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  • Acute restraint stress induces rapid changes in central redox status and protective antioxidant genes in rats

    Author(s)
    Spiers, Jereme G
    Chen, Hsiao-Jou Cortina
    Cuffe, James SM
    Sernia, Conrad
    Lavidis, Nickolas A
    Griffith University Author(s)
    Cuffe, James S.
    Year published
    2016
    Metadata
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    Abstract
    The stress-induced imbalance in reduction/oxidation (redox) state has been proposed to play a major role in the etiology of neurological disorders. However, the relationship between psychological stress, central redox state, and potential protective mechanisms within specific neural regions has not been well characterized. In this study, we have used an acute psychological stress to demonstrate the dynamic changes that occur in the redox system of hippocampal and striatal tissue. Outbred male Wistar rats were subject to 0 (control), 60, 120, or 240 min of acute restraint stress and the hippocampus and striatum were cryodissected ...
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    The stress-induced imbalance in reduction/oxidation (redox) state has been proposed to play a major role in the etiology of neurological disorders. However, the relationship between psychological stress, central redox state, and potential protective mechanisms within specific neural regions has not been well characterized. In this study, we have used an acute psychological stress to demonstrate the dynamic changes that occur in the redox system of hippocampal and striatal tissue. Outbred male Wistar rats were subject to 0 (control), 60, 120, or 240 min of acute restraint stress and the hippocampus and striatum were cryodissected for redox assays and relative gene expression. Restraint stress significantly elevated oxidative status and lipid peroxidation, while decreasing glutathione ratios overall indicative of oxidative stress in both neural regions. These biochemical changes were prevented by prior administration of the glucocorticoid receptor antagonist, RU-486. The hippocampus also demonstrated increased glutathione peroxidase 1 and 4 antioxidant expression which was not observed in the striatum, while both regions displayed robust upregulation of the antioxidant, metallothionein 1a. This was observed with concurrent upregulation of 11β-hydroxysteroid dehydrogenase 1, a local reactivator of corticosterone, in addition to decreased expression of the cytosolic regulatory subunit of superoxide-producing enzyme, NADPH-oxidase. Together, this study demonstrates distinctive regional redox profiles following acute stress exposure, in addition to identifying differential capabilities in managing oxidative challenges via altered antioxidant gene expression in the hippocampus and striatum.
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    Journal Title
    Psychoneuroendocrinology
    Volume
    67
    DOI
    https://doi.org/10.1016/j.psyneuen.2016.02.005
    Subject
    Biomedical and clinical sciences
    Clinical sciences not elsewhere classified
    Psychology
    Publication URI
    http://hdl.handle.net/10072/173682
    Collection
    • Journal articles

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