An appraisal of the antiparkinsonian activity of piribedil in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets
Identifieur interne : 000463 ( Istex/Corpus ); précédent : 000462; suivant : 000464An appraisal of the antiparkinsonian activity of piribedil in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets
Auteurs : Lance Smith ; Maria De Salvia ; Jenner ; C. David MarsdenSource :
- Movement Disorders [ 0885-3185 ] ; 1996-03.
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- KwdEn :
Abstract
The D2 dopamine agonist piribedil is not widely used in the treatment of Parkinson's disease because it was thought to be effective mainly on parkinsonian tremor and to produce a high incidence of peripheral side effects, particular nausea. In this study, we used 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–treated primates to reevaluate the antiparkinsonian ability of piribedil after its oral administration in the presence or absence of domperidone pretreatment. Adult common marmosets (Callithrix jacchus) were treated with the nigral toxin MPTP to induce a parkinsonian syndrome characterised primarily by brady kinesia and other motor deficits. Oral administration of a solution of piribedil [1–(3,4–methylenedioxybenzyl)–4–(2–pyrimidinyl) piperazine] produced a dose–related reversal of all MPTP locomotor and behavioural deficits. However, this effect was short lived and associated with unwanted effects, particular nausea and retching, which clearly hindered locomotion. In contrast, after pretreatment with the peripheral dopamine antagonist domperidone, administration of piribedil did not induce nausea or retching in MPTP‐treated marmosets. In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. These data indicate that piribedil should be an effective monotherapy for Parkinson's disease.
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DOI: 10.1002/mds.870110203
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In this study, we used 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–treated primates to reevaluate the antiparkinsonian ability of piribedil after its oral administration in the presence or absence of domperidone pretreatment. Adult common marmosets (Callithrix jacchus) were treated with the nigral toxin MPTP to induce a parkinsonian syndrome characterised primarily by brady kinesia and other motor deficits. Oral administration of a solution of piribedil [1–(3,4–methylenedioxybenzyl)–4–(2–pyrimidinyl) piperazine] produced a dose–related reversal of all MPTP locomotor and behavioural deficits. However, this effect was short lived and associated with unwanted effects, particular nausea and retching, which clearly hindered locomotion. In contrast, after pretreatment with the peripheral dopamine antagonist domperidone, administration of piribedil did not induce nausea or retching in MPTP‐treated marmosets. In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. 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In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. 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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="1996-03"></date><biblScope unit="vol">11</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="125">125</biblScope><biblScope unit="page" to="135">135</biblScope></imprint></monogr><idno type="istex">3A8D5EC6C2F8DD45D6D5B30A233600CFF5E52960</idno><idno type="DOI">10.1002/mds.870110203</idno><idno type="ArticleID">MDS870110203</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The D2 dopamine agonist piribedil is not widely used in the treatment of Parkinson's disease because it was thought to be effective mainly on parkinsonian tremor and to produce a high incidence of peripheral side effects, particular nausea. In this study, we used 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–treated primates to reevaluate the antiparkinsonian ability of piribedil after its oral administration in the presence or absence of domperidone pretreatment. Adult common marmosets (Callithrix jacchus) were treated with the nigral toxin MPTP to induce a parkinsonian syndrome characterised primarily by brady kinesia and other motor deficits. Oral administration of a solution of piribedil [1–(3,4–methylenedioxybenzyl)–4–(2–pyrimidinyl) piperazine] produced a dose–related reversal of all MPTP locomotor and behavioural deficits. However, this effect was short lived and associated with unwanted effects, particular nausea and retching, which clearly hindered locomotion. In contrast, after pretreatment with the peripheral dopamine antagonist domperidone, administration of piribedil did not induce nausea or retching in MPTP‐treated marmosets. In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. These data indicate that piribedil should be an effective monotherapy for Parkinson's disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Piribedil</term></item><item><term>Parkinson's disease</term></item><item><term>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</term></item><item><term>Common marmosets</term></item><item><term>Locomotor activity</term></item><item><term>Behavioural deficits</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="1995-08-03">Registration</change><change when="1996-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3A8D5EC6C2F8DD45D6D5B30A233600CFF5E52960/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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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</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>University Department of Clinical Neurology, Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, England</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Piribedil</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</keyword><keyword xml:id="kwd4">Common marmosets</keyword><keyword xml:id="kwd5">Locomotor activity</keyword><keyword xml:id="kwd6">Behavioural deficits</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The D2 dopamine agonist piribedil is not widely used in the treatment of Parkinson's disease because it was thought to be effective mainly on parkinsonian tremor and to produce a high incidence of peripheral side effects, particular nausea. In this study, we used 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–treated primates to reevaluate the antiparkinsonian ability of piribedil after its oral administration in the presence or absence of domperidone pretreatment. Adult common marmosets <i>(Callithrix jacchus)</i> were treated with the nigral toxin MPTP to induce a parkinsonian syndrome characterised primarily by brady kinesia and other motor deficits. Oral administration of a solution of piribedil [1–(3,4–methylenedioxybenzyl)–4–(2–pyrimidinyl) piperazine] produced a dose–related reversal of all MPTP locomotor and behavioural deficits. However, this effect was short lived and associated with unwanted effects, particular nausea and retching, which clearly hindered locomotion. In contrast, after pretreatment with the peripheral dopamine antagonist domperidone, administration of piribedil did not induce nausea or retching in MPTP‐treated marmosets. In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. These data indicate that piribedil should be an effective monotherapy for Parkinson's disease.</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>An appraisal of the antiparkinsonian activity of piribedil in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ANTIPARKINSONIAN ACTIONS OF PIRIBEDIL</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>An appraisal of the antiparkinsonian activity of piribedil in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐treated common marmosets</title></titleInfo><name type="personal"><namePart type="given">Lance</namePart><namePart type="family">Smith</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">De Salvia</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Prof.</namePart><namePart type="family">Jenner</namePart><affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, Biomedical Sciences Division, King's College, London, England</affiliation><description>Correspondence: Pharmacology Group, Biomedical Sciences Division, King's College London, 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 Clinical Neurology, Institute of Neurology, The 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">1996-03</dateIssued><dateValid encoding="w3cdtf">1995-08-03</dateValid><copyrightDate encoding="w3cdtf">1996</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">6</extent><extent unit="references">21</extent></physicalDescription><abstract lang="en">The D2 dopamine agonist piribedil is not widely used in the treatment of Parkinson's disease because it was thought to be effective mainly on parkinsonian tremor and to produce a high incidence of peripheral side effects, particular nausea. In this study, we used 1–methyl–4–phenyl–1,2,3,6–tetrahydropyridine (MPTP)–treated primates to reevaluate the antiparkinsonian ability of piribedil after its oral administration in the presence or absence of domperidone pretreatment. Adult common marmosets (Callithrix jacchus) were treated with the nigral toxin MPTP to induce a parkinsonian syndrome characterised primarily by brady kinesia and other motor deficits. Oral administration of a solution of piribedil [1–(3,4–methylenedioxybenzyl)–4–(2–pyrimidinyl) piperazine] produced a dose–related reversal of all MPTP locomotor and behavioural deficits. However, this effect was short lived and associated with unwanted effects, particular nausea and retching, which clearly hindered locomotion. In contrast, after pretreatment with the peripheral dopamine antagonist domperidone, administration of piribedil did not induce nausea or retching in MPTP‐treated marmosets. In these animals, piribedil caused a more marked and and longer lasting enhancement of locomotor activity and a further reduction in behavioural deficits than that observed after administration of piribedil alone. In addition, piribedil induced increased vigilance and awareness. These data show that piribedil can reverse akinesia and rigidity in MPTP‐treated primates. In addition, they show the drug to be effective without peripheral side effects when used in conjuction with domperidone. These data indicate that piribedil should be an effective monotherapy for Parkinson's disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>Piribedil</topic><topic>Parkinson's disease</topic><topic>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine</topic><topic>Common marmosets</topic><topic>Locomotor activity</topic><topic>Behavioural deficits</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>1996</date><detail type="volume"><caption>vol.</caption><number>11</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>125</start><end>135</end><total>11</total></extent></part></relatedItem><identifier type="istex">3A8D5EC6C2F8DD45D6D5B30A233600CFF5E52960</identifier><identifier type="DOI">10.1002/mds.870110203</identifier><identifier type="ArticleID">MDS870110203</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1996 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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