Jaturaporn ChagkutipPiyarat GovitrapongSirirat KlongpanichpakManuchair EbadiUniversity of North DakotaThe Institute of Science and Technology for Research and Development, Mahidol UniversityMahidol University2018-06-212018-06-212005-05-01Neurochemical Research. Vol.30, No.5 (2005), 633-639036431902-s2.0-23944473836https://repository.li.mahidol.ac.th/handle/20.500.14594/16349The molecular mechanism of 1-methyl-4-phenylpyridinium (MPP+), a Parkinsonism-inducing neurotoxin, has been studied in PC12 cells. The cells treated with MPP+(100 μM) induced a rapid increase in phosphorylation of tyrosine residues of several proteins, including synaptophysin, a major 38 kDa synaptic vesicle protein implicated in exocytosis. An accelerated release of dopamine by MPP+correlated with phosphorylation of synaptophysin. Exposing the cells to MPP+triggered reactive oxygen species (ROS) generation within 60 min of treatment and the said effect was blocked by mazindol, a dopamine uptake blocker. In addition, pretreatment with 50-100 μM of selegiline, a selective MAO-B inhibitor, significantly suppressed MPP+-mediated ROS generation. These effects of MPP+result in the generation of ROS, which may be involved in neuronal degeneration seen in Parkinson's disease. © 2005 Springer Science+Business Media, Inc.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyNeuroscienceArticleSCOPUS10.1007/s11064-005-2751-8