4.6 Article

Prolonged Exposure to Social Stress Impairs Homeostatic Sleep Regulation

期刊

FRONTIERS IN NEUROSCIENCE
卷 15, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fnins.2021.633955

关键词

homeostatic sleep; slow wave amplitude; NREM sleep; chronic social defeat; sleep pressure; process S

资金

  1. NYUAD Annual Research Budget, Brain and Behavior Research Foundation [NARSAD: 22715]
  2. NYUAD Research Enhancement Fund, NYU Research Enhancement Fund, Al Jalila Research Foundation [AJF20163]
  3. L'OREAL-UNESCO [4500385541]
  4. For Women in Science (FWIS) Middle East Fellowship
  5. NYUAD Post-Graduation Fellowship Program: AYT

向作者/读者索取更多资源

Stress and sleep are tightly regulated through the interaction of homeostatic and circadian processes. Chronic stress can lead to deficient sleep homeostasis, but the understanding of how chronic stress affects sleep regulation and the differences in adaptation to stress on sleep remains limited.
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-naive 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.

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