Journal
NEUROCHEMICAL RESEARCH
Volume 31, Issue 7, Pages 851-860Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-006-9088-9
Keywords
1-methyl-4-phenylpyridinium; 6-hydroxydopamine; mitochondrial membrane permeability; intracellular Ca2+ homeostasis; PC12 cells
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1-Methyl-4-phenylpyridinium (MPP+) or 6-hydroxydopamine (6-OHDA) caused a nuclear damage, the mitochondrial membrane permeability changes, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species and the depletion of GSH in PC12 cells. Nicardipine (a calcium channel blocker), EGTA (an extracellular calcium chelator), BAPTA-AM (a cell permeable calcium chelator) and calmodulin antagonists (W-7 and calmidazolium) attenuated the MPP+-induced mitochondrial damage and cell death. In contrast, the compounds did not reduce the toxicity of 6-OHDA. Treatment with MPP+ or 6-OHDA evoked the elevation of intracellular Ca2+ levels. Unlike cell injury, addition of nicardipine, BAPTA-AM and calmodulin antagonists prevented the elevation of intracellular Ca(2+)levels due to both toxins. The results show that the MPP+-induced formation of the mitochondrial permeability transition seems to be mediated by elevation of intracellular Ca2+ levels and calmodulin action. In contrast, the 6-OHDA-induced cell death seems to be mediated by Ca2+-independent manner.
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