Journal
BRAIN RESEARCH
Volume 1243, Issue -, Pages 167-173Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2008.09.057
Keywords
ATP content; MPTP; Near-infrared light; Neurotoxicity; Parkinson's disease; Rotenone
Categories
Funding
- NIH/NICAM [R21AT003002]
- NIH/NEI [EY018441]
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Parkinson's disease (PD) is a movement disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to nigrostriatal degeneration. The inhibition of mitochondrial respiratory chain complex I and oxidative stress-induced damage have been implicated in the pathogenesis of PD. The present study used these specific mitochondrial complex I inhibitors (rotenone and 1-methyl-4-phenylpyridinium or MPP+) on striatal and cortical neurons in culture. The goal was to test our hypothesis that pretreatment with near-infrared light (NIR) via light-emitting diode (LED) had a greater beneficial effect on primary neurons grown in media with rotenone or MPP+ than those with or without LED treatment during exposure to poisons. Striatal and visual cortical neurons from newborn rats were cultured in a media with or without 200 nM of rotenone or 250 mu M of MPP+ for 48 h. They were treated with NIR-LED twice a day before, during, and both before and during the exposure to the poison. Results indicate that pretreatment with NIR-LED significantly suppressed rotenone- or MPP+-induced apoptosis in both striatal and cortical neurons (P<0.001), and that pretreatment plus LED treatment during neurotoxin exposure was significantly better than LED treatment alone during exposure to neurotoxins. In addition, MPP+ induced a decrease in neuronal ATP levels (to 48% of control level) that was reversed significantly to 70% of control by NIR-LED pretreatment. These data suggest that LED pretreatment is an effective. adjunct preventative therapy in rescuing neurons from neurotoxins linked to PD. 2008 Elsevier B.V. All rights reserved.
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