Nonhuman primates: translational models for predicting antipsychotic-induced movement disorders.
Identifieur interne : 000658 ( PubMed/Corpus ); précédent : 000657; suivant : 000659Nonhuman primates: translational models for predicting antipsychotic-induced movement disorders.
Auteurs : Roger D. Porsolt ; Vincent Castagné ; Eric Hayes ; David VirleySource :
- The Journal of pharmacology and experimental therapeutics [ 1521-0103 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Antipsychotic Agents (adverse effects), Catalepsy (chemically induced), Catalepsy (physiopathology), Disease Models, Animal, Dyskinesia, Drug-Induced (physiopathology), Dystonia (chemically induced), Dystonia (physiopathology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Primates (physiology), Psychomotor Agitation (physiopathology), Rats.
- MESH :
- chemical , adverse effects : Antipsychotic Agents.
- chemically induced : Catalepsy, Dystonia, Parkinson Disease, Secondary.
- physiology : Primates.
- physiopathology : Catalepsy, Dyskinesia, Drug-Induced, Dystonia, Parkinson Disease, Secondary, Psychomotor Agitation.
- Animals, Disease Models, Animal, Rats.
Abstract
Repeated haloperidol treatment administered to nonhuman primates (NHPs) over several months or even years leads to the gradual appearance of drug-induced dystonic reactions in the orofacial region (mouth opening, tongue protrusion or retraction, bar biting) and in the whole body (writhing of the limbs and trunk, bar grasping). The propensity of antipsychotics to induce dystonia in NHPs is not correlated with their propensity to induce catalepsy in rodents, suggesting that the two types of effects are dissociated and may represent distinct aspects of the extrapyramidal symptoms induced by antipsychotics. In view of the clear homology to clinically observed phenomena, antipsychotic-induced dystonias in antipsychotic-primed NHPs would appear to possess a high degree of translational validity. These NHP phenomena could therefore serve as a useful model for predicting the occurrence of similar abnormal movements with novel substances developed for the treatment of schizophrenia or other psychotic disorders. Moreover, the NHP dystonia model could possibly serve as a biomarker for substances that will eventually cause tardive dyskinesia in patients.
DOI: 10.1124/jpet.113.207209
PubMed: 24030013
Links to Exploration step
pubmed:24030013Le document en format XML
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Porsolt</name><affiliation><nlm:affiliation>Porsolt Research Center, Porsolt SAS (France), Le Genest-Saint-Isle, France.</nlm:affiliation></affiliation></author><author><name sortKey="Castagne, Vincent" sort="Castagne, Vincent" uniqKey="Castagne V" first="Vincent" last="Castagné">Vincent Castagné</name></author><author><name sortKey="Hayes, Eric" sort="Hayes, Eric" uniqKey="Hayes E" first="Eric" last="Hayes">Eric Hayes</name></author><author><name sortKey="Virley, David" sort="Virley, David" uniqKey="Virley D" first="David" last="Virley">David Virley</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:24030013</idno><idno type="pmid">24030013</idno><idno type="doi">10.1124/jpet.113.207209</idno><idno type="wicri:Area/PubMed/Corpus">000658</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000658</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Nonhuman primates: translational models for predicting antipsychotic-induced movement disorders.</title><author><name sortKey="Porsolt, Roger D" sort="Porsolt, Roger D" uniqKey="Porsolt R" first="Roger D" last="Porsolt">Roger D. Porsolt</name><affiliation><nlm:affiliation>Porsolt Research Center, Porsolt SAS (France), Le Genest-Saint-Isle, France.</nlm:affiliation></affiliation></author><author><name sortKey="Castagne, Vincent" sort="Castagne, Vincent" uniqKey="Castagne V" first="Vincent" last="Castagné">Vincent Castagné</name></author><author><name sortKey="Hayes, Eric" sort="Hayes, Eric" uniqKey="Hayes E" first="Eric" last="Hayes">Eric Hayes</name></author><author><name sortKey="Virley, David" sort="Virley, David" uniqKey="Virley D" first="David" last="Virley">David Virley</name></author></analytic><series><title level="j">The Journal of pharmacology and experimental therapeutics</title><idno type="eISSN">1521-0103</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antipsychotic Agents (adverse effects)</term><term>Catalepsy (chemically induced)</term><term>Catalepsy (physiopathology)</term><term>Disease Models, Animal</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Dystonia (chemically induced)</term><term>Dystonia (physiopathology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Primates (physiology)</term><term>Psychomotor Agitation (physiopathology)</term><term>Rats</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antipsychotic Agents</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Catalepsy</term><term>Dystonia</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Primates</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Catalepsy</term><term>Dyskinesia, Drug-Induced</term><term>Dystonia</term><term>Parkinson Disease, Secondary</term><term>Psychomotor Agitation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Rats</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Repeated haloperidol treatment administered to nonhuman primates (NHPs) over several months or even years leads to the gradual appearance of drug-induced dystonic reactions in the orofacial region (mouth opening, tongue protrusion or retraction, bar biting) and in the whole body (writhing of the limbs and trunk, bar grasping). The propensity of antipsychotics to induce dystonia in NHPs is not correlated with their propensity to induce catalepsy in rodents, suggesting that the two types of effects are dissociated and may represent distinct aspects of the extrapyramidal symptoms induced by antipsychotics. In view of the clear homology to clinically observed phenomena, antipsychotic-induced dystonias in antipsychotic-primed NHPs would appear to possess a high degree of translational validity. These NHP phenomena could therefore serve as a useful model for predicting the occurrence of similar abnormal movements with novel substances developed for the treatment of schizophrenia or other psychotic disorders. Moreover, the NHP dystonia model could possibly serve as a biomarker for substances that will eventually cause tardive dyskinesia in patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24030013</PMID><DateCreated><Year>2013</Year><Month>11</Month><Day>19</Day></DateCreated><DateCompleted><Year>2014</Year><Month>01</Month><Day>23</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-0103</ISSN><JournalIssue CitedMedium="Internet"><Volume>347</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Journal of pharmacology and experimental therapeutics</Title><ISOAbbreviation>J. Pharmacol. Exp. Ther.</ISOAbbreviation></Journal><ArticleTitle>Nonhuman primates: translational models for predicting antipsychotic-induced movement disorders.</ArticleTitle><Pagination><MedlinePgn>542-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1124/jpet.113.207209</ELocationID><Abstract><AbstractText>Repeated haloperidol treatment administered to nonhuman primates (NHPs) over several months or even years leads to the gradual appearance of drug-induced dystonic reactions in the orofacial region (mouth opening, tongue protrusion or retraction, bar biting) and in the whole body (writhing of the limbs and trunk, bar grasping). The propensity of antipsychotics to induce dystonia in NHPs is not correlated with their propensity to induce catalepsy in rodents, suggesting that the two types of effects are dissociated and may represent distinct aspects of the extrapyramidal symptoms induced by antipsychotics. In view of the clear homology to clinically observed phenomena, antipsychotic-induced dystonias in antipsychotic-primed NHPs would appear to possess a high degree of translational validity. These NHP phenomena could therefore serve as a useful model for predicting the occurrence of similar abnormal movements with novel substances developed for the treatment of schizophrenia or other psychotic disorders. Moreover, the NHP dystonia model could possibly serve as a biomarker for substances that will eventually cause tardive dyskinesia in patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Porsolt</LastName><ForeName>Roger D</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Porsolt Research Center, Porsolt SAS (France), Le Genest-Saint-Isle, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castagné</LastName><ForeName>Vincent</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Hayes</LastName><ForeName>Eric</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Virley</LastName><ForeName>David</ForeName><Initials>D</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>09</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Pharmacol Exp Ther</MedlineTA><NlmUniqueID>0376362</NlmUniqueID><ISSNLinking>0022-3565</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014150">Antipsychotic Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014150" MajorTopicYN="N">Antipsychotic Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002375" MajorTopicYN="N">Catalepsy</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004421" MajorTopicYN="N">Dystonia</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011323" MajorTopicYN="N">Primates</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011595" MajorTopicYN="N">Psychomotor Agitation</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>9</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>9</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>1</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24030013</ArticleId><ArticleId IdType="pii">jpet.113.207209</ArticleId><ArticleId IdType="doi">10.1124/jpet.113.207209</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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