Increased apoptosis in rat brain after rapid eye movement sleep loss
Increased apoptosis in rat brain after rapid eye movement sleep loss
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DOI：
10.1016/j.neuroscience.2006.06.026
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发表时间：
2006-10-13
期刊：
影响因子：
3.3
通讯作者：
Mallick, B. N.
中科院分区：
文献类型：
--
作者：
Biswas, S.;Mishra, P.;Mallick, B. N.
快速眼动（REM）睡眠丧失损害了几个生理，行为和细胞过程;然而，其作用机制尚不清楚。为了了解REM睡眠剥夺对神经元损伤和细胞凋亡的影响，在位于与REM睡眠调节相关或不相关的区域的对照和实验大鼠脑神经元中使用多种细胞凋亡标记物进行研究。此外，还研究了REM睡眠剥夺对神经元细胞骨架蛋白、肌动蛋白和微管蛋白的影响。据观察，REM睡眠剥夺后，大鼠大脑中的神经元数量显着增加，对凋亡标记物呈阳性，然而，在大鼠允许进行REM睡眠后，这些神经元趋于恢复;对照组大鼠不受影响。此外，还观察到REM睡眠剥夺减少了神经元中肌动蛋白和微管蛋白的量，证实了我们先前关于这种剥夺后神经元大小和形状变化的报道。这些发现表明，REM睡眠的可能功能之一是保护神经元免受损伤和凋亡。(c)2006年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Rapid eye movement (REM) sleep loss impairs several physiological, behavioral and cellular processes; however, the mechanism of action was unknown. To understand the effects of REM sleep deprivation on neuronal damage and apoptosis, studies were conducted using multiple apoptosis markers in control and experimental rat brain neurons located in areas either related to or unrelated to REM sleep regulation. Furthermore, the effects of REM sleep deprivation were also studied on neuronal cytoskeletal proteins, actin and tubulin. It was observed that after REM sleep deprivation a significantly increased number of neurons in the rat brain were positive to apoptotic markers, which however, tended to recover after the rats were allowed to undergo REM sleep; the control rats were not affected. Further, it was also observed that REM sleep deprivation decreased amounts of actin and tubulin in neurons confirming our previous reports of changes in neuronal size and shape after such deprivation. These findings suggest that one of the possible functions of REM sleep is to protect neurons from damage and apoptosis. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.