Short-term total sleep deprivation in the rat increases antioxidant responses in multiple brain regions without impairing spontaneous alternation behavior.

TitleShort-term total sleep deprivation in the rat increases antioxidant responses in multiple brain regions without impairing spontaneous alternation behavior.
Publication TypeJournal Article
Year of Publication2010
AuthorsRamanathan, L, Hu S, Frautschy SA, Siegel JM
JournalBehavioural brain research
Volume207
Issue2
Pagination305-9
Date Published2010 Mar 5
ISSN1872-7549
KeywordsAnimals, Antioxidants, Behavior, Animal, Brain, Exploratory Behavior, Glutathione, Glutathione Peroxidase, Hexokinase, Male, Maze Learning, Rats, Rats, Sprague-Dawley, sleep deprivation, Superoxide Dismutase, Time Factors
Abstract

Total sleep deprivation (TSD) induces a broad spectrum of cognitive, behavioral and cellular changes. We previously reported that long term (5-11 days) TSD in the rat, by the disk-over-water method, decreases the activity of the antioxidant enzyme superoxide dismutase (SOD) in the brainstem and hippocampus. To gain insight into the mechanisms causing cognitive impairment, here we explore the early associations between metabolic activity, antioxidant responses and working memory (one form of cognitive impairment). Specifically we investigated the impact of short-term (6h) TSD, by gentle handling, on the levels of the endogenous antioxidant, total glutathione (GSHt), and the activities of the antioxidative enzymes, SOD and glutathione peroxidase (GPx). Short-term TSD had no significant impact on SOD activity, but increased GSHt levels in the rat cortex, brainstem and basal forebrain, and GPx activity in the rat hippocampus and cerebellum. We also observed increased activity of hexokinase, (HK), the rate limiting enzyme of glucose metabolism, in the rat cortex and hypothalamus. We further showed that 6h of TSD leads to increased exploratory behavior to a new environment, without impairing spontaneous alternation behavior (SAB) in the Y maze. We conclude that acute (6h) sleep loss may trigger compensatory mechanisms (like increased antioxidant responses) that prevent initial deterioration in working memory.

DOI10.1111/j.1365-2869.2012.01023.x
Alternate JournalBehav. Brain Res.