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
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023752%3A_____%2F20%3A43920303" target="_blank" >RIV/00023752:_____/20:43920303 - isvavai.cz</a>
Alternative codes found
RIV/67985823:_____/20:00531295 RIV/68081715:_____/20:00531295 RIV/00216208:11310/20:10413207
Result on the web
<a href="https://www.sciencedirect.com/science/article/pii/S0278584620302694" target="_blank" >https://www.sciencedirect.com/science/article/pii/S0278584620302694</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.pnpbp.2020.109953" target="_blank" >10.1016/j.pnpbp.2020.109953</a>
Alternative languages
Result language
angličtina
Original language name
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
Original language description
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.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30215 - Psychiatry
Result continuities
Project
<a href="/en/project/GA17-07070S" target="_blank" >GA17-07070S: Effect of lithium on Na+/K+-ATPase activity and functional consequences of oxidative stress; from animal model to bipolar patients</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2020
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Progress in Neuro-Psychopharmacology & Biological Psychiatry
ISSN
0278-5846
e-ISSN
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Volume of the periodical
102
Issue of the periodical within the volume
109953
Country of publishing house
GB - UNITED KINGDOM
Number of pages
16
Pages from-to
1-16
UT code for WoS article
000548248400011
EID of the result in the Scopus database
2-s2.0-85084368234