Neurobehavioral Anomalies in the Pitx3/ak Murine Model of Parkinson's Disease and MPTP.
Identifieur interne : 000276 ( PubMed/Curation ); précédent : 000275; suivant : 000277Neurobehavioral Anomalies in the Pitx3/ak Murine Model of Parkinson's Disease and MPTP.
Auteurs : Mohammed Filali [Canada] ; Robert Lalonde [France]Source :
- Behavior genetics [ 1573-3297 ] ; 2016.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Animals, Behavior, Animal, Brain (physiopathology), Disease Models, Animal, Dopamine (metabolism), Female, Hindlimb (physiopathology), Homeodomain Proteins (genetics), Male, Mice, Inbred C57BL, Motor Activity, Mutation (genetics), Parkinson Disease (physiopathology), Phenotype, Transcription Factors (genetics).
- MESH :
- chemical , genetics : Homeodomain Proteins, Transcription Factors.
- chemical , metabolism : Dopamine.
- chemical : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- genetics : Mutation.
- physiopathology : Brain, Hindlimb, Parkinson Disease.
- Animals, Behavior, Animal, Disease Models, Animal, Female, Male, Mice, Inbred C57BL, Motor Activity, Phenotype.
Abstract
Pitx3/ak null mutants are characterized by basal ganglia pathology in a manner resembling Parkinson's disease (PD), with decline in substantia nigra cell numbers as well as striatal tyrosine hydroxylase expression. Although young adult Pitx3/ak mutants were deficient in motor coordination tests, they were more active than non-transgenic controls in the open-field, unlike PD-related bradykinesia. On the SHIRPA primary screen, the mutants displayed body tremor, hyperactivity in the viewing jar, anomalies in eye morphology as well as a higher degree of hindlimb clasping and myoclonic jumping. Increased hindlimb clasping time and rotorod deficits seen in mutants were also exhibited by mice injected with MPTP, indicating an influence of dopamine on these behaviors.
DOI: 10.1007/s10519-015-9753-3
PubMed: 26477573
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wicri:level="1"><nlm:affiliation>Faculty of Sciences, University of Rouen, Mont-Saint-Aignan, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Faculty of Sciences, University of Rouen, Mont-Saint-Aignan</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26477573</idno><idno type="pmid">26477573</idno><idno type="doi">10.1007/s10519-015-9753-3</idno><idno type="wicri:Area/PubMed/Corpus">000276</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000276</idno><idno type="wicri:Area/PubMed/Curation">000276</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000276</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neurobehavioral Anomalies in the Pitx3/ak Murine Model of Parkinson's Disease and MPTP.</title><author><name sortKey="Filali, Mohammed" sort="Filali, Mohammed" uniqKey="Filali M" first="Mohammed" last="Filali">Mohammed Filali</name><affiliation wicri:level="1"><nlm:affiliation>Functional Analysis of Animal Behavior Platform, CHUQ Research Center and Department of Molecular Medicine, Laval University, 2705 Blvd Laurier, Québec, QC, G1V 4G2, Canada. mohammed.filali@crchul.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Functional Analysis of Animal Behavior Platform, CHUQ Research Center and Department of Molecular Medicine, Laval University, 2705 Blvd Laurier, Québec, QC, G1V 4G2</wicri:regionArea></affiliation></author><author><name sortKey="Lalonde, Robert" sort="Lalonde, Robert" uniqKey="Lalonde R" first="Robert" last="Lalonde">Robert Lalonde</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Sciences, University of Rouen, Mont-Saint-Aignan, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Faculty of Sciences, University of Rouen, Mont-Saint-Aignan</wicri:regionArea></affiliation></author></analytic><series><title level="j">Behavior genetics</title><idno type="eISSN">1573-3297</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Animals</term><term>Behavior, Animal</term><term>Brain (physiopathology)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Female</term><term>Hindlimb (physiopathology)</term><term>Homeodomain Proteins (genetics)</term><term>Male</term><term>Mice, Inbred C57BL</term><term>Motor Activity</term><term>Mutation (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Phenotype</term><term>Transcription Factors (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Homeodomain Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Hindlimb</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Behavior, Animal</term><term>Disease Models, Animal</term><term>Female</term><term>Male</term><term>Mice, Inbred C57BL</term><term>Motor Activity</term><term>Phenotype</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pitx3/ak null mutants are characterized by basal ganglia pathology in a manner resembling Parkinson's disease (PD), with decline in substantia nigra cell numbers as well as striatal tyrosine hydroxylase expression. Although young adult Pitx3/ak mutants were deficient in motor coordination tests, they were more active than non-transgenic controls in the open-field, unlike PD-related bradykinesia. On the SHIRPA primary screen, the mutants displayed body tremor, hyperactivity in the viewing jar, anomalies in eye morphology as well as a higher degree of hindlimb clasping and myoclonic jumping. Increased hindlimb clasping time and rotorod deficits seen in mutants were also exhibited by mice injected with MPTP, indicating an influence of dopamine on these behaviors.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26477573</PMID><DateCreated><Year>2016</Year><Month>02</Month><Day>12</Day></DateCreated><DateCompleted><Year>2017</Year><Month>01</Month><Day>09</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1573-3297</ISSN><JournalIssue CitedMedium="Internet"><Volume>46</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Behavior genetics</Title><ISOAbbreviation>Behav. 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Increased hindlimb clasping time and rotorod deficits seen in mutants were also exhibited by mice injected with MPTP, indicating an influence of dopamine on these behaviors.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Filali</LastName><ForeName>Mohammed</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Functional Analysis of Animal Behavior Platform, CHUQ Research Center and Department of Molecular Medicine, Laval University, 2705 Blvd Laurier, Québec, QC, G1V 4G2, Canada. mohammed.filali@crchul.ulaval.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lalonde</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Faculty of Sciences, University of Rouen, Mont-Saint-Aignan, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychology, ICONES Laboratory EA 4699, 76821, Mont-Saint-Aignan, 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