GSTπ expression mediates dopaminergic neuron sensitivity in experimental parkinsonism

Michelle Smeyne, Justin Boyd, Kennie Raviie Shepherd, Yun Jiao, Brooks Barnes Pond, Matthew Hatler, Roland Wolf, Colin Henderson, Richard Jay Smeyne (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    69 Citations (Scopus)


    The cause of 95% of Parkinson's disease (PD) cases is unknown. It is hypothesized that PD arises from an interaction of free-radical-generating agents with an underlying genetic susceptibility to these compounds. Here we use the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of parkinsonism to examine the role of a dual function protein, GSTπ, in dopaminergic neuron death. GSTπ is the only GST family member expressed in substantia nigra neurons. GSTπ reduction by pharmacological blockade, RNA inhibition, and gene targeting increases sensitivity to 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine, suggesting that differential expression of GSTπ contributes to the sensitivity to xenobiotics in the substantia nigra and may influence the pathogenesis of reactive oxygen species-induced neurological disorders including PD.

    Original languageEnglish
    Pages (from-to)1977-1982
    Number of pages6
    JournalProceedings of the National Academy of Sciences of the United States of America
    Issue number6
    Publication statusPublished - 6 Feb 2007


    • Detoxification
    • Glutathione
    • Oxidative stress
    • Parkinson's disease
    • Substantia nigra

    ASJC Scopus subject areas

    • General


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