Prevention of levodopa‐induced dyskinesias by a selective NR1A/2B N‐methyl‐D‐aspartate receptor antagonist in parkinsonian monkeys: Implication of preproenkephalin
Identifieur interne : 002C11 ( Main/Corpus ); précédent : 002C10; suivant : 002C12Prevention of levodopa‐induced dyskinesias by a selective NR1A/2B N‐methyl‐D‐aspartate receptor antagonist in parkinsonian monkeys: Implication of preproenkephalin
Auteurs : Marc Morissette ; Mehdi Dridi ; Frédéric Calon ; Abdallah Hadj Tahar ; Leonard T. Meltzer ; Paul J. Bédard ; Thérèse Di PaoloSource :
- Movement Disorders [ 0885-3185 ] ; 2006-01.
English descriptors
Abstract
Enkephalin is reported to play an important role in the pathophysiology of levodopa (LD) ‐induced dyskinesias. The present study investigated the effect of chronic treatment with a selective NR1A/2B N‐methyl‐D‐aspartate (NMDA) receptor antagonist, CI‐1041, on the expression of preproenkephalin‐A (PPE‐A) in brains of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) ‐treated monkeys in relation to the development of LD‐induced dyskinesias. Four MPTP‐monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP‐monkeys received LD/benserazide plus CI‐1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline‐treated MPTP monkeys were also included. MPTP‐treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE‐A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline‐treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI‐1041 normalizes PPE‐A mRNA expression and prevents the development of LD‐induced dyskinesias in an animal model of Parkinson disease. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20654
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ISTEX:DE7517848667D0FEB06AA3F8B46C2E74A33A4989Le document en format XML
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The present study investigated the effect of chronic treatment with a selective NR1A/2B N‐methyl‐D‐aspartate (NMDA) receptor antagonist, CI‐1041, on the expression of preproenkephalin‐A (PPE‐A) in brains of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) ‐treated monkeys in relation to the development of LD‐induced dyskinesias. Four MPTP‐monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP‐monkeys received LD/benserazide plus CI‐1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline‐treated MPTP monkeys were also included. MPTP‐treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE‐A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline‐treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI‐1041 normalizes PPE‐A mRNA expression and prevents the development of LD‐induced dyskinesias in an animal model of Parkinson disease. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Marc Morissette PhD</name><affiliations><json:string>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</json:string><json:string>Faculty of Pharmacy, Laval University, Quebec, Canada</json:string></affiliations></json:item><json:item><name>Mehdi Dridi MSc</name><affiliations><json:string>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</json:string><json:string>Faculty of Pharmacy, Laval University, Quebec, Canada</json:string></affiliations></json:item><json:item><name>Frédéric Calon PhD</name><affiliations><json:string>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</json:string><json:string>Faculty of Pharmacy, Laval University, Quebec, Canada</json:string></affiliations></json:item><json:item><name>Abdallah Hadj Tahar PhD</name><affiliations><json:string>Neuroscience Research Unit, Laval University Medical Centre, Quebec, Canada</json:string></affiliations></json:item><json:item><name>Leonard T. 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Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. 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Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. 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Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/mds.v21:1</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2006-01">January 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="20" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20654</doi><idGroup><id type="unit" value="MDS20654"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2005 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2004-11-05"></event><event type="manuscriptRevised" date="2005-02-02"></event><event type="manuscriptAccepted" 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href="file:MDS.MDS20654.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="48"></count><count type="wordTotal" number="5721"></count></countGroup><titleGroup><title type="main" xml:lang="en">Prevention of levodopa‐induced dyskinesias by a selective NR1A/2B <i>N</i>‐methyl‐<sc>D</sc>‐aspartate receptor antagonist in parkinsonian monkeys: Implication of preproenkephalin</title><title type="short" xml:lang="en">Glutamate Antagonist and Enkephalin</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Marc</givenNames><familyName>Morissette</familyName><degrees>PhD</degrees></personName><contactDetails><email>therese.dipaolo@crchul.ulaval.ca</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Mehdi</givenNames><familyName>Dridi</familyName><degrees>MSc</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Frédéric</givenNames><familyName>Calon</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Abdallah Hadj</givenNames><familyName>Tahar</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Leonard T.</givenNames><familyName>Meltzer</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af3 #af5"><personName><givenNames>Paul J.</givenNames><familyName>Bédard</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Thérèse</givenNames><familyName>Di Paolo</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Faculty of Pharmacy, Laval University, Quebec, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Neuroscience Research Unit, Laval University Medical Centre, Quebec, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Pfizer Global Research & Development, Ann Arbor Laboratories, Ann Arbor, Michigan, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="CA" type="organization"><unparsedAffiliation>Faculty of Medicine, Laval University, Quebec, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">MPTP</keyword><keyword xml:id="kwd2">glutamate receptor</keyword><keyword xml:id="kwd3">preproenkephalin</keyword><keyword xml:id="kwd4">Parkinson's disease</keyword><keyword xml:id="kwd5">dyskinesia</keyword><keyword xml:id="kwd6">levodopa</keyword></keywordGroup><fundingInfo><fundingAgency>Canadian Institutes of Health Research</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Novartis Canada and the Neuroscience Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Fonds de la recherche en santé du Quebec</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Government of Tunisia</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Enkephalin is reported to play an important role in the pathophysiology of levodopa (LD) ‐induced dyskinesias. The present study investigated the effect of chronic treatment with a selective NR1A/2B <i>N</i>‐methyl‐<sc>D</sc>‐aspartate (NMDA) receptor antagonist, CI‐1041, on the expression of preproenkephalin‐A (PPE‐A) in brains of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) ‐treated monkeys in relation to the development of LD‐induced dyskinesias. Four MPTP‐monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP‐monkeys received LD/benserazide plus CI‐1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline‐treated MPTP monkeys were also included. MPTP‐treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE‐A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline‐treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI‐1041 normalizes PPE‐A mRNA expression and prevents the development of LD‐induced dyskinesias in an animal model of Parkinson disease. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Prevention of levodopa‐induced dyskinesias by a selective NR1A/2B N‐methyl‐D‐aspartate receptor antagonist in parkinsonian monkeys: Implication of preproenkephalin</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Glutamate Antagonist and Enkephalin</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Prevention of levodopa‐induced dyskinesias by a selective NR1A/2B</title></titleInfo><name type="personal"><namePart type="given">Marc</namePart><namePart type="family">Morissette</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</affiliation><affiliation>Faculty of Pharmacy, Laval University, Quebec, Canada</affiliation><description>Correspondence: Molecular Endocrinology and Oncology Research Center, Laval University Medical Center, CHUL, 2705 Laurier Blvd, Quebec, QC, Canada G1V 4G2</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mehdi</namePart><namePart type="family">Dridi</namePart><namePart type="termsOfAddress">MSc</namePart><affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</affiliation><affiliation>Faculty of Pharmacy, Laval University, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frédéric</namePart><namePart type="family">Calon</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</affiliation><affiliation>Faculty of Pharmacy, Laval University, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Abdallah Hadj</namePart><namePart type="family">Tahar</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Unit, Laval University Medical Centre, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Leonard T.</namePart><namePart type="family">Meltzer</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Pfizer Global Research & Development, Ann Arbor Laboratories, Ann Arbor, Michigan, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paul J.</namePart><namePart type="family">Bédard</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neuroscience Research Unit, Laval University Medical Centre, Quebec, Canada</affiliation><affiliation>Faculty of Medicine, Laval University, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thérèse</namePart><namePart type="family">Di Paolo</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Molecular Endocrinology and Oncology Research Centre, Laval University Medical Centre, Quebec, Canada</affiliation><affiliation>Faculty of Pharmacy, Laval University, Quebec, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2006-01</dateIssued><dateCaptured encoding="w3cdtf">2004-11-05</dateCaptured><dateValid encoding="w3cdtf">2005-02-04</dateValid><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="references">48</extent><extent unit="words">5721</extent></physicalDescription><abstract lang="en">Enkephalin is reported to play an important role in the pathophysiology of levodopa (LD) ‐induced dyskinesias. The present study investigated the effect of chronic treatment with a selective NR1A/2B N‐methyl‐D‐aspartate (NMDA) receptor antagonist, CI‐1041, on the expression of preproenkephalin‐A (PPE‐A) in brains of 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) ‐treated monkeys in relation to the development of LD‐induced dyskinesias. Four MPTP‐monkeys received LD/benserazide alone; they all developed dyskinesias. Four other MPTP‐monkeys received LD/benserazide plus CI‐1041; only one of them developed mild dyskinesias at the end of the fourth week of treatment. Four normal monkeys and four saline‐treated MPTP monkeys were also included. MPTP‐treated monkeys had extensive and similar striatal dopamine denervation. An increase of PPE‐A mRNA levels assayed by in situ hybridization was observed in the lateral putamen (rostral and caudal) and caudate nucleus (rostral) of saline‐treated MPTP monkeys compared to controls, whereas no change or a small increase was observed in their medial parts. Striatal PPE‐A mRNA levels remained elevated in LD‐treated MPTP monkeys, whereas cotreatment with CI‐1041 brought them back to control values. These findings suggest that chronic blockade of striatal NR1A/2B NMDA receptors with CI‐1041 normalizes PPE‐A mRNA expression and prevents the development of LD‐induced dyskinesias in an animal model of Parkinson disease. © 2005 Movement Disorder Society</abstract><note type="funding">Canadian Institutes of Health Research</note><note type="funding">Novartis Canada and the Neuroscience Foundation</note><note type="funding">Fonds de la recherche en santé du Quebec</note><note type="funding">Government of Tunisia</note><subject lang="en"><genre>Keywords</genre><topic>MPTP</topic><topic>glutamate receptor</topic><topic>preproenkephalin</topic><topic>Parkinson's disease</topic><topic>dyskinesia</topic><topic>levodopa</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>9</start><end>17</end><total>9</total></extent></part></relatedItem><identifier type="istex">DE7517848667D0FEB06AA3F8B46C2E74A33A4989</identifier><identifier type="DOI">10.1002/mds.20654</identifier><identifier type="ArticleID">MDS20654</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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