Age-dependent dopaminergic dysfunction in Nurr1 knockout mice.
Identifieur interne : 000203 ( PubMed/Corpus ); précédent : 000202; suivant : 000204Age-dependent dopaminergic dysfunction in Nurr1 knockout mice.
Auteurs : Chuantao Jiang ; Xinhua Wan ; Yi He ; Tianhong Pan ; Joseph Jankovic ; Weidong LeSource :
- Experimental neurology [ 0014-4886 ] ; 2005.
English descriptors
- KwdEn :
- Aging (genetics), Aging (metabolism), Animals, DNA-Binding Proteins (biosynthesis), DNA-Binding Proteins (deficiency), DNA-Binding Proteins (genetics), Dopamine (genetics), Dopamine (metabolism), Female, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nuclear Receptor Subfamily 4, Group A, Member 2, Transcription Factors (biosynthesis), Transcription Factors (deficiency), Transcription Factors (genetics).
- MESH :
- chemical , biosynthesis : DNA-Binding Proteins, Transcription Factors.
- chemical , deficiency : DNA-Binding Proteins, Transcription Factors.
- genetics : Aging, DNA-Binding Proteins, Dopamine, Transcription Factors.
- metabolism : Aging, Dopamine.
- Animals, Female, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Nuclear Receptor Subfamily 4, Group A, Member 2.
Abstract
The Nurr1 gene, which codes for a transcriptional factor in the nuclear receptor superfamily, plays an important role in the development of the mesencephalic dopaminergic (DAergic) system. To study the age-dependent effects of Nurr1 expression in maintaining mature nigrostriatal DAergic neuronal function, we examined motor behaviors, determined nigrostriatal dopamine (DA) levels and the number of nigral DAergic neurons, and measured the expression of several DAergic neuron-associated genes in heterozygous Nurr1-deficient (Nurr1+/-) and wild-type mice of different ages. In contrast to the same-aged, wild-type mice, old Nurr1+/- mice (>15 months) had a significant decrease in both rotarod performance and locomotor activities, suggesting a motor impairment that is analogous to parkinsonian deficit. Furthermore, the abnormal motor behaviors in old Nurr1+/- mice were associated with decreased DA levels in the striatum, decreased number of DAergic neurons in the nigra, and reduced expression of Nurr1 and DA transporter in the nigra. Our data indicate that Nurr1 plays an important role in the functional maintenance and survival of nigral DAergic neurons and suggest that the Nurr1+/- mouse is a useful animal model to study the pathogenesis of Parkinson disease (PD) and to explore disease-modifying strategies.
DOI: 10.1016/j.expneurol.2004.08.035
PubMed: 15589522
Links to Exploration step
pubmed:15589522Le document en format XML
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To study the age-dependent effects of Nurr1 expression in maintaining mature nigrostriatal DAergic neuronal function, we examined motor behaviors, determined nigrostriatal dopamine (DA) levels and the number of nigral DAergic neurons, and measured the expression of several DAergic neuron-associated genes in heterozygous Nurr1-deficient (Nurr1+/-) and wild-type mice of different ages. In contrast to the same-aged, wild-type mice, old Nurr1+/- mice (>15 months) had a significant decrease in both rotarod performance and locomotor activities, suggesting a motor impairment that is analogous to parkinsonian deficit. Furthermore, the abnormal motor behaviors in old Nurr1+/- mice were associated with decreased DA levels in the striatum, decreased number of DAergic neurons in the nigra, and reduced expression of Nurr1 and DA transporter in the nigra. Our data indicate that Nurr1 plays an important role in the functional maintenance and survival of nigral DAergic neurons and suggest that the Nurr1+/- mouse is a useful animal model to study the pathogenesis of Parkinson disease (PD) and to explore disease-modifying strategies.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15589522</PMID><DateCreated><Year>2004</Year><Month>12</Month><Day>13</Day></DateCreated><DateCompleted><Year>2005</Year><Month>02</Month><Day>18</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0014-4886</ISSN><JournalIssue CitedMedium="Print"><Volume>191</Volume><Issue>1</Issue><PubDate><Year>2005</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Experimental neurology</Title><ISOAbbreviation>Exp. Neurol.</ISOAbbreviation></Journal><ArticleTitle>Age-dependent dopaminergic dysfunction in Nurr1 knockout mice.</ArticleTitle><Pagination><MedlinePgn>154-62</MedlinePgn></Pagination><Abstract><AbstractText>The Nurr1 gene, which codes for a transcriptional factor in the nuclear receptor superfamily, plays an important role in the development of the mesencephalic dopaminergic (DAergic) system. To study the age-dependent effects of Nurr1 expression in maintaining mature nigrostriatal DAergic neuronal function, we examined motor behaviors, determined nigrostriatal dopamine (DA) levels and the number of nigral DAergic neurons, and measured the expression of several DAergic neuron-associated genes in heterozygous Nurr1-deficient (Nurr1+/-) and wild-type mice of different ages. In contrast to the same-aged, wild-type mice, old Nurr1+/- mice (>15 months) had a significant decrease in both rotarod performance and locomotor activities, suggesting a motor impairment that is analogous to parkinsonian deficit. Furthermore, the abnormal motor behaviors in old Nurr1+/- mice were associated with decreased DA levels in the striatum, decreased number of DAergic neurons in the nigra, and reduced expression of Nurr1 and DA transporter in the nigra. Our data indicate that Nurr1 plays an important role in the functional maintenance and survival of nigral DAergic neurons and suggest that the Nurr1+/- mouse is a useful animal model to study the pathogenesis of Parkinson disease (PD) and to explore disease-modifying strategies.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Chuantao</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Parkinson Disease Research Laboratory, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Xinhua</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Yi</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Pan</LastName><ForeName>Tianhong</ForeName><Initials>T</Initials></Author><Author 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