کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739244 | 1046868 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Increased sensitivity of striatal dopamine release to H2O2 upon chronic rotenone treatment
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کلمات کلیدی
DAQDOPACEFs3,4-dihydroxyphenylacetic acid - 3،4-دی هیدروکسی فنیل اسیدهای اسیدDMSO - DMSOl-DOPA - L-DOPAACh - آهAcetylcholine - استیل کولینElectrical field stimulation - تحریک الکتریکی میدانANOVA - تحلیل واریانس Analysis of varianceone-way analysis of variance - تحلیل واریانس یک راههDopamine - دوپامینdopamine quinone - دوپامین کینونDimethyl sulfoxide - دیمتیل سولفواکسیدhomovanillic acid - هومووانیلیک اسیدHVA - چهhigh performance liquid chromatography - کروماتوگرافی مایع با کارایی بالاHPLC - کروماتوگرافی مایعی کارا
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
It is believed that both mitochondrial dysfunction and oxidative stress play important roles in the pathogenesis of Parkinson's disease (PD). We studied the effect of chronic systemic exposure to the mitochondrial inhibitor rotenone on the uptake, content, and release of striatal neurotransmitters upon neuronal activity and oxidative stress, the latter simulated by H2O2 perfusion. The dopamine content in the rat striatum is decreased simultaneously with the progressive loss of tyrosine hydroxylase (TH) immunoreactivity in response to chronic intravenous rotenone infusion. However, surviving dopaminergic neurons take up and release only a slightly lower amount of dopamine (DA) in response to electrical stimulation. Striatal dopaminergic neurons showed increased susceptibility to oxidative stress by H2O2, responding with enhanced release of DA and with formation of an unidentified metabolite, which is most likely the toxic dopamine quinone (DAQ). In contrast, the uptake of [3H]choline and the electrically induced release of acetylcholine increased, in coincidence with a decline in its D2 receptor-mediated dopaminergic control. Thus, oxidative stress-induced dysregulation of DA release/uptake based on a mitochondrial deficit might underlie the selective vulnerability of dopaminergic transmission in PD, causing a self-amplifying production of reactive oxygen species, and thereby contributing to the progressive degeneration of dopaminergic neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 1, 1 July 2005, Pages 133-142
Journal: Free Radical Biology and Medicine - Volume 39, Issue 1, 1 July 2005, Pages 133-142
نویسندگان
Elisaveta Milusheva, Mária Baranyi, Ágnes Kittel, Beáta Sperlágh, E. Sylvester Vizi,