Linked Life Data

20620130

Source:http://linkedlifedata.com/resource/pubmed/id/20620130

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-8-23
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1872-6240
pubmed:author
pubmed:issnType
Electronic
pubmed:day
17
pubmed:volume
1352
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
214-22
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Impaired in vivo dopamine release in parkin knockout mice.
pubmed:affiliation
Department of Neurology, Juntendo University School of Medicine, Bunkyo-ku, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't