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.

中文翻译：

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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 我们研究了丰富的环境 (EE) 这一经典的表观遗传学范例是否可以预防慢性睡眠剥夺 (SD) 引起的细胞可塑性损伤。方法 我们通过改进的多平台方法 (MMPM) 在小鼠中进行 SD。SD 组小鼠被剥夺睡眠 18 ha 天。此外，慢性 SD 组中的一半小鼠每天暴露于 EE 刺激 6 小时。免疫染色分析了海马齿状回 (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，而EE则完全逆转了这一过程。SD可诱导小鼠海马神经胶质增生，EE可延缓该过程。结论 我们的结果表明，慢性 SD 可能会损害海马 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。