The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP‐treated and levodopa‐primed common marmosets
Identifieur interne : 000016 ( Istex/Corpus ); précédent : 000015; suivant : 000017The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP‐treated and levodopa‐primed common marmosets
Auteurs : Ronald K. B. Pearce ; Lance A. Smith ; Michael J. Jackson ; Tara Banerji ; Jorgen Scheel-Krüger ; Peter JennerSource :
- Movement Disorders [ 0885-3185 ] ; 2002-09.
English descriptors
Abstract
The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L‐dopa) dosing and subsequent re‐challenge with L‐dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated L‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L‐dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L‐dopa priming may relate to actions on D1 receptor‐linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L‐dopa–induced dyskinesias complicate treatment. © 2002 Movement Disorder Society
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DOI: 10.1002/mds.10238
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We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated L‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. 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Pearce MD, PhD, FRCPC</name><affiliations><json:string>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</json:string><json:string>Department of Neurology, Charing Cross Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Lance A. Smith MSc PhD</name><affiliations><json:string>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Michael J. Jackson BSc</name><affiliations><json:string>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Tara Banerji MBBS, BSc</name><affiliations><json:string>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Jorgen Scheel‐Krüger PhD</name><affiliations><json:string>NeuroSearch, Smedeland, Glostrup, Denmark</json:string></affiliations></json:item><json:item><name>Peter Jenner PhD, DSc</name><affiliations><json:string>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>L‐dopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dyskinesia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MPTP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine reuptake blockers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>marmosets</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L‐dopa) dosing and subsequent re‐challenge with L‐dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated L‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L‐dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L‐dopa priming may relate to actions on D1 receptor‐linked pathways. 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We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated L‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L‐dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L‐dopa priming may relate to actions on D1 receptor‐linked pathways. 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href="file:MDS.MDS10238.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="55"></count><count type="wordTotal" number="4881"></count></countGroup><titleGroup><title type="main" xml:lang="en">The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP‐treated and levodopa‐primed common marmosets</title><title type="short" xml:lang="en">Brasofensine in MPTP‐Treated Marmosets</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Ronald K.B.</givenNames><familyName>Pearce</familyName><degrees>MD, PhD, FRCPC</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Lance A.</givenNames><familyName>Smith</familyName><degrees>MSc PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael J.</givenNames><familyName>Jackson</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tara</givenNames><familyName>Banerji</familyName><degrees>MBBS, BSc</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jorgen</givenNames><familyName>Scheel‐Krüger</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Peter</givenNames><familyName>Jenner</familyName><degrees>PhD, DSc</degrees></personName><contactDetails><email>div.pharm@kcl.ac.uk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Department of Neurology, Charing Cross Hospital, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="DK" type="organization"><unparsedAffiliation>NeuroSearch, Smedeland, Glostrup, Denmark</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1"><sc>L</sc>‐dopa</keyword><keyword xml:id="kwd2">dyskinesia</keyword><keyword xml:id="kwd3">MPTP</keyword><keyword xml:id="kwd4">dopamine reuptake blockers</keyword><keyword xml:id="kwd5">Parkinson's disease</keyword><keyword xml:id="kwd6">marmosets</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (<sc>L</sc>‐dopa) dosing and subsequent re‐challenge with <sc>L</sc>‐dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of <sc>L</sc>‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated <sc>L</sc>‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of <sc>L</sc>‐dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous <sc>L</sc>‐dopa priming may relate to actions on D<sub>1</sub> receptor‐linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when <sc>L</sc>‐dopa–induced dyskinesias complicate treatment. © 2002 Movement Disorder Society</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>The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP‐treated and levodopa‐primed common marmosets</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Brasofensine in MPTP‐Treated Marmosets</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The monoamine reuptake blocker brasofensine reverses akinesia without dyskinesia in MPTP‐treated and levodopa‐primed common marmosets</title></titleInfo><name type="personal"><namePart type="given">Ronald K.B.</namePart><namePart type="family">Pearce</namePart><namePart type="termsOfAddress">MD, PhD, FRCPC</namePart><affiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</affiliation><affiliation>Department of Neurology, Charing Cross Hospital, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lance A.</namePart><namePart type="family">Smith</namePart><namePart type="termsOfAddress">MSc PhD</namePart><affiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael J.</namePart><namePart type="family">Jackson</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tara</namePart><namePart type="family">Banerji</namePart><namePart type="termsOfAddress">MBBS, BSc</namePart><affiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jorgen</namePart><namePart type="family">Scheel‐Krüger</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>NeuroSearch, Smedeland, Glostrup, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Jenner</namePart><namePart type="termsOfAddress">PhD, DSc</namePart><affiliation>Division of Pharmacology & Therapeutics, Guy's, King's and St. Thomas’ School of Biomedical Sciences, London, United Kingdom</affiliation><description>Correspondence: Division of Pharmacology & Therapeutics, Guy's, King's and St Thomas' School of Biomedical Sciences, King's College, London SE1 1UL, United Kingdom</description><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">New York</placeTerm></place><dateIssued encoding="w3cdtf">2002-09</dateIssued><dateCaptured encoding="w3cdtf">2001-01-17</dateCaptured><dateValid encoding="w3cdtf">2002-02-25</dateValid><copyrightDate encoding="w3cdtf">2002</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">55</extent><extent unit="words">4881</extent></physicalDescription><abstract lang="en">The common marmoset develops motor deficits after MPTP treatment and exhibits dyskinesia after chronic levodopa (L‐dopa) dosing and subsequent re‐challenge with L‐dopa and other dopaminergic agents. We report on the actions of the potent monoamine reuptake blocker brasofensine on motor disability, locomotor activity, and dyskinesia in the 1‐methyl‐4‐1, 2,3,6‐tetrahydropyridine (MPTP) ‐treated marmoset model of Parkinson's disease. Oral administration of brasofensine (0.25, 0.5, 1.0, or 2.5 mg/kg) to MPTP‐treated marmosets produced a long‐lasting, dose‐dependent increase in locomotor activity and reduction in disability scores. In addition, coadministration of the lowest dose of brasofensine (0.25 mg/kg orally) with a threshold oral dose of L‐dopa (2.5 mg/kg) caused a marked increase in locomotor activity, greater than that produced by either drug alone. In other MPTP‐treated marmosets previously primed to exhibit dyskinesia by repeated L‐dopa dosing, brasofensine effectively reversed akinesia with a naturalistic and prolonged motor response without the appearance of dyskinesia or stereotypy. This finding contrasts with the severe dyskinesia, stereotypy, and hyperkinesis produced by equivalent doses of L‐dopa. The ability of brasofensine to produce a prolonged and naturalistic antiparkinsonian response without eliciting dyskinesia after previous L‐dopa priming may relate to actions on D1 receptor‐linked pathways. These findings suggest that monoamine reuptake blockade may be of value in the treatment of Parkinson's disease, both early in the disease course and when L‐dopa–induced dyskinesias complicate treatment. © 2002 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>L‐dopa</topic><topic>dyskinesia</topic><topic>MPTP</topic><topic>dopamine reuptake blockers</topic><topic>Parkinson's disease</topic><topic>marmosets</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>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>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>877</start><end>886</end><total>10</total></extent></part></relatedItem><identifier type="istex">AF5A50DEADD417F68F96E20F0D16EAF3E8EA642A</identifier><identifier type="DOI">10.1002/mds.10238</identifier><identifier type="ArticleID">MDS10238</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorders 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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