Postsurgery sleep deprivation is a common complication that severely deteriorates the quality of life of patients. Here we aim to investigate the effects and mechanism of enriched environment in ameliorating sleep deprivation and memory impairments. Hernia repair surgery was performed on rats to induce sleep deprivation. Enriched environment (EE) was used to treat rats with sleep deprivation, and open field and Y-maze tests were performed to compare behavioral parameters of sleep deprivation rats with or without EE treatments to those of normal rats. To understand the mechanism, neurotrophic and growth factors including BDNF, NGF, NT-3 and GDNF were analyzed using enzyme-linked immunosorbent assay (ELISA). AMPAR subunits, including GluA1-A3, and GABAA receptor α1 subunit expression in hippocampus tissues were assessed using western blot. EE restored normal levels of anxiety index and freezing behavior in open field test and level of alternation in Y-maze test, suggesting the reduction of anxiolytic effects and spatial memory impairment induced by sleep deprivation. EE increased BDNF levels and reduced NT-3 levels in sleep deprivation rats. GluA1/GluA2 ratio was increased by EE. GABAA receptor α1 subunit expression was decreased by EE. EE is effective in ameliorating the detrimental effects of sleep deprivation in spatial memory impairment, and restoring normal levels of neurotrophic factors, which are potentially mediated by attenuating the changes in AMPAR subunit expression and reducing GABAA receptor α1 subunit expression. These data provide supporting evidences for the use of EE to treat adverse outcomes of sleep deprivation induced by surgery.

中文翻译：

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丰富的环境改善了手术后睡眠剥夺后大鼠的记忆障碍

术后睡眠剥夺是一种常见的并发症，严重影响患者的生活质量。在这里，我们旨在研究丰富环境在改善睡眠剥夺和记忆障碍方面的作用和机制。对大鼠进行疝气修复手术以诱导睡眠剥夺。使用富集环境（EE）治疗睡眠剥夺大鼠，并进行旷场和 Y 迷宫试验，比较睡眠剥夺大鼠与正常大鼠和有或没有 EE 治疗的行为参数。为了了解其机制，使用酶联免疫吸附测定 (ELISA) 分析了神经营养和生长因子，包括 BDNF、NGF、NT-3 和 GDNF。使用蛋白质印迹评估海马组织中的 AMPAR 亚基，包括 GluA1-A3 和 GABAA 受体α1 亚基表达。EE 恢复了旷场测试中焦虑指数和冻结行为的正常水平以及 Y 迷宫测试中的交替水平，表明减少了由睡眠剥夺引起的抗焦虑作用和空间记忆障碍。EE 增加了睡眠剥夺大鼠的 BDNF 水平并降低了 NT-3 水平。EE 增加了 GluA1/GluA2 比率。GABAA 受体α1 亚基表达被EE 降低。EE 可有效改善睡眠剥夺对空间记忆障碍的不利影响，并恢复神经营养因子的正常水平，这可能是通过减弱 AMPAR 亚基表达的变化和降低 GABAA 受体α1 亚基表达来介导的。这些数据为使用 EE 治疗手术引起的睡眠剥夺的不良后果提供了支持证据。