Introduction The neurophysiological mechanisms underlying long-term neurological and cognitive disorders associated with chronic sleep restriction (CSR) are not fully understood. Here we evaluated how the sleep-wake cycle changes during and after a period of sleep restriction in rats, and whether CSR results in neurodegeneration in monoaminergic brain structures. Methods For CSR, 7-8-month-old Wistar rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 5 days on the orbital shaker. Telemetric sleep recordings were made before, during, and after CSR. Neurodegeneration in brain monoaminergic structures was assessed immunohistochemically. Results During SD, wakefulness comprised 85% of the total registration time; the remaining time was represented by drowsiness with low EEG delta power. Rapid eye movement sleep (REMS) was absent. During CSR, slow-wave sleep (SWS) and REMS were reduced by 62% and 57%. Total SWS time during SO periods increased on the first CSR day, but decreased to the baseline by the fifth CSR day. SWS EEG delta power (a measure of sleep intensity) decreased gradually from the first to the fifth CSR day. REMS total time remained elevated during all SO periods. During the first recovery day after CSR, SWS did not change, but REMS increased by 30%. No changes in total sleep time were found on the second recovery day but sleep intensity was decreased. In 14 days after CSR, all sleep parameters returned to the baseline. We revealed a loss of 24% of noradrenergic locus coeruleus neurons, 29% and 17% of dopaminergic neurons in the substantia nigra, the ventral tegmental area as well as in their striatal terminals. Conclusion We consider CSR as a damaging factor leading to a gradual suppression of homeostatic mechanisms governing sleep recovery. CSR can provoke neurodegeneration in monoaminergic structures involved in the regulation of emotional behavior, sleep, and autonomic functions. Support (if any) Ministry of Science and Higher Education of the Russian Federation grant (No. 075-15-2020-916 dated November 13, 2020) for the establishment and development of the Pavlovsky Center “Integrative Physiology for Medicine, High-Tech Healthcare and Stress Resilience Technologies”.

中文翻译：

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112 慢性睡眠限制会破坏慢波睡眠稳态调节并损害大鼠大脑中的单胺能结构

简介 与慢性睡眠限制 (CSR) 相关的长期神经和认知障碍的神经生理机制尚不完全清楚。在这里，我们评估了大鼠在睡眠限制期间和之后的睡眠-觉醒周期如何变化，以及 CSR 是否导致单胺能脑结构的神经变性。方法 对于 CSR，7-8 个月大的 Wistar 大鼠在轨道振动器上连续 5 天经历 3 小时的睡眠剥夺 (SD) 和 1 小时的睡眠机会 (SO) 循环。在 CSR 之前、期间和之后进行遥测睡眠记录。免疫组化评估脑单胺能结构中的神经变性。结果 在 SD 期间，清醒占总注册时间的 85%；剩余时间由低 EEG delta 功率的嗜睡表示。没有快速眼动睡眠（REMS）。在 CSR 期间，慢波睡眠 (SWS) 和 REMS 减少了 62% 和 57%。SO 期间的总 SWS 时间在 CSR 的第一天增加，但在 CSR 的第五天减少到基线。从第一天到第五天，SWS EEG delta 功率（睡眠强度的衡量标准）逐渐下降。在所有 SO 期间，REMS 总时间保持升高。在 CSR 后的第一个恢复日，SWS 没有变化，但 REMS 增加了 30%。在恢复的第二天，总睡眠时间没有变化，但睡眠强度有所降低。在 CSR 后的 14 天内，所有睡眠参数恢复到基线。我们发现黑质、腹侧被盖区及其纹状体末端有 24% 的去甲肾上腺素能蓝斑神经元、29% 和 17% 的多巴胺能神经元丢失。结论 我们认为企业社会责任是一个破坏性因素，会导致控制睡眠恢复的稳态机制逐渐受到抑制。企业社会责任可引起与情绪行为、睡眠和自主神经功能调节有关的单胺能结构的神经变性。支持（如果有）俄罗斯联邦科学和高等教育部拨款（2020 年 11 月 13 日第 075-15-2020-916 号），用于建立和发展巴甫洛夫斯基中心“医学、高科技综合生理学”医疗保健和压力恢复技术”。