The monoamine reuptake inhibitor BTS 74 398 fails to evoke established dyskinesia but does not synergise with levodopa in MPTP‐treated primates
Identifieur interne : 000F44 ( Istex/Corpus ); précédent : 000F43; suivant : 000F45The monoamine reuptake inhibitor BTS 74 398 fails to evoke established dyskinesia but does not synergise with levodopa in MPTP‐treated primates
Auteurs : Matthew J. Hansard ; Lance A. Smith ; Michael J. Jackson ; Sharon C. Cheetham ; Peter JennerSource :
- Movement Disorders [ 0885-3185 ] ; 2004-01.
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- KwdEn :
Abstract
Long‐term treatment of Parkinson's disease (PD) with levodopa (L‐dopa) induces dyskinesia that, once established, is provoked by each dose of L‐dopa or a dopamine (DA) agonist. In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with L‐dopa and whether co‐administration of BTS 74 398 with L‐dopa potentiates motor behaviour and dyskinesia induced by acute L‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of L‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal L‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by L‐dopa alone and there was no alteration in the dyskinesia provoked by L‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with L‐dopa. The lack of synergy with L‐dopa may suggest different sites of drug action. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10596
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ISTEX:9786D3DEE263A88180D758AEAD02B14FDD26BBBFLe document en format XML
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Smith</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Jackson, Michael J" sort="Jackson, Michael J" uniqKey="Jackson M" first="Michael J." last="Jackson">Michael J. Jackson</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Cheetham, Sharon C" sort="Cheetham, Sharon C" uniqKey="Cheetham S" first="Sharon C." last="Cheetham">Sharon C. 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Jackson</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Cheetham, Sharon C" sort="Cheetham, Sharon C" uniqKey="Cheetham S" first="Sharon C." last="Cheetham">Sharon C. Cheetham</name><affiliation><mods:affiliation>RenaSci Consultancy Ltd., Nottingham, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Jenner, Peter" sort="Jenner, Peter" uniqKey="Jenner P" first="Peter" last="Jenner">Peter Jenner</name><affiliation><mods:affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-01">2004-01</date><biblScope unit="vol">19</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="15">15</biblScope><biblScope unit="page" to="21">21</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9786D3DEE263A88180D758AEAD02B14FDD26BBBF</idno><idno type="DOI">10.1002/mds.10596</idno><idno type="ArticleID">MDS10596</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>BTS 74 398</term><term>MPTP</term><term>Parkinson's disease</term><term>dyskinesia</term><term>marmosets</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Long‐term treatment of Parkinson's disease (PD) with levodopa (L‐dopa) induces dyskinesia that, once established, is provoked by each dose of L‐dopa or a dopamine (DA) agonist. In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with L‐dopa and whether co‐administration of BTS 74 398 with L‐dopa potentiates motor behaviour and dyskinesia induced by acute L‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of L‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal L‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by L‐dopa alone and there was no alteration in the dyskinesia provoked by L‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with L‐dopa. The lack of synergy with L‐dopa may suggest different sites of drug action. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Matthew J. Hansard BSc, PhD</name><affiliations><json:string>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Lance A. Smith MSc, PhD</name><affiliations><json:string>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Michael J. Jackson BSc</name><affiliations><json:string>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Sharon C. Cheetham MSc, PhD</name><affiliations><json:string>RenaSci Consultancy Ltd., Nottingham, United Kingdom</json:string></affiliations></json:item><json:item><name>Peter Jenner FRPharm, DSc</name><affiliations><json:string>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</json:string></affiliations></json:item></author><subject><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>BTS 74 398</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>marmosets</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Long‐term treatment of Parkinson's disease (PD) with levodopa (L‐dopa) induces dyskinesia that, once established, is provoked by each dose of L‐dopa or a dopamine (DA) agonist. In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with L‐dopa and whether co‐administration of BTS 74 398 with L‐dopa potentiates motor behaviour and dyskinesia induced by acute L‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of L‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal L‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by L‐dopa alone and there was no alteration in the dyskinesia provoked by L‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with L‐dopa. 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In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with L‐dopa and whether co‐administration of BTS 74 398 with L‐dopa potentiates motor behaviour and dyskinesia induced by acute L‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of L‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal L‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by L‐dopa alone and there was no alteration in the dyskinesia provoked by L‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with L‐dopa. 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In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with <sc>L</sc>‐dopa and whether co‐administration of BTS 74 398 with <sc>L</sc>‐dopa potentiates motor behaviour and dyskinesia induced by acute <sc>L</sc>‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of <sc>L</sc>‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal <sc>L</sc>‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by <sc>L</sc>‐dopa alone and there was no alteration in the dyskinesia provoked by <sc>L</sc>‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with <sc>L</sc>‐dopa. The lack of synergy with <sc>L</sc>‐dopa may suggest different sites of drug action. © 2003 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 inhibitor BTS 74 398 fails to evoke established dyskinesia but does not synergise with levodopa in MPTP‐treated primates</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Dyskinesia and Monoamine Reuptake Inhibition</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The monoamine reuptake inhibitor BTS 74 398 fails to evoke established dyskinesia but does not synergise with levodopa in MPTP‐treated primates</title></titleInfo><name type="personal"><namePart type="given">Matthew J.</namePart><namePart type="family">Hansard</namePart><namePart type="termsOfAddress">BSc, PhD</namePart><affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, 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>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, 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>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sharon C.</namePart><namePart type="family">Cheetham</namePart><namePart type="termsOfAddress">MSc, PhD</namePart><affiliation>RenaSci Consultancy Ltd., Nottingham, United Kingdom</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">FRPharm, DSc</namePart><affiliation>Neurodegenerative Disease Research Centre, Guy's, King's and St. Thomas' School of Biomedical Sciences, King's College, London, United Kingdom</affiliation><description>Correspondence: Neurodegenerative Disease Research Centre, GKT 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">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2004-01</dateIssued><dateCaptured encoding="w3cdtf">2002-08-07</dateCaptured><dateValid encoding="w3cdtf">2003-07-04</dateValid><copyrightDate encoding="w3cdtf">2004</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">2</extent><extent unit="references">35</extent><extent unit="words">4460</extent></physicalDescription><abstract lang="en">Long‐term treatment of Parkinson's disease (PD) with levodopa (L‐dopa) induces dyskinesia that, once established, is provoked by each dose of L‐dopa or a dopamine (DA) agonist. In contrast, monoamine reuptake inhibitors may reverse motor deficits in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated primates without provoking established involuntary movements. We now examine whether the potent monoamine reuptake blocker BTS 74 398 induces established dyskinesia in MPTP‐treated common marmosets primed previously with L‐dopa and whether co‐administration of BTS 74 398 with L‐dopa potentiates motor behaviour and dyskinesia induced by acute L‐dopa treatment. Administration of BTS 74 398 (2.5, 5.0, or 10.0 mg/kg, p.o.) in MPTP‐treated common marmosets increased locomotor activity and reduced motor disability in a dose‐related manner but did not provoke involuntary movements. BTS 74 398 (2.5, 5.0, or 10.0 mg/kg p.o.) co‐administered with a threshold dose of L‐dopa (2.5 mg/kg p.o.) did not evoke a motor response or induce dyskinesia. Similarly, concomitant administration of BTS 74 398 (5.0 mg/kg p.o.) with a submaximal L‐dopa dose (12.5 mg/kg p.o.) did not potentiate the motor response produced by L‐dopa alone and there was no alteration in the dyskinesia provoked by L‐dopa challenge. BTS 74 398 reverses motor abnormalities in MPTP‐treated marmosets without evoking established dyskinesia but no additive improvement occurs when administered in combination with L‐dopa. The lack of synergy with L‐dopa may suggest different sites of drug action. © 2003 Movement Disorder Society</abstract><note type="funding">British Biological Science Research Council</note><note type="funding">Parkinson's Disease Society</note><note type="funding">National Parkinson's Disease Foundation</note><note type="funding">Knoll Ltd.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>BTS 74 398</topic><topic>dyskinesia</topic><topic>MPTP</topic><topic>marmosets</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></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>2004</date><detail type="volume"><caption>vol.</caption><number>19</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>15</start><end>21</end><total>7</total></extent></part></relatedItem><identifier type="istex">9786D3DEE263A88180D758AEAD02B14FDD26BBBF</identifier><identifier type="DOI">10.1002/mds.10596</identifier><identifier type="ArticleID">MDS10596</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 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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