The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys
Identifieur interne : 000487 ( Istex/Corpus ); précédent : 000486; suivant : 000488The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys
Auteurs : R. J. Vermeulen ; Drukarch ; M. C. R. Sahadat ; C. Goosen ; E. C. Wolters ; J. C. StoofSource :
- Movement Disorders [ 0885-3185 ] ; 1994.
English descriptors
- KwdEn :
Abstract
At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D2 receptor agonist. However, in general the clinical efficacy of D2 agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D1 receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D1 agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D2 agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D1 receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D1 and D2 receptors as compared with stimulation of both receptors alone.
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DOI: 10.1002/mds.870090613
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ISTEX:DB773F4F248D62B2386EC24C0587FD28D04DBBDELe document en format XML
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Sahadat</name><affiliation><mods:affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Goosen, C" sort="Goosen, C" uniqKey="Goosen C" first="C." last="Goosen">C. Goosen</name><affiliation><mods:affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Wolters, E C" sort="Wolters, E C" uniqKey="Wolters E" first="E. C." last="Wolters">E. C. Wolters</name><affiliation><mods:affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</mods:affiliation></affiliation></author><author><name sortKey="Stoof, J C" sort="Stoof, J C" uniqKey="Stoof J" first="J. C." last="Stoof">J. C. Stoof</name><affiliation><mods:affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><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="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="1994">1994</date><biblScope unit="vol">9</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="664">664</biblScope><biblScope unit="page" to="672">672</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DB773F4F248D62B2386EC24C0587FD28D04DBBDE</idno><idno type="DOI">10.1002/mds.870090613</idno><idno type="ArticleID">MDS870090613</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1‐Methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine</term><term>D1 receptor</term><term>D2 receptor</term><term>Dopamine</term><term>Monkey</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D2 receptor agonist. However, in general the clinical efficacy of D2 agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D1 receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D1 agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D2 agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D1 receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D1 and D2 receptors as compared with stimulation of both receptors alone.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>R. J. Vermeulen</name><affiliations><json:string>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</json:string><json:string>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</json:string></affiliations></json:item><json:item><name>Dr. Drukarch</name><affiliations><json:string>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</json:string></affiliations></json:item><json:item><name>M. C. R. Sahadat</name><affiliations><json:string>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</json:string></affiliations></json:item><json:item><name>C. Goosen</name><affiliations><json:string>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</json:string></affiliations></json:item><json:item><name>E. C. Wolters</name><affiliations><json:string>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</json:string></affiliations></json:item><json:item><name>J. C. Stoof</name><affiliations><json:string>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>D1 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>D2 receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>1‐Methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Monkey</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D2 receptor agonist. However, in general the clinical efficacy of D2 agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D1 receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D1 agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D2 agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D1 receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D1 and D2 receptors as compared with stimulation of both receptors alone.</abstract><qualityIndicators><score>7.508</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 828 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1350</abstractCharCount><pdfWordCount>5783</pdfWordCount><pdfCharCount>34845</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>209</abstractWordCount></qualityIndicators><title>The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys</title><genre><json:string>Serial article</json:string></genre><host><volume>9</volume><pages><total>9</total><last>672</last><first>664</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>1994</publicationDate><copyrightDate>1994</copyrightDate><doi><json:string>10.1002/mds.870090613</json:string></doi><id>DB773F4F248D62B2386EC24C0587FD28D04DBBDE</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/DB773F4F248D62B2386EC24C0587FD28D04DBBDE/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/DB773F4F248D62B2386EC24C0587FD28D04DBBDE/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/DB773F4F248D62B2386EC24C0587FD28D04DBBDE/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys</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>1994</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys</title><author><persName><forename type="first">R. J.</forename><surname>Vermeulen</surname></persName><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation></author><author><persName><surname>Drukarch</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, the Netherlands</p></note><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation></author><author><persName><forename type="first">M. C. R.</forename><surname>Sahadat</surname></persName><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation></author><author><persName><forename type="first">C.</forename><surname>Goosen</surname></persName><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation></author><author><persName><forename type="first">E. C.</forename><surname>Wolters</surname></persName><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation></author><author><persName><forename type="first">J. C.</forename><surname>Stoof</surname></persName><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</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="1994"></date><biblScope unit="vol">9</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="664">664</biblScope><biblScope unit="page" to="672">672</biblScope></imprint></monogr><idno type="istex">DB773F4F248D62B2386EC24C0587FD28D04DBBDE</idno><idno type="DOI">10.1002/mds.870090613</idno><idno type="ArticleID">MDS870090613</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1994</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D2 receptor agonist. However, in general the clinical efficacy of D2 agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D1 receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D1 agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D2 agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D1 receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D1 and D2 receptors as compared with stimulation of both receptors alone.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Dopamine</term></item><item><term>D1 receptor</term></item><item><term>D2 receptor</term></item><item><term>1‐Methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine</term></item><item><term>Monkey</term></item><item><term>Parkinson's disease</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="1994">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DB773F4F248D62B2386EC24C0587FD28D04DBBDE/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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J.</givenNames><familyName>Vermeulen</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>B.</givenNames><familyName>Drukarch</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>M. C. R.</givenNames><familyName>Sahadat</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>C.</givenNames><familyName>Goosen</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>E. C.</givenNames><familyName>Wolters</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>J. C.</givenNames><familyName>Stoof</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CH" type="organization"><unparsedAffiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="NL" type="organization"><unparsedAffiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Dopamine</keyword><keyword xml:id="kwd2">D<sub>1</sub> receptor</keyword><keyword xml:id="kwd3">D<sub>2</sub> receptor</keyword><keyword xml:id="kwd4">1‐Methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine</keyword><keyword xml:id="kwd5">Monkey</keyword><keyword xml:id="kwd6">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D<sub>2</sub> receptor agonist. However, in general the clinical efficacy of D<sub>2</sub> agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D<sub>1</sub> receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D<sub>1</sub> agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D<sub>2</sub> agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D<sub>1</sub> receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D<sub>1</sub> and D<sub>2</sub> receptors as compared with stimulation of both receptors alone.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>The dopamine D1 agonist SKF 81297 and the dopamine D2 agonist LY 171555 act synergistically to stimulate motor behavior of 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine‐lesioned parkinsonian rhesus monkeys</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MOTOR EFFECTS OF D1 AND D2 RECEPTOR STIMULATION</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The dopamine D</title></titleInfo><name type="personal"><namePart type="given">R. J.</namePart><namePart type="family">Vermeulen</namePart><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Drukarch</namePart><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation><description>Correspondence: Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, the Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. C. R.</namePart><namePart type="family">Sahadat</namePart><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Goosen</namePart><affiliation>TNO Medical Biological Laboratory, Rijswijk, the Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E. C.</namePart><namePart type="family">Wolters</namePart><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. C.</namePart><namePart type="family">Stoof</namePart><affiliation>Graduate School Neurosciences Amsterdam, Research Institute Neurosciences, Department of Neurology, Vrije Universiteit, Amsterdam</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">1994</dateIssued><copyrightDate encoding="w3cdtf">1994</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">50</extent></physicalDescription><abstract lang="en">At present, the pharmacotherapy of Parkinson's disease (PD) consists mainly of L‐dihydroxyphenylalanine (L‐DOPA) and/or dopamine D2 receptor agonist. However, in general the clinical efficacy of D2 agonists is less than that of L‐DOPA. Therefore, attention is being focussed on the role of the D1 receptor as a target for therapeutic intervention in PD. Recently, we reported that SKF 81297 is a selective D1 agonist that stimulates motor behavior of unilaterally MPTP (1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine)‐lesioned rhesus monkeys. Presently, we studied the effect of coadministration of SKF 81297 and the D2 agonist LY 171555 using the same model of PD. Coadministration of behaviorally active doses of SKF 81297 (0.3 mg/kg) and LY 171555 (0.01 mg/kg) resulted in a prolongation of the motor stimulation induced by either of the drugs alone. Neither administration of SKF 81297, in a dose of 0.03 mg/kg, nor of LY 171555, in a dose of 0.003 mg/kg, were behaviorally active, whereas the combined administration of these compounds induced a significant stimulation of motor behavior. These data suggest that (a) D1 receptor stimulation will prove to be useful in the treatment of PD and (b) better therapeutic results will be obtained by simultaneous stimulation of D1 and D2 receptors as compared with stimulation of both receptors alone.</abstract><subject lang="en"><genre>Keywords</genre><topic>Dopamine</topic><topic>D1 receptor</topic><topic>D2 receptor</topic><topic>1‐Methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine</topic><topic>Monkey</topic><topic>Parkinson's disease</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>1994</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>664</start><end>672</end><total>9</total></extent></part></relatedItem><identifier type="istex">DB773F4F248D62B2386EC24C0587FD28D04DBBDE</identifier><identifier type="DOI">10.1002/mds.870090613</identifier><identifier type="ArticleID">MDS870090613</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1994 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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