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Na+/K+-ATPase and lipid peroxidation in forebrain cortex and hippocampus of sleep-deprived rats treated with therapeutic lithium concentration for different periods of time

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    SYSNO ASEP0531295
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    TitleNa+/K+-ATPase and lipid peroxidation in forebrain cortex and hippocampus of sleep-deprived rats treated with therapeutic lithium concentration for different periods of time
    Author(s) Vošahlíková, Miroslava (FGU-C) RID, ORCID, SAI
    Roubalová, Lenka (FGU-C) RID, ORCID, SAI
    Cechová, Kristína (FGU-C) RID, ORCID
    Kaufman, Jonáš (FGU-C)
    Musil, Stanislav (UIACH-O) RID, ORCID
    Mikšík, Ivan (FGU-C) RID, ORCID, SAI
    Alda, M. (CZ)
    Svoboda, Petr (FGU-C) RID, ORCID
    Article number109953
    Source TitleProgress in Neuro-Psychopharmacology & Biological Psychiatry. - : Elsevier - ISSN 0278-5846
    Roč. 102, Aug 30 (2020)
    Number of pages16 s.
    Languageeng - English
    CountryUS - United States
    Keywordslithium ; sleep deprivation ; Na+/K+-ATPase ; lipid peroxidation ; rat brain
    Subject RIVED - Physiology
    OECD categoryPhysiology (including cytology)
    Subject RIV - cooperationInstitute of Analytical Chemistry - Analytical Chemistry, Separation
    R&D ProjectsGA17-07070S GA ČR - Czech Science Foundation (CSF)
    Method of publishingLimited access
    Institutional supportFGU-C - RVO:67985823 ; UIACH-O - RVO:68081715
    UT WOS000548248400011
    EID SCOPUS85084368234
    DOI10.1016/j.pnpbp.2020.109953
    AnnotationLithium (Li) is a typical mood stabilizer and the first choice for treatment of bipolar disorder (BD). Despite an extensive clinical use of Li, its mechanisms of action remain widely different and debated. In this work, we studied the time-course of the therapeutic Li effects on ouabain-sensitive Na+/K+-ATPase in forebrain cortex and hippocampus of rats exposed to 3-day sleep deprivation (SD). We also monitored lipid peroxidation as malondialdehyde (MDA) production. In samples of plasma collected from all experimental groups of animals, Li concentrations were followed by ICP-MS. The acute (1 day), short-term (7 days) and chronic (28 days) treatment of rats with Li resulted in large decrease of Na+/K+-ATPase activity in both brain parts. At the same time, SD of control, Li-untreated rats increased Na+/K+-ATPase along with increased production of MDA. The SD-induced increase of Na+/K+-ATPase and MDA was attenuated in Li-treated rats. While SD results in a positive change of Na+/K+-ATPase, the inhibitory effect of Li treatment may be interpreted as a pharmacological mechanism causing a normalization of the stress-induced shift and return the Na+/K+-ATPase back to control level. We conclude that SD alone up-regulates Na+/K+-ATPase together with increased peroxidative damage of lipids. Chronic treatment of rats with Li before SD, protects the brain tissue against this type of damage and decreases Na+/K+-ATPase level back to control level.
    WorkplaceInstitute of Physiology
    ContactLucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400
    Year of Publishing2021
    Electronic addresshttps://doi.org/10.1016/j.pnpbp.2020.109953
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