LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors
Identifieur interne : 001302 ( Main/Exploration ); précédent : 001301; suivant : 001303LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors
Auteurs : Kelly M. Hinkle [États-Unis] ; Mei Yue [États-Unis] ; Bahareh Behrouz [États-Unis] ; Justus C. D Chsel [États-Unis] ; Sarah J. Lincoln [États-Unis] ; Erin E. Bowles [États-Unis] ; Joel E. Beevers [États-Unis] ; Brittany Dugger [États-Unis] ; Beate Winner [Allemagne] ; Iryna Prots [Allemagne] ; Caroline B. Kent [États-Unis] ; Kenya Nishioka [États-Unis] ; Wen-Lang Lin [États-Unis] ; Dennis W. Dickson [États-Unis] ; Christopher J. Janus [États-Unis] ; Matthew J. Farrer [États-Unis, Canada] ; Heather L. Melrose [États-Unis]Source :
- Molecular Neurodegeneration [ 1750-1326 ] ; 2012.
Abstract
Mutations in the
We created mice lacking exon 41 that encodes the activation hinge of the kinase domain of LRRK2. We have performed a comprehensive analysis of these mice up to 20 months of age, including evaluation of dopamine storage, release, uptake and synthesis, behavioral testing, dendritic spine and proliferation/neurogenesis analysis.
Our results show that the dopaminergic system was not functionally comprised in
Url:
DOI: 10.1186/1750-1326-7-25
PubMed: 22647713
PubMed Central: 3441373
Affiliations:
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knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors</title>
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knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors</title>
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<author><name sortKey="Beevers, Joel E" sort="Beevers, Joel E" uniqKey="Beevers J" first="Joel E" last="Beevers">Joel E. Beevers</name>
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<author><name sortKey="Winner, Beate" sort="Winner, Beate" uniqKey="Winner B" first="Beate" last="Winner">Beate Winner</name>
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<country xml:lang="fr">Allemagne</country>
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<author><name sortKey="Nishioka, Kenya" sort="Nishioka, Kenya" uniqKey="Nishioka K" first="Kenya" last="Nishioka">Kenya Nishioka</name>
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<author><name sortKey="Lin, Wen Lang" sort="Lin, Wen Lang" uniqKey="Lin W" first="Wen-Lang" last="Lin">Wen-Lang Lin</name>
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<author><name sortKey="Janus, Christopher J" sort="Janus, Christopher J" uniqKey="Janus C" first="Christopher J" last="Janus">Christopher J. Janus</name>
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<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Neuroscience, Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, Florida, 32610</wicri:regionArea>
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<author><name sortKey="Farrer, Matthew J" sort="Farrer, Matthew J" uniqKey="Farrer M" first="Matthew J" last="Farrer">Matthew J. Farrer</name>
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<country xml:lang="fr">États-Unis</country>
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<affiliation wicri:level="1"><nlm:aff id="I4">Department of Medical Genetics, University of British Columbia, Vancouver, V6T 285, Canada</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Department of Medical Genetics, University of British Columbia, Vancouver, V6T 285</wicri:regionArea>
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<author><name sortKey="Melrose, Heather L" sort="Melrose, Heather L" uniqKey="Melrose H" first="Heather L" last="Melrose">Heather L. Melrose</name>
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<front><div type="abstract" xml:lang="en"><p>Mutations in the <italic>LRRK2</italic>
gene are the most common cause of genetic Parkinson’s disease. Although the mechanisms behind the pathogenic effects of <italic>LRRK2</italic>
mutations are still not clear, data emerging from <italic>in vitro</italic>
and <italic>in vivo</italic>
models suggests roles in regulating neuronal polarity, neurotransmission, membrane and cytoskeletal dynamics and protein degradation.</p>
<p>We created mice lacking exon 41 that encodes the activation hinge of the kinase domain of LRRK2. We have performed a comprehensive analysis of these mice up to 20 months of age, including evaluation of dopamine storage, release, uptake and synthesis, behavioral testing, dendritic spine and proliferation/neurogenesis analysis.</p>
<p>Our results show that the dopaminergic system was not functionally comprised in <italic>LRRK2</italic>
knockout mice. However, <italic>LRRK2</italic>
knockout mice displayed abnormal exploratory activity in the open-field test. Moreover, <italic>LRRK2</italic>
knockout mice stayed longer than their wild type littermates on the accelerated rod during rotarod testing. Finally, we confirm that loss of LRRK2 caused degeneration in the kidney, accompanied by a progressive enhancement of autophagic activity and accumulation of autofluorescent material, but without evidence of biphasic changes.</p>
</div>
</front>
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<li>Canada</li>
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<name sortKey="Lin, Wen Lang" sort="Lin, Wen Lang" uniqKey="Lin W" first="Wen-Lang" last="Lin">Wen-Lang Lin</name>
<name sortKey="Lincoln, Sarah J" sort="Lincoln, Sarah J" uniqKey="Lincoln S" first="Sarah J" last="Lincoln">Sarah J. Lincoln</name>
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<country name="Canada"><noRegion><name sortKey="Farrer, Matthew J" sort="Farrer, Matthew J" uniqKey="Farrer M" first="Matthew J" last="Farrer">Matthew J. Farrer</name>
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