Stimulatory role of calcium in rapid eye movement sleep deprivation-induced noradrenaline-mediated increase in Na-K-ATPase activity in rat brain

被引:28
作者
Das, G. [1 ]
Gopalakrishnan, A. [1 ]
Faisal, M. [1 ]
Mallick, B. N. [1 ]
机构
[1] Jawaharlal Nehru Univ, Sch Life Sci, New Delhi 110067, India
关键词
brain excitability; Ca2+; lipid peroxidation; Na-K-ATPase; noradrenaline; REM sleep;
D O I
10.1016/j.neuroscience.2008.04.069
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Rapid eye movement (REM) sleep deprivation elevates noradrenaline level, which upon acting on alpha1-adrenoceptors increases Na-K-ATPase activity; however, the detailed intracellular mechanism of action was unknown. Since membrane integrity is crucial for maintaining Na-K-ATPase activity as well as ionic exchange and noradrenaline affects membrane lipid-peroxidation, we proposed that the deprivation might modulate membrane lipid-peroxidation, which would modulate intracellular ionic concentration and thereby increase Na-K-ATPase activity. Hence, in this in vivo and in vitro study, rats were deprived of REM sleep for 4 days by the flowerpot method and suitable control experiments were conducted. The deprivation simultaneously decreased membrane lipid-peroxidation as well as increased Na-K-ATPase activity by its dephosphorylation and all the effects were induced by noradrenaline. Further, in vitro experiments showed that hydrogen peroxide (H2O2)-induced enhanced lipid-peroxidation increased synaptosomal calcium (Ca2+)-influx, which was also prevented by noradrenaline and nifidipine, an L-type Ca2+-channel blocker. Additionally, both nifidipine and cyclopiazonic acid, which have opposite effects on intracellular Ca2+-concentration, prevented deprivation induced increased Na-K-ATPase activity. We propose that REM sleep deprivation elevates noradrenaline level in the brain that acting on alphal-adrenoceptor simultaneously reduces membrane lipid-peroxidation but activates phospholipase-C, resulting in closure of L-type Ca2+-channel and releasing membrane bound Ca2+; the latter then dephosphorylates Na-K-ATPase, the active form, causing its increased activity. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:76 / 89
页数:14
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