Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Identifieur interne : 000779 ( Istex/Corpus ); précédent : 000778; suivant : 000780Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
Auteurs : Naomi P. Visanji ; Jordi Gomez-Ramirez ; Tom H. Johnston ; Donna Pires ; Valerie Voon ; Jonathan M. Brotchie ; Susan H. FoxSource :
- Movement Disorders [ 0885-3185 ] ; 2006-11.
English descriptors
Abstract
Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society
Url:
DOI: 10.1002/mds.21073
Links to Exploration step
ISTEX:D66C7CD0F71954996563291D61D0CDCC2B400A5FLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P." last="Visanji">Naomi P. Visanji</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gomez Amirez, Jordi" sort="Gomez Amirez, Jordi" uniqKey="Gomez Amirez J" first="Jordi" last="Gomez-Ramirez">Jordi Gomez-Ramirez</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H." last="Johnston">Tom H. Johnston</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Pires, Donna" sort="Pires, Donna" uniqKey="Pires D" first="Donna" last="Pires">Donna Pires</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Voon, Valerie" sort="Voon, Valerie" uniqKey="Voon V" first="Valerie" last="Voon">Valerie Voon</name><affiliation><mods:affiliation>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Current Address: Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name><affiliation><mods:affiliation>Division of Neurology, University of Toronto, Toronto, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D66C7CD0F71954996563291D61D0CDCC2B400A5F</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1002/mds.21073</idno><idno type="url">https://api.istex.fr/document/D66C7CD0F71954996563291D61D0CDCC2B400A5F/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000779</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><author><name sortKey="Visanji, Naomi P" sort="Visanji, Naomi P" uniqKey="Visanji N" first="Naomi P." last="Visanji">Naomi P. Visanji</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Gomez Amirez, Jordi" sort="Gomez Amirez, Jordi" uniqKey="Gomez Amirez J" first="Jordi" last="Gomez-Ramirez">Jordi Gomez-Ramirez</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H." last="Johnston">Tom H. Johnston</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Pires, Donna" sort="Pires, Donna" uniqKey="Pires D" first="Donna" last="Pires">Donna Pires</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Voon, Valerie" sort="Voon, Valerie" uniqKey="Voon V" first="Valerie" last="Voon">Valerie Voon</name><affiliation><mods:affiliation>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Current Address: Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</mods:affiliation></affiliation></author><author><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name><affiliation><mods:affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H." last="Fox">Susan H. Fox</name><affiliation><mods:affiliation>Division of Neurology, University of Toronto, Toronto, Canada</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="2006-11">2006-11</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1879">1879</biblScope><biblScope unit="page" to="1891">1891</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">D66C7CD0F71954996563291D61D0CDCC2B400A5F</idno><idno type="DOI">10.1002/mds.21073</idno><idno type="ArticleID">MDS21073</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MPTP‐lesioned primate</term><term>Parkinson's disease</term><term>animal model</term><term>psychosis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Naomi P. Visanji PhD</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Jordi Gomez‐Ramirez PhD</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Tom H. Johnston PhD</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Donna Pires</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Valerie Voon MD</name><affiliations><json:string>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</json:string><json:string>Current Address: Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</json:string></affiliations></json:item><json:item><name>Jonathan M. Brotchie PhD</name><affiliations><json:string>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</json:string></affiliations></json:item><json:item><name>Susan H. Fox MD, PhD</name><affiliations><json:string>Division of Neurology, University of Toronto, Toronto, Canada</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>psychosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>animal model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MPTP‐lesioned primate</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society</abstract><qualityIndicators><score>7.244</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1467</abstractCharCount><pdfWordCount>7656</pdfWordCount><pdfCharCount>51441</pdfCharCount><pdfPageCount>13</pdfPageCount><abstractWordCount>187</abstractWordCount></qualityIndicators><title>Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><genre><json:string>Serial article</json:string></genre><host><volume>21</volume><pages><total>13</total><last>1891</last><first>1879</first></pages><issn><json:string>0885-3185</json:string></issn><issue>11</issue><subject><json:item><value>Research 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>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1002/mds.21073</json:string></doi><id>D66C7CD0F71954996563291D61D0CDCC2B400A5F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/D66C7CD0F71954996563291D61D0CDCC2B400A5F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/D66C7CD0F71954996563291D61D0CDCC2B400A5F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D66C7CD0F71954996563291D61D0CDCC2B400A5F/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</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>2006</date></publicationStmt><notesStmt><note>Parkinson Society Canada New Investigator Award</note><note>Edmond J. Safra Philanthropic Foundation</note><note>Krembil Neuroscience Fund</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><author><persName><forename type="first">Naomi P.</forename><surname>Visanji</surname><roleName type="degree">PhD</roleName></persName><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Jordi</forename><surname>Gomez‐Ramirez</surname><roleName type="degree">PhD</roleName></persName><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Tom H.</forename><surname>Johnston</surname><roleName type="degree">PhD</roleName></persName><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Donna</forename><surname>Pires</surname></persName><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Valerie</forename><surname>Voon</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</affiliation><affiliation>Current Address: Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation></author><author><persName><forename type="first">Jonathan M.</forename><surname>Brotchie</surname><roleName type="degree">PhD</roleName></persName><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation></author><author><persName><forename type="first">Susan H.</forename><surname>Fox</surname><roleName type="degree">MD, PhD</roleName></persName><note type="correspondence"><p>Correspondence: Division of Neurology, Movement Disorders Clinic MCL7‐421, Toronto Western Hospital, 399, Bathurst Street, Toronto, Ontario M5V 2S8, Canada</p></note><affiliation>Division of Neurology, University of Toronto, Toronto, Canada</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="2006-11"></date><biblScope unit="vol">21</biblScope><biblScope unit="issue">11</biblScope><biblScope unit="page" from="1879">1879</biblScope><biblScope unit="page" to="1891">1891</biblScope></imprint></monogr><idno type="istex">D66C7CD0F71954996563291D61D0CDCC2B400A5F</idno><idno type="DOI">10.1002/mds.21073</idno><idno type="ArticleID">MDS21073</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>psychosis</term></item><item><term>animal model</term></item><item><term>MPTP‐lesioned primate</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-12-02">Received</change><change when="2006-04-19">Registration</change><change when="2006-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D66C7CD0F71954996563291D61D0CDCC2B400A5F/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="110"><doi origin="wiley" registered="yes">10.1002/mds.v21:11</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">11</numbering></numberingGroup><coverDate startDate="2006-11">November 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.21073</doi><idGroup><id type="unit" value="MDS21073"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2006 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2005-12-02"></event><event type="manuscriptAccepted" date="2006-04-19"></event><event type="publishedOnlineEarlyUnpaginated" date="2006-09-07"></event><event type="firstOnline" date="2006-09-07"></event><event type="publishedOnlineFinalForm" date="2006-11-08"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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">1879</numbering><numbering type="pageLast">1891</numbering></numberingGroup><correspondenceTo>Division of Neurology, Movement Disorders Clinic MCL7‐421, Toronto Western Hospital, 399, Bathurst Street, Toronto, Ontario M5V 2S8, Canada</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS21073.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="6"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="74"></count><count type="wordTotal" number="8383"></count></countGroup><titleGroup><title type="main" xml:lang="en">Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title><title type="short" xml:lang="en">Primate Model of Psychosis‐Like Behavior</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Naomi P.</givenNames><familyName>Visanji</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jordi</givenNames><familyName>Gomez‐Ramirez</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tom H.</givenNames><familyName>Johnston</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Donna</givenNames><familyName>Pires</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2" currentRef="#curr1"><personName><givenNames>Valerie</givenNames><familyName>Voon</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jonathan M.</givenNames><familyName>Brotchie</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3" corresponding="yes"><personName><givenNames>Susan H.</givenNames><familyName>Fox</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>sfox@uhnresearch.ca</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Division of Neurology, University of Toronto, Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="US"><unparsedAffiliation>Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">psychosis</keyword><keyword xml:id="kwd3">animal model</keyword><keyword xml:id="kwd4">MPTP‐lesioned primate</keyword></keywordGroup><fundingInfo><fundingAgency>Parkinson Society Canada New Investigator Award</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Edmond J. Safra Philanthropic Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Krembil Neuroscience Fund</fundingAgency></fundingInfo><supportingInformation><p> This article includes supplementary video clips, available online at <url href="http://www.interscience.wiley.com/jpages/0885-3185/suppmat"> http://www.interscience.wiley.com/jpages/0885‐3185/suppmat </url></p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds21073:jws-mds"></mediaResource><caption> Segment 1. Normal: an untreated marmoset showing normal level of motor activity and alertness. Segment 2. Parkinsonian untreated: following MPTP treatment, this animal demonstrates reduced motor activity, akinesia, hunched posture, and reduced blink rate. The animal is less reactive to stimuli and does not respond to close up filming. Segment 3. MPTP‐lesioned marmoset following long‐term levodopa therapy with levodopa‐induced dyskinesia: involuntary movements of all limbs, mixture of chorea and dystonia. Segment 4. Hyperkinesia: fast ballistic movements. Segment 5. Tracking: following nonapparent stimuli. Segment 6. Staring: this animal was eating and then stopped and was staring at a nonapparent stimulus for several seconds before resuming eating activity. Segment 7. Side‐to‐side jumping: this animal exhibits repetitive purposeless stereotypies (see Segment 8). Segment 8. Running in circles. Segment 9. Fiddling with bars: this animal repetitively grasps and scrabbles at corner of cage bars. Also exhibits lower limb dyskinesia. This video presentation has been abbreviated. The full version will appear on theMovementDisorders DVD Supplement, which is issued bi‐annually. </caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society</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>Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Primate Model of Psychosis‐Like Behavior</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Naomi P.</namePart><namePart type="family">Visanji</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jordi</namePart><namePart type="family">Gomez‐Ramirez</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tom H.</namePart><namePart type="family">Johnston</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donna</namePart><namePart type="family">Pires</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Valerie</namePart><namePart type="family">Voon</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Psychiatry, Toronto Western Hospital, Toronto, Canada</affiliation><affiliation>Current Address: Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jonathan M.</namePart><namePart type="family">Brotchie</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Toronto Western Research Institute, Toronto Western Hospital, Toronto, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Susan H.</namePart><namePart type="family">Fox</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Division of Neurology, University of Toronto, Toronto, Canada</affiliation><description>Correspondence: Division of Neurology, Movement Disorders Clinic MCL7‐421, Toronto Western Hospital, 399, Bathurst Street, Toronto, Ontario M5V 2S8, Canada</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">2006-11</dateIssued><dateCaptured encoding="w3cdtf">2005-12-02</dateCaptured><dateValid encoding="w3cdtf">2006-04-19</dateValid><copyrightDate encoding="w3cdtf">2006</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="tables">1</extent><extent unit="references">74</extent><extent unit="words">8383</extent></physicalDescription><abstract lang="en">Investigation of the pathophysiology of psychosis in Parkinson's disease (PD), as well as the assessment of potential novel therapeutics, has been limited by the lack of a well‐validated animal model. MPTP‐lesioned primates exhibit abnormal behaviors that are distinct from dyskinesia and parkinsonism and may represent behavioral correlates of neural processes related to psychosis in PD. Here we assess four types of behavior—agitation, hallucinatory‐like responses to nonapparent stimuli, obsessive grooming, and stereotypies that are termed “psychosis‐like”—and define their pharmacology using a psychosis‐like behavior rating scale. By assessing the actions of drugs known to enhance or attenuate psychosis in PD patients, we find that the pharmacology of these behaviors recapitulates, in several respects, the pharmacology of psychosis in PD. Thus, levodopa and apomorphine elicited psychosis‐like behaviors. Amantadine significantly decreased levodopa‐induced dyskinesia but exacerbated psychosis‐like behaviors. Haloperidol reduced psychosis‐like behaviors but at the expense of increased parkinsonian disability while the atypical neuroleptics clozapine and quetiapine reduced psychosis‐like behaviors without significant effect on parkinsonian disability. The response of different components of the psychotomimetic behavior suggested the involvement of both dopaminergic and nondopaminergic mechanisms in their expression. © 2006 Movement Disorder Society</abstract><note type="funding">Parkinson Society Canada New Investigator Award</note><note type="funding">Edmond J. Safra Philanthropic Foundation</note><note type="funding">Krembil Neuroscience Fund</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>psychosis</topic><topic>animal model</topic><topic>MPTP‐lesioned primate</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><note type="content"> This article includes supplementary video clips, available online at http://www.interscience.wiley.com/jpages/0885‐3185/suppmatSupporting Info Item: Segment 1. Normal: an untreated marmoset showing normal level of motor activity and alertness. Segment 2. Parkinsonian untreated: following MPTP treatment, this animal demonstrates reduced motor activity, akinesia, hunched posture, and reduced blink rate. The animal is less reactive to stimuli and does not respond to close up filming. Segment 3. MPTP‐lesioned marmoset following long‐term levodopa therapy with levodopa‐induced dyskinesia: involuntary movements of all limbs, mixture of chorea and dystonia. Segment 4. Hyperkinesia: fast ballistic movements. Segment 5. Tracking: following nonapparent stimuli. Segment 6. Staring: this animal was eating and then stopped and was staring at a nonapparent stimulus for several seconds before resuming eating activity. Segment 7. Side‐to‐side jumping: this animal exhibits repetitive purposeless stereotypies (see Segment 8). Segment 8. Running in circles. Segment 9. Fiddling with bars: this animal repetitively grasps and scrabbles at corner of cage bars. Also exhibits lower limb dyskinesia. This video presentation has been abbreviated. The full version will appear on theMovementDisorders DVD Supplement, which is issued bi‐annually. - </note><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>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1879</start><end>1891</end><total>13</total></extent></part></relatedItem><identifier type="istex">D66C7CD0F71954996563291D61D0CDCC2B400A5F</identifier><identifier type="DOI">10.1002/mds.21073</identifier><identifier type="ArticleID">MDS21073</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 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 000779 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 000779 | 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:D66C7CD0F71954996563291D61D0CDCC2B400A5F
|texte= Pharmacological characterization of psychosis‐like behavior in the MPTP‐lesioned nonhuman primate model of Parkinson's disease
}}
| This area was generated with Dilib version V0.6.23. |  |