Khadrawy_2011_Transl.Res_157_100

Several studies revealed the importance of paradoxical sleep as a homeostatic mechanism by which the brain can control oxidative stress. The aim of the present study is to investigate the effect of 72 h of paradoxical sleep deprivation on the oxidative stress markers and its insults on the activities of Na(+), K(+)-ATPase and acetylcholinesterase in the cortex and hippocampus of albino rat. Animals were subjected to paradoxical sleep deprivation for 72 h. At the end of the experiment, the rats were sacrificed, and catalase activity, levels of reduced glutathione, lipid peroxidation, and nitric oxide were assayed together with the activities of Na(+), K(+)-ATPase and acetylcholinesterase in the cortex and hippocampus. The present study revealed a significant increase in lipid peroxidation accompanied by a significant decrease in reduced glutathione in the cortex and hippocampus. Na(+), K(+)-ATPase decreased significantly in both areas. However, acetylcholinesterase showed a significant increase in the investigated brain regions. The present data showed that 72 h of paradoxical sleep deprivation induced oxidative stress in the cortex and hippocampus. It could be suggested that the inhibition of Na(+), K(+)-ATPase and the increased acetylcholinesterase activity may underlie memory impairment, increased brain excitability, and anxiety induced by paradoxical sleep deprivation.