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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 ASEP 0531295 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title 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 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, ORCIDArticle number 109953 Source Title Progress in Neuro-Psychopharmacology & Biological Psychiatry. - : Elsevier - ISSN 0278-5846
Roč. 102, Aug 30 (2020)Number of pages 16 s. Language eng - English Country US - United States Keywords lithium ; sleep deprivation ; Na+/K+-ATPase ; lipid peroxidation ; rat brain Subject RIV ED - Physiology OECD category Physiology (including cytology) Subject RIV - cooperation Institute of Analytical Chemistry - Analytical Chemistry, Separation R&D Projects GA17-07070S GA ČR - Czech Science Foundation (CSF) Method of publishing Limited access Institutional support FGU-C - RVO:67985823 ; UIACH-O - RVO:68081715 UT WOS 000548248400011 EID SCOPUS 85084368234 DOI 10.1016/j.pnpbp.2020.109953 Annotation Lithium (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. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2021 Electronic address https://doi.org/10.1016/j.pnpbp.2020.109953
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