Publication: Mechanism of 1-methyl-4-phenylpyridinium-induced dopamine release from PC12 cells
Issued Date
2005-05-01
Resource Type
ISSN
03643190
Other identifier(s)
2-s2.0-23944473836
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Neurochemical Research. Vol.30, No.5 (2005), 633-639
Suggested Citation
Jaturaporn Chagkutip, Piyarat Govitrapong, Sirirat Klongpanichpak, Manuchair Ebadi Mechanism of 1-methyl-4-phenylpyridinium-induced dopamine release from PC12 cells. Neurochemical Research. Vol.30, No.5 (2005), 633-639. doi:10.1007/s11064-005-2751-8 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/16349
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Mechanism of 1-methyl-4-phenylpyridinium-induced dopamine release from PC12 cells
Abstract
The 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.