Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations
Identifieur interne : 002199 ( Main/Corpus ); précédent : 002198; suivant : 002200Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations
Auteurs : Philippe Huot ; Tom H. Johnston ; Tayyeba Darr ; Lili-Naz Hazrati ; Naomi P. Visanji ; Donna Pires ; Jonathan M. Brotchie ; Susan H. FoxSource :
- Movement Disorders [ 0885-3185 ] ; 2010-07-30.
English descriptors
Abstract
Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT2A) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT2A receptor levels may be involved in VH in PD. Autoradiographic binding using [3H]‐ketanserin and spiperone, to define 5‐HT2A receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [3H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, P = 0.039). Additionally, there was a significant increase in the levels of 5‐HT2A receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, P = 0.0297). These results suggest that enhanced 5‐HT2A‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT2A antagonist activity are effective at alleviating this debilitating complication. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23083
Links to Exploration step
ISTEX:9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title><author><name sortKey="Huot, Philippe" sort="Huot, Philippe" uniqKey="Huot P" first="Philippe" last="Huot">Philippe Huot</name><affiliation><mods:affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, 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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Darr, Tayyeba" sort="Darr, Tayyeba" uniqKey="Darr T" first="Tayyeba" last="Darr">Tayyeba Darr</name><affiliation><mods:affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hazrati, Lili Az" sort="Hazrati, Lili Az" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name><affiliation><mods:affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><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>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, 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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, 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 Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/mds.23083</idno><idno type="url">https://api.istex.fr/document/9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002199</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title><author><name sortKey="Huot, Philippe" sort="Huot, Philippe" uniqKey="Huot P" first="Philippe" last="Huot">Philippe Huot</name><affiliation><mods:affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, 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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Darr, Tayyeba" sort="Darr, Tayyeba" uniqKey="Darr T" first="Tayyeba" last="Darr">Tayyeba Darr</name><affiliation><mods:affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><author><name sortKey="Hazrati, Lili Az" sort="Hazrati, Lili Az" uniqKey="Hazrati L" first="Lili-Naz" last="Hazrati">Lili-Naz Hazrati</name><affiliation><mods:affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author><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>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, 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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, 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 Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</mods:affiliation></affiliation><affiliation><mods:affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</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="2010-07-30">2010-07-30</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1399">1399</biblScope><biblScope unit="page" to="1408">1408</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8</idno><idno type="DOI">10.1002/mds.23083</idno><idno type="ArticleID">MDS23083</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5‐HT2A receptors</term><term>Parkinson's disease</term><term>autoradiography</term><term>serotonin</term><term>visual hallucinations</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT2A) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT2A receptor levels may be involved in VH in PD. Autoradiographic binding using [3H]‐ketanserin and spiperone, to define 5‐HT2A receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [3H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, P = 0.039). Additionally, there was a significant increase in the levels of 5‐HT2A receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, P = 0.0297). These results suggest that enhanced 5‐HT2A‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT2A antagonist activity are effective at alleviating this debilitating complication. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Philippe Huot MD, MSc, FRCPC, DABPN</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string><json:string>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Tom H. Johnston PhD</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Tayyeba Darr BSc</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Lili‐Naz Hazrati MD, PhD, FRCPC</name><affiliations><json:string>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Naomi P. Visanji PhD</name><affiliations><json:string>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Donna Pires RVT</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Jonathan M. Brotchie PhD</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string></affiliations></json:item><json:item><name>Susan H. Fox MRCP(UK), PhD</name><affiliations><json:string>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</json:string><json:string>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, 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>serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5‐HT2A receptors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>visual hallucinations</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>autoradiography</value></json:item></subject><articleId><json:string>MDS23083</json:string></articleId><language><json:string>eng</json:string></language><abstract>Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT2A) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT2A receptor levels may be involved in VH in PD. Autoradiographic binding using [3H]‐ketanserin and spiperone, to define 5‐HT2A receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [3H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, P = 0.039). Additionally, there was a significant increase in the levels of 5‐HT2A receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, P = 0.0297). These results suggest that enhanced 5‐HT2A‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT2A antagonist activity are effective at alleviating this debilitating complication. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1673</abstractCharCount><pdfWordCount>5285</pdfWordCount><pdfCharCount>35229</pdfCharCount><pdfPageCount>10</pdfPageCount><abstractWordCount>252</abstractWordCount></qualityIndicators><title>Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title><genre><json:string>article</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>10</total><last>1408</last><first>1399</first></pages><issn><json:string>0885-3185</json:string></issn><issue>10</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23083</json:string></doi><id>9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>Dean's New Staff Award (SHF)</note><note>Cure Parkinson's Trust</note><note>Krembil Foundation (JMB)</note><note>Edmond J. Safra Philanthropic Foundation</note><note>Parkinson Society Canada</note><note>United Kingdom Parkinson's Disease Society Tissue Bank at Imperial College</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title><author><persName><forename type="first">Philippe</forename><surname>Huot</surname></persName><roleName type="degree">MD, MSc, FRCPC, DABPN</roleName><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Tom H.</forename><surname>Johnston</surname></persName><roleName type="degree">PhD</roleName><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Tayyeba</forename><surname>Darr</surname></persName><roleName type="degree">BSc</roleName><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Lili‐Naz</forename><surname>Hazrati</surname></persName><roleName type="degree">MD, PhD, FRCPC</roleName><affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Naomi P.</forename><surname>Visanji</surname></persName><roleName type="degree">PhD</roleName><affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Donna</forename><surname>Pires</surname></persName><roleName type="degree">RVT</roleName><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Jonathan M.</forename><surname>Brotchie</surname></persName><roleName type="degree">PhD</roleName><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation></author><author><persName><forename type="first">Susan H.</forename><surname>Fox</surname></persName><roleName type="degree">MRCP(UK), PhD</roleName><note type="correspondence"><p>Correspondence: Movement Disorder Clinic, MCL7.421, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, ON, Canada M5T 2S8</p></note><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</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="2010-07-30"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1399">1399</biblScope><biblScope unit="page" to="1408">1408</biblScope></imprint></monogr><idno type="istex">9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8</idno><idno type="DOI">10.1002/mds.23083</idno><idno type="ArticleID">MDS23083</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT2A) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT2A receptor levels may be involved in VH in PD. Autoradiographic binding using [3H]‐ketanserin and spiperone, to define 5‐HT2A receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [3H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, P = 0.039). Additionally, there was a significant increase in the levels of 5‐HT2A receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, P = 0.0297). These results suggest that enhanced 5‐HT2A‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT2A antagonist activity are effective at alleviating this debilitating complication. © 2010 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>serotonin</term></item><item><term>5‐HT2A receptors</term></item><item><term>visual hallucinations</term></item><item><term>autoradiography</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="2009-10-08">Received</change><change when="2010-02-12">Registration</change><change when="2010-07-30">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8/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="100"><doi origin="wiley" registered="yes">10.1002/mds.v25:10</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">10</numbering></numberingGroup><coverDate startDate="2010-07-30">30 July 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="100" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23083</doi><idGroup><id type="unit" value="MDS23083"></id></idGroup><countGroup><count type="pageTotal" number="10"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2009-10-08"></event><event type="manuscriptRevised" date="2010-01-28"></event><event type="manuscriptAccepted" date="2010-02-12"></event><event type="firstOnline" date="2010-03-29"></event><event type="publishedOnlineFinalForm" date="2010-07-23"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-03-29"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.5.2 mode:FullText source:FullText result:FullText" date="2011-06-21"></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">1399</numbering><numbering type="pageLast">1408</numbering></numberingGroup><correspondenceTo>Movement Disorder Clinic, MCL7.421, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, ON, Canada M5T 2S8</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23083.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="2"></count><count type="referenceTotal" number="58"></count><count type="wordTotal" number="6675"></count></countGroup><titleGroup><title type="main" xml:lang="en">Increased 5‐HT<sub>2A</sub> receptors in the temporal cortex of parkinsonian patients with visual hallucinations<link href="#fn1"></link></title><title type="short" xml:lang="en">5‐HT<sub>2A</sub> Receptors in Visual Hallucinations</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Philippe</givenNames><familyName>Huot</familyName><degrees>MD, MSc, FRCPC, DABPN</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tom H.</givenNames><familyName>Johnston</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tayyeba</givenNames><familyName>Darr</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Lili‐Naz</givenNames><familyName>Hazrati</familyName><degrees>MD, PhD, FRCPC</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Naomi P.</givenNames><familyName>Visanji</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Donna</givenNames><familyName>Pires</familyName><degrees>RVT</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jonathan M.</givenNames><familyName>Brotchie</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Susan H.</givenNames><familyName>Fox</familyName><degrees>MRCP(UK), PhD</degrees></personName><contactDetails><email>sfox@uhnresearch.ca</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">serotonin</keyword><keyword xml:id="kwd3">5‐HT<sub>2A</sub> receptors</keyword><keyword xml:id="kwd4">visual hallucinations</keyword><keyword xml:id="kwd5">autoradiography</keyword></keywordGroup><fundingInfo><fundingAgency>Dean's New Staff Award (SHF)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Cure Parkinson's Trust</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Krembil Foundation (JMB)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Edmond J. Safra Philanthropic Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Parkinson Society Canada</fundingAgency></fundingInfo><fundingInfo><fundingAgency>United Kingdom Parkinson's Disease Society Tissue Bank at Imperial College</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT<sub>2A</sub>) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT<sub>2A</sub> receptor levels may be involved in VH in PD. Autoradiographic binding using [<sup>3</sup>H]‐ketanserin and spiperone, to define 5‐HT<sub>2A</sub> receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [<sup>3</sup>H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, <i>P</i> = 0.039). Additionally, there was a significant increase in the levels of 5‐HT<sub>2A</sub> receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, <i>P</i> = 0.0297). These results suggest that enhanced 5‐HT<sub>2A</sub>‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT<sub>2A</sub> antagonist activity are effective at alleviating this debilitating complication. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>5‐HT2A Receptors in Visual Hallucinations</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Increased 5‐HT</title></titleInfo><name type="personal"><namePart type="given">Philippe</namePart><namePart type="family">Huot</namePart><namePart type="termsOfAddress">MD, MSc, FRCPC, DABPN</namePart><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, 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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tayyeba</namePart><namePart type="family">Darr</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lili‐Naz</namePart><namePart type="family">Hazrati</namePart><namePart type="termsOfAddress">MD, PhD, FRCPC</namePart><affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naomi P.</namePart><namePart type="family">Visanji</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donna</namePart><namePart type="family">Pires</namePart><namePart type="termsOfAddress">RVT</namePart><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</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>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, 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">MRCP(UK), PhD</namePart><affiliation>Division of Brain Imaging & Behaviour Systems ‐ Neuroscience, Toronto Western Research Institute,Toronto Western Hospital, University Health Network, Toronto, Ontario, Canada</affiliation><affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Toronto, Ontario, Canada</affiliation><description>Correspondence: Movement Disorder Clinic, MCL7.421, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Toronto, ON, Canada M5T 2S8</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-07-30</dateIssued><dateCaptured encoding="w3cdtf">2009-10-08</dateCaptured><dateValid encoding="w3cdtf">2010-02-12</dateValid><copyrightDate encoding="w3cdtf">2010</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">3</extent><extent unit="tables">2</extent><extent unit="references">58</extent><extent unit="words">6675</extent></physicalDescription><abstract lang="en">Well‐formed visual hallucinations (VH) are common in patients with Parkinson's disease (PD). The pathophysiology of VH in PD is unknown but may involve structures mediating visual processing such as the inferior temporal cortex. Serotonergic type 2A (5‐HT2A) receptors have been linked to many psychiatric disorders, including psychosis. We hypothesized that enhanced 5‐HT2A receptor levels may be involved in VH in PD. Autoradiographic binding using [3H]‐ketanserin and spiperone, to define 5‐HT2A receptors, was performed in 6 PD patients with VH, 6 PD patients without VH, and 5 healthy, age‐matched controls. The cerebral regions studied included the orbitofrontal cortex, inferolateral temporal cortex, motor cortex, striatum, and substantia nigra. There was a significant (45.6%) increase in the levels of [3H]‐ketanserin binding in the inferolateral temporal cortex of PD patients with VH when compared with PD patients without VH (54.3 ± 5.2 fmol/mg vs. 37.3 ± 4.3 fmol/mg, P = 0.039). Additionally, there was a significant increase in the levels of 5‐HT2A receptors in the motor cortex of all PD patients taken as a group when compared with controls (57.8 ± 5.7 fmol/mg vs. 41.2 ± 2.6 fmol/mg, P = 0.0297). These results suggest that enhanced 5‐HT2A‐mediated neurotransmission in the inferolateral temporal cortex, a critical structure in visual processing, might be associated with the development of VH in PD. Our results provide new insights into the pathophysiology of VH in PD and provide an anatomical basis to explain why compounds with 5‐HT2A antagonist activity are effective at alleviating this debilitating complication. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">Dean's New Staff Award (SHF)</note><note type="funding">Cure Parkinson's Trust</note><note type="funding">Krembil Foundation (JMB)</note><note type="funding">Edmond J. Safra Philanthropic Foundation</note><note type="funding">Parkinson Society Canada</note><note type="funding">United Kingdom Parkinson's Disease Society Tissue Bank at Imperial College</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>serotonin</topic><topic>5‐HT2A receptors</topic><topic>visual hallucinations</topic><topic>autoradiography</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1399</start><end>1408</end><total>10</total></extent></part></relatedItem><identifier type="istex">9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8</identifier><identifier type="DOI">10.1002/mds.23083</identifier><identifier type="ArticleID">MDS23083</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002199 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 002199 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:9FA0C11FCE42AD5AF1DE47FA08B25B23B6FAF7D8
|texte= Increased 5‐HT2A receptors in the temporal cortex of parkinsonian patients with visual hallucinations
}}
| This area was generated with Dilib version V0.6.23. |  |