Possible Mechanism Involved in Sleep Deprivation-Induced Memory Dysfunction

被引:14
|
作者
Kalonia, H. [1 ]
Bishnoi, M. [1 ]
Kumar, A. [1 ]
机构
[1] Punjab Univ, Univ Inst Pharmaceut Sci, Chandigarh 160014, India
来源
METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY | 2008年 / 30卷 / 07期
关键词
Acetylcholinesterase; Oxidative stress; Sleep deprivation;
D O I
10.1358/mf.2008.30.7.1186074
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Sleep deprivation disrupts various vital biological and metabolic processes that are necessary for health. The present study was designed to investigate the possible mechanisms a(sleep deprivation-induced memory dysfunction by using different behavioral, biochemical and neurochemical parameters. Hale Wistar rats were sleep deprived for 72 It using a grid suspended over water Elevated phis maze, passive avoidance and Morris water maze tests were used to assess memory retention in 72-h sleep-deprived animals. Various electrophisiological (sleep-wake cycle), biochemical (lipid peroxidation. reduced glutathione, nitrite, catalase, acetylcholinesterase) and neurochemical parameters (norepinephrine, dopamine and serotonin) were also assessed Sleep deprivation resulted in memory dysfunction in all the behavioral paradigms, alteration in the sleep-wake cycle (delayed sleep latency, shortening of rapid eve movement [REM] and non-REM [NREM] sleep and increased waking period) and oxidative stress (increased lipid peroxidation and nitrite levels, depletion of reduced glutathione and catalase activity). In addition, increased levels of acetylcholinesterase (AChE, the enzyme responsible for the degradation of acetycholine) and reduction in norepinephrine and dopamine levels were seen in 72-h sleep-deprived animals. In conclusion. sleep deprivation-induced memory deficits may possibly be due to the combined effect of oxidative damage and alterations in neurotransmitter levels. Copyright 2008 Prous Science, S.A.U. or its licensors. All rights reserved.
引用
收藏
页码:529 / 535
页数:7
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