Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets
Identifieur interne : 000B51 ( Istex/Corpus ); précédent : 000B50; suivant : 000B52Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets
Auteurs : Lance A. Smith ; Ariel Gordin ; Jenner ; C. David MarsdenSource :
- Movement Disorders [ 0885-3185 ] ; 1997-11.
English descriptors
- KwdEn :
Abstract
Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.
Url:
DOI: 10.1002/mds.870120616
Links to Exploration step
ISTEX:72FAAC5BF6A29EED81F9A337BFC2F161071D71FFLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title><author><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</mods:affiliation></affiliation></author><author><name sortKey="Gordin, Ariel" sort="Gordin, Ariel" uniqKey="Gordin A" first="Ariel" last="Gordin">Ariel Gordin</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</mods:affiliation></affiliation></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><affiliation><mods:affiliation>Orion Research Center, Espoo, Finland</mods:affiliation></affiliation></author><author><name sortKey="Marsden, C David" sort="Marsden, C David" uniqKey="Marsden C" first="C. David" last="Marsden">C. David Marsden</name><affiliation><mods:affiliation>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, England</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:72FAAC5BF6A29EED81F9A337BFC2F161071D71FF</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1002/mds.870120616</idno><idno type="url">https://api.istex.fr/document/72FAAC5BF6A29EED81F9A337BFC2F161071D71FF/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000B51</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title><author><name sortKey="Smith, Lance A" sort="Smith, Lance A" uniqKey="Smith L" first="Lance A." last="Smith">Lance A. Smith</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</mods:affiliation></affiliation></author><author><name sortKey="Gordin, Ariel" sort="Gordin, Ariel" uniqKey="Gordin A" first="Ariel" last="Gordin">Ariel Gordin</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</mods:affiliation></affiliation></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><affiliation><mods:affiliation>Orion Research Center, Espoo, Finland</mods:affiliation></affiliation></author><author><name sortKey="Marsden, C David" sort="Marsden, C David" uniqKey="Marsden C" first="C. David" last="Marsden">C. David Marsden</name><affiliation><mods:affiliation>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, England</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="1997-11">1997-11</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="935">935</biblScope><biblScope unit="page" to="945">945</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">72FAAC5BF6A29EED81F9A337BFC2F161071D71FF</idno><idno type="DOI">10.1002/mds.870120616</idno><idno type="ArticleID">MDS870120616</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Behavioral disability</term><term>COMT inhibitor</term><term>Carbidopa</term><term>Entacapone</term><term>Levodopa</term><term>Locomotor activity</term><term>MPTP</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Lance A. Smith</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</json:string></affiliations></json:item><json:item><name>Ariel Gordin</name><affiliations><json:string>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</json:string></affiliations></json:item><json:item><name>Dr. Jenner</name><affiliations><json:string>Orion Research Center, Espoo, Finland</json:string></affiliations></json:item><json:item><name>C. David Marsden</name><affiliations><json:string>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, England</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Locomotor activity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Behavioral disability</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>COMT inhibitor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Entacapone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Carbidopa</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.</abstract><qualityIndicators><score>6.984</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 827.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1428</abstractCharCount><pdfWordCount>4548</pdfWordCount><pdfCharCount>29716</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>203</abstractWordCount></qualityIndicators><title>Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title><genre><json:string>Serial article</json:string></genre><host><volume>12</volume><pages><total>11</total><last>945</last><first>935</first></pages><issn><json:string>0885-3185</json:string></issn><issue>6</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1002/mds.870120616</json:string></doi><id>72FAAC5BF6A29EED81F9A337BFC2F161071D71FF</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/72FAAC5BF6A29EED81F9A337BFC2F161071D71FF/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/72FAAC5BF6A29EED81F9A337BFC2F161071D71FF/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/72FAAC5BF6A29EED81F9A337BFC2F161071D71FF/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title><author><persName><forename type="first">Lance A.</forename><surname>Smith</surname></persName><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</affiliation></author><author><persName><forename type="first">Ariel</forename><surname>Gordin</surname></persName><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</affiliation></author><author><persName><surname>Jenner</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, U.K.</p></note><affiliation>Orion Research Center, Espoo, Finland</affiliation></author><author><persName><forename type="first">C. David</forename><surname>Marsden</surname></persName><affiliation>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, England</affiliation></author></analytic><monogr><title level="j">Movement Disorders</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="1997-11"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="935">935</biblScope><biblScope unit="page" to="945">945</biblScope></imprint></monogr><idno type="istex">72FAAC5BF6A29EED81F9A337BFC2F161071D71FF</idno><idno type="DOI">10.1002/mds.870120616</idno><idno type="ArticleID">MDS870120616</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Locomotor activity</term></item><item><term>Behavioral disability</term></item><item><term>MPTP</term></item><item><term>COMT inhibitor</term></item><item><term>Entacapone</term></item><item><term>Levodopa</term></item><item><term>Carbidopa</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="1996-10-23">Received</change><change when="1997-02-16">Registration</change><change when="1997-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/72FAAC5BF6A29EED81F9A337BFC2F161071D71FF/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="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="60"><doi origin="wiley" registered="yes">10.1002/mds.v12:6</doi><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue">6</numbering></numberingGroup><coverDate startDate="1997-11">November 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="16" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870120616</doi><idGroup><id type="unit" value="MDS870120616"></id></idGroup><countGroup><count type="pageTotal" number="11"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1997 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1996-10-23"></event><event type="manuscriptRevised" date="1997-02-07"></event><event type="manuscriptAccepted" date="1997-02-16"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4.7 mode:FullText source:HeaderRef result:HeaderRef" date="2011-02-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">935</numbering><numbering type="pageLast">945</numbering></numberingGroup><correspondenceTo>Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, U.K.</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870120616.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="24"></count></countGroup><titleGroup><title type="main" xml:lang="en">Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title><title type="short" xml:lang="en">ENTACAPONE POTENTIATES ANTIPARKINSONIAN EFFECTS OF LEVODOPA</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Lance A.</givenNames><familyName>Smith</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ariel</givenNames><familyName>Gordin</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Peter</givenNames><familyName>Jenner</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>C. David</givenNames><familyName>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; Orion‐Farmos</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FI" type="organization"><unparsedAffiliation>Orion Research Center, Espoo, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London, England</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Locomotor activity</keyword><keyword xml:id="kwd2">Behavioral disability</keyword><keyword xml:id="kwd3">MPTP</keyword><keyword xml:id="kwd4">COMT inhibitor</keyword><keyword xml:id="kwd5">Entacapone</keyword><keyword xml:id="kwd6">Levodopa</keyword><keyword xml:id="kwd7">Carbidopa</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.</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>Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ENTACAPONE POTENTIATES ANTIPARKINSONIAN EFFECTS OF LEVODOPA</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets</title></titleInfo><name type="personal"><namePart type="given">Lance A.</namePart><namePart type="family">Smith</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ariel</namePart><namePart type="family">Gordin</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England; Orion‐Farmos</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Jenner</namePart><affiliation>Orion Research Center, Espoo, Finland</affiliation><description>Correspondence: Pharmacology Group, Biomedical Sciences Division, King's College London, Manresa Road, London SW3 6LX, U.K.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C. David</namePart><namePart type="family">Marsden</namePart><affiliation>University Department of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, 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">1997-11</dateIssued><dateCaptured encoding="w3cdtf">1996-10-23</dateCaptured><dateValid encoding="w3cdtf">1997-02-16</dateValid><copyrightDate encoding="w3cdtf">1997</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">5</extent><extent unit="tables">3</extent><extent unit="references">24</extent></physicalDescription><abstract lang="en">Oral administration of levodopa (L‐dopa) (2.5–25.0 mg/kg) plus carbidopa (12.5 mg/kg p.o.) to MPTP‐treated common marmosets produced a dose‐related increase in locomotor activity and a corresponding decrease in motor disability. Pretreatment with the peripheral COMT inhibitor entacapone (12.5 mg/kg p.o.) enhanced the intensity and duration of the increase in locomotor activity and the reversal of motor disability produced by a threshold dose of L‐dopa (2.5 mg/kg p.o.) plus carbidopa. By contrast, entacapone pretreatment did not potentiate the increased locomotor activity or reversal of motor disability produced by a near‐maximal dose of L‐dopa (12.5 mg/kg p.o.) plus carbidopa. The effects of entacapone (5.0–25.0 mg/kg p.o.) were dose related, with doses of >12.5 mg/kg tending to produce less potentiation of L‐dopa's effects compared to lower doses. Pretreatment with entacapone (12.5 mg/kg p.o.) without carbidopa caused a short‐lasting enhancement of L‐dopa's (12.5 mg/kg p.o.) action, whereas pretreatment with carbidopa (12.5 mg/kg p.o.) alone had a more dramatic effect. However, pretreatment with both carbidopa and entacapone produced the greatest overall motor response. In conclusion, entacapone enhances the motor response produced by a low threshold dose of L‐dopa plus carbidopa. However, optimization of both the dose of L‐dopa and entacapone appears necessary to obtain the maximal therapeutic response.</abstract><subject lang="en"><genre>Keywords</genre><topic>Locomotor activity</topic><topic>Behavioral disability</topic><topic>MPTP</topic><topic>COMT inhibitor</topic><topic>Entacapone</topic><topic>Levodopa</topic><topic>Carbidopa</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>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>1997</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>935</start><end>945</end><total>11</total></extent></part></relatedItem><identifier type="istex">72FAAC5BF6A29EED81F9A337BFC2F161071D71FF</identifier><identifier type="DOI">10.1002/mds.870120616</identifier><identifier type="ArticleID">MDS870120616</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 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)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000B51 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000B51 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:72FAAC5BF6A29EED81F9A337BFC2F161071D71FF
|texte= Entacapone enhances levodopa‐induced reversal of motor disability in MPTP‐treated common marmosets
}}
| This area was generated with Dilib version V0.6.23. |  |