Document Detail


Impaired in vivo dopamine release in parkin knockout mice.
MedLine Citation:
PMID:  20620130     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
parkin is the most frequent causative gene among familial Parkinson's disease (PD). Although parkin deficiency induces autosomal recessive juvenile parkinsonism (AR-JP, PARK2) in humans, parkin knockout (PKO) mice consistently show few signs of dopaminergic degeneration. We aimed to directly measure evoked extracellular dopamine (DA) overflow in the striatum with in vivo voltammetry. The amplitude of evoked DA overflow was low in PKO mice. The half-life time of evoked DA overflow was long in PKO mice suggesting lower release and uptake of dopamine. Facilitation of DA overflow by repetitive stimulation enhanced in the older PKO mice. Decreased dopamine release and uptake in young PKO mice suggest early pre-symptomatic changes in dopamine neurotransmission, while the enhanced facilitation in the older PKO mice may reflect a compensatory adaptation in dopamine function during the late pre-symptomatic phase of Parkinson's disease. Our results showed parkin deficiency may affect DA release in PKO mice, although it does not cause massive nigral degeneration or parkinsonian symptoms as in humans.
Authors:
Genko Oyama; Kenji Yoshimi; Shihoko Natori; Yoko Chikaoka; Yong-Ri Ren; Manabu Funayama; Yasushi Shimo; Ryosuke Takahashi; Taizo Nakazato; Shigeru Kitazawa; Nobutaka Hattori
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-08
Journal Detail:
Title:  Brain research     Volume:  1352     ISSN:  1872-6240     ISO Abbreviation:  Brain Res.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-23     Completed Date:  2010-12-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  214-22     Citation Subset:  IM    
Affiliation:
Department of Neurology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
3,4-Dihydroxyphenylacetic Acid / metabolism
Aging / physiology
Animals
Body Weight
Corpus Striatum / physiology*
Dopamine / metabolism*,  secretion*
Homovanillic Acid / metabolism
Hydroxyindoleacetic Acid / metabolism
Mice
Mice, Knockout
Motor Activity / physiology
Nerve Fibers / drug effects,  physiology
Nomifensine / pharmacology
Prosencephalon / drug effects,  physiology
Ubiquitin-Protein Ligases / deficiency*
Chemical
Reg. No./Substance:
102-32-9/3,4-Dihydroxyphenylacetic Acid; 24526-64-5/Nomifensine; 306-08-1/Homovanillic Acid; 54-16-0/Hydroxyindoleacetic Acid; EC 6.3.2.19/Ubiquitin-Protein Ligases; EC 6.3.2.19/parkin protein

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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