region><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></country><country name="Russie"><noRegion><name sortKey="Gainetdinov, Raul R" sort="Gainetdinov, Raul R" uniqKey="Gainetdinov R" first="Raul R" last="Gainetdinov">Raul R. Gainetdinov</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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