Abstract：
: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.
journal_name
Brain Resjournal_title
Brain researchauthors
Oyama G,Yoshimi K,Natori S,Chikaoka Y,Ren YR,Funayama M,Shimo Y,Takahashi R,Nakazato T,Kitazawa S,Hattori Ndoi
10.1016/j.brainres.2010.06.065subject
Has Abstractpub_date
2010-09-17 00:00:00pages
214-22eissn
0006-8993issn
1872-6240pii
S0006-8993(10)01491-5journal_volume
1352pub_type
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