De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Identifieur interne : 000890 ( Istex/Corpus ); précédent : 000889; suivant : 000891De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset
Auteurs : Ronald K. B. Pearce ; Tara Banerji ; Jenner ; C. David MarsdenSource :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
English descriptors
- KwdEn :
Abstract
In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.
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DOI: 10.1002/mds.870130207
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We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ronald K. B. 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We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p > 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. 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B.</forename><surname>Pearce</surname></persName><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation></author><author><persName><forename type="first">Tara</forename><surname>Banerji</surname></persName><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation></author><author><persName><surname>Jenner</surname><roleName type="degree">Professor</roleName></persName><note type="correspondence"><p>Correspondence: Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, England</p></note><affiliation>National Hospital for Neurology and Neurosurgery, King's College, London, England</affiliation></author><author><persName><forename type="first">C.</forename><surname>David Marsden</surname></persName><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-03"></date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="234">234</biblScope><biblScope unit="page" to="241">241</biblScope></imprint></monogr><idno type="istex">982D4676EE3271FE1ABC9DB732BA6A99D80145F1</idno><idno type="DOI">10.1002/mds.870130207</idno><idno type="ArticleID">MDS870130207</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dyskinesia</term></item><item><term>Parkinson's disease</term></item><item><term>Ropinirole</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-04-28">Received</change><change when="1997-07-14">Registration</change><change when="1998-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/982D4676EE3271FE1ABC9DB732BA6A99D80145F1/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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B.</givenNames><familyName>Pearce</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tara</givenNames><familyName>Banerji</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><honorifics>Professor</honorifics><givenNames>Peter</givenNames><familyName>Jenner</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>C.</givenNames><familyName>David Marsden</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>National Hospital for Neurology and Neurosurgery, King's College, London, England</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Dyskinesia</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">Ropinirole</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In contrast to levodopa (<sc>L</sc>‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and <sc>L</sc>‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, <sc>L</sc>‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. <sc>L</sc>‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the <sc>L</sc>‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with <sc>L</sc>‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of <sc>L</sc>‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than <sc>L</sc>‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once <sc>L</sc>‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in <sc>L</sc>‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>De novo administration of ropinirole and bromocriptine induces less dyskinesia than L‐dopa in the MPTP‐treated marmoset</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ROPINIROLE AND DYSKINESIA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>De novo administration of ropinirole and bromocriptine induces less dyskinesia than</title></titleInfo><name type="personal"><namePart type="given">Ronald K. B.</namePart><namePart type="family">Pearce</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tara</namePart><namePart type="family">Banerji</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Professor</namePart><namePart type="family">Jenner</namePart><affiliation>National Hospital for Neurology and Neurosurgery, King's College, London, England</affiliation><description>Correspondence: Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, England</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">David Marsden</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-03</dateIssued><dateCaptured encoding="w3cdtf">1997-04-28</dateCaptured><dateValid encoding="w3cdtf">1997-07-14</dateValid><copyrightDate encoding="w3cdtf">1998</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">42</extent></physicalDescription><abstract lang="en">In contrast to levodopa (L‐dopa), de novo administration of the D2‐like receptor agonist bromocriptine to patients with Parkinson's disease (PD) or to 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated subhuman primates is not associated with the onset of significant dyskinesia. We now compare the ability of the novel D2‐like selective dopamine agonist ropinirole with that of bromocriptine and L‐dopa to induce dyskinesia in MPTP‐treated common marmosets. MPTP‐treated common marmosets were treated with placebo, L‐dopa plus carbidopa, ropinirole, or bromocriptine daily for 30 days (n = 4 per group) in doses that were titrated to similarly increase locomotion and improve motor disability. L‐dopa rapidly induced dyskinesia of moderate to severe intensity, whereas ropinirole and bromocriptine produced mild dyskinesia over the course of the study that was significantly less severe than in the L‐dopa‐treated group (p < 0.05). However, in a separate group of marmosets previously primed with L‐dopa to exhibit dyskinesia, ropinirole administration elicited severe dyskinesias comparable with that of L‐dopa in a dosedependent fashion. Ropinirole, in common with bromocriptine, has a lesser tendency than L‐dopa to produce dyskinesia while similarly improving motor performance in drug‐naive MPTP‐treated marmosets. However, in common with other dopamine agonists, ropinirole will elicit comparable dyskinesia once L‐dopa priming has occurred. These results predict a similar response to ropinirole and other long‐acting dopamine agonists in L‐dopa‐naive patients with PD and emphasize the importance of avoiding initial dyskinesia induction through early use of dopamine agonist drugs.</abstract><subject lang="en"><genre>Keywords</genre><topic>Dyskinesia</topic><topic>Parkinson's disease</topic><topic>Ropinirole</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><subject><genre>article category</genre><topic>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>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>234</start><end>241</end><total>8</total></extent></part></relatedItem><identifier type="istex">982D4676EE3271FE1ABC9DB732BA6A99D80145F1</identifier><identifier type="DOI">10.1002/mds.870130207</identifier><identifier type="ArticleID">MDS870130207</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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