Enriched environment can reverse chronic sleep deprivation-induced damage to cellular plasticity in the dentate gyrus of the hippocampus.

IF 1.8 4区 医学 Q4 NEUROSCIENCES Translational Neuroscience Pub Date : 2023-01-01 DOI:10.1515/tnsci-2022-0280
Xue Shixing, Hou Xueyan, Ren Yuan, Tang Wei, Wang Wei
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Abstract

Objective: We studied whether enriched environment (EE), a classic epigenetics paradigm, can prevent cellular plasticity damage caused by chronic sleep deprivation (SD).

Methods: We performed SD in mice by a modified multi-platform method (MMPM). Mice in the SD group were deprived of sleep for 18 h a day. In addition, half of the mice in the chronic SD group were exposed to EE stimuli for 6 h per day. Immunostaining analyzed neurogenesis and neural progenitor cell-differentiated phenotypes in the hippocampal dentate gyrus (DG) region.

Result: At 13 weeks, compared with the control group, SD severely impaired the proliferation and differentiation of neural stem cells, and EE completely reversed the process. SD can induce gliosis in the mouse hippocampus, and EE can delay the process.

Conclusion: Our results suggest that chronic SD may damage the neurogenesis in the DG of the hippocampus. However, enrichment stimulation can reverse the processing by promoting neuronal repair related to neuronal plasticity.

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丰富的环境可以逆转慢性睡眠剥夺引起的海马齿状回细胞可塑性损伤。
目的:研究富环境(EE)作为一种典型的表观遗传学模式是否能预防慢性睡眠剥夺(SD)引起的细胞可塑性损伤。方法:采用改良的多平台法(MMPM)对小鼠进行SD。SD组小鼠每天被剥夺18小时的睡眠。此外,慢性SD组中一半的小鼠每天暴露于情感表达刺激6小时。免疫染色分析海马齿状回(DG)区域的神经发生和神经祖细胞分化表型。结果:在13周时,与对照组相比,SD严重损害了神经干细胞的增殖和分化,EE完全逆转了这一过程。SD可诱导小鼠海马神经胶质化,EE可延缓该过程。结论:慢性SD可能损害海马DG的神经发生。然而,富集刺激可以通过促进与神经元可塑性相关的神经元修复来逆转这一过程。
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来源期刊
CiteScore
3.00
自引率
4.80%
发文量
45
审稿时长
>12 weeks
期刊介绍: Translational Neuroscience provides a closer interaction between basic and clinical neuroscientists to expand understanding of brain structure, function and disease, and translate this knowledge into clinical applications and novel therapies of nervous system disorders.
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