Radwan Basma, Yanez Touzet Alvaro, Hammami Soaad, Chaudhury Dipesh
Department of Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates.
MBChB Medicine, The University of Manchester, Manchester, United Kingdom.
Front Neurosci. 2021 Feb 22;15:633955. doi: 10.3389/fnins.2021.633955. eCollection 2021.
Stress and sleep are tightly regulated as a result of the substantial overlap in neurotransmitter signaling and regulatory pathways between the neural centers that modulate mood and sleep-wake cycle. The chronicity of the stressor and variability in coping with it are major determinants of the psychiatric outcomes and subsequent effect on sleep. The regulation of sleep is mediated by the interaction of a homeostatic and a circadian process according to the two-process model. Chronic stress induces stress-related disorders which are associated with deficient sleep homeostasis. However, little is known about how chronic stress affects sleep homeostasis and whether the differences in adaptation to stress distinctively influence sleep. Therefore, we assessed sleep homeostasis in C57BL6/J mice following exposure to 15-d of chronic social defeat stress. We implemented wake:sleep ratio as a behavioral correlate of sleep pressure. Both stress-resilient and stress-susceptible mice displayed deficient sleep homeostasis in post-stress baseline sleep. This was due to poor temporal correlation between frontal slow wave activity (SWA) power and sleep pressure in the dark/active phase. Moreover, the buildup rate of sleep pressure in the dark was lower in susceptible mice in comparison to stress-naïve mice. Additionally, 4-h SD in the dark caused a deficient sleep recovery response in susceptible mice characterized by non-rapid eye movement (NREM) sleep loss. Our findings provide evidence of deficient homeostatic sleep process (S) in baseline sleep in stress-exposed mice, while impaired sleep recovery following a mild enforced wakefulness experienced during the dark was only detected in stress-susceptible mice. This alludes to the differential homeostatic adaptation to stress between susceptible and resilient mice and its effect on sleep regulation.
由于调节情绪和睡眠 - 觉醒周期的神经中枢之间神经递质信号传导和调节途径存在大量重叠,压力和睡眠受到严格调控。应激源的长期性以及应对方式的变异性是精神疾病后果及后续对睡眠影响的主要决定因素。根据双过程模型,睡眠的调节由稳态过程和昼夜节律过程的相互作用介导。慢性应激会引发与睡眠稳态不足相关的应激相关障碍。然而,关于慢性应激如何影响睡眠稳态以及对应激的适应差异是否会独特地影响睡眠,我们知之甚少。因此,我们评估了C57BL6/J小鼠在暴露于15天慢性社会挫败应激后的睡眠稳态。我们采用觉醒:睡眠比率作为睡眠压力的行为相关指标。应激耐受型和应激敏感型小鼠在应激后基线睡眠中均表现出睡眠稳态不足。这是由于在黑暗/活跃期额叶慢波活动(SWA)功率与睡眠压力之间的时间相关性较差。此外,与未经历应激的小鼠相比,敏感型小鼠在黑暗中的睡眠压力累积速率较低。另外,黑暗中4小时的睡眠剥夺导致敏感型小鼠出现以非快速眼动(NREM)睡眠丧失为特征的睡眠恢复反应不足。我们的研究结果提供了证据,表明应激暴露小鼠的基线睡眠中存在稳态睡眠过程(S)不足,而仅在应激敏感型小鼠中检测到黑暗期间经历轻度强制觉醒后睡眠恢复受损。这暗示了敏感型和耐受型小鼠对应激的稳态适应差异及其对睡眠调节的影响。