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自愿运动可改善睡眠剥夺的青春期小鼠的突触修剪缺陷。

Voluntary exercise ameliorates synaptic pruning deficits in sleep-deprived adolescent mice.

机构信息

Graduate Institute of Anatomy and Cell Biology, National Taiwan University, Taipei, Taiwan, ROC.

Division of Environmental Health and Occupational Medicine, National Health Research Institutes, Miaoli, Taiwan, ROC.

出版信息

Brain Behav Immun. 2021 Mar;93:96-110. doi: 10.1016/j.bbi.2020.12.017. Epub 2020 Dec 24.

Abstract

Adolescence is a critical period for brain development and adequate sleep during this period is essential for physical function and mental health. Emerging evidence has detailed the neurological impacts of sleep insufficiency on adolescents, as was unveiled by our previous study, microglia, one of the crucial contributors to synaptic pruning, is functionally disrupted by lack of sleep. Here, we provided evidence featuring the protective effect and the underlying mechanisms of voluntary exercise (VE) on microglial functions in an adolescent 72 h sleep deprivation (SD) model. We identified that the aberrant hippocampal neuronal activity and impaired short-term memory performance in sleep-deprived mice were prevented by 11 days of VE. VE significantly normalized the SD-induced dendritic spine increment and maintained the microglial phagocytic ability in sleep-deprived mice. Moreover, we found that the amendment of the noradrenergic signal in the central nervous system may explain the preventative effects of VE on the abnormalities of microglial and neuronal functions caused by SD. These data suggested that VE may confer protection to the microglia-mediated synaptic pruning in the sleep-deprived adolescent brains. Therefore, physical exercise could be a beneficial health practice for the adolescents that copes the adverse influence of inevitable sleep insufficiency.

摘要

青春期是大脑发育的关键时期,在此期间充足的睡眠对于身体功能和心理健康至关重要。我们之前的研究揭示了睡眠不足对青少年的神经影响,新出现的证据详细说明了睡眠不足对小胶质细胞的功能障碍的影响,小胶质细胞是突触修剪的关键贡献者之一。在这里,我们提供了证据,证明在青少年 72 小时睡眠剥夺 (SD) 模型中,自愿运动 (VE) 对小胶质细胞功能具有保护作用和潜在机制。我们发现,11 天的 VE 可预防睡眠剥夺小鼠海马神经元活动异常和短期记忆能力受损。VE 还可使睡眠剥夺小鼠中 SD 诱导的树突棘增加正常化,并维持小胶质细胞的吞噬能力。此外,我们发现中枢神经系统去甲肾上腺素信号的改变可能解释了 VE 对 SD 引起的小胶质细胞和神经元功能异常的预防作用。这些数据表明,VE 可能为睡眠剥夺青少年大脑中的小胶质细胞介导的突触修剪提供保护。因此,体育锻炼可能是一种有益的健康实践,可以帮助青少年应对不可避免的睡眠不足的不利影响。

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