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Sleep deprivation and stress: a reciprocal relationship.

ABSTRACT: Sleep is highly conserved across evolution, suggesting vital biological functions that are yet to be fully understood. Animals and humans experiencing partial sleep restriction usually exhibit detrimental physiological responses, while total and prolonged sleep loss could lead to death. The perturbation of sleep homeostasis is usually accompanied by an increase in hypothalamic-pituitary-adrenal (HPA) axis activity, leading to a rise in circulating levels of stress hormones (e.g. cortisol in humans, corticosterone in rodents). Such hormones follow a circadian release pattern under undisturbed conditions and participate in the regulation of sleep. The investigation of the consequences of sleep deprivation, from molecular changes to behavioural alterations, has been used to study the fundamental functions of sleep. However, the reciprocal relationship between sleep and the activity of the HPA axis is problematic when investigating sleep using traditional sleep-deprivation protocols that can induce stress per se. This is especially true in studies using rodents in which sleep deprivation is achieved by exogenous, and potentially stressful, sensory-motor stimulations that can undoubtedly confuse their conclusions. While more research is needed to explore the mechanisms underlying sleep loss and health, avoiding stress as a confounding factor in sleep-deprivation studies is therefore crucial. This review examines the evidence of the intricate links between sleep and stress in the context of experimental sleep deprivation, and proposes a more sophisticated research framework for sleep-deprivation procedures that could benefit from recent progress in biotechnological tools for precise neuromodulation, such as chemogenetics and optogenetics, as well as improved automated real-time sleep-scoring algorithms.

SUBMITTER: Nollet M

PROVIDER: S-EPMC7202382 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature

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Sleep deprivation and stress: a reciprocal relationship.

Nollet Mathieu M Wisden William W Franks Nicholas P NP

Interface focus 20200417 3

Sleep is highly conserved across evolution, suggesting vital biological functions that are yet to be fully understood. Animals and humans experiencing partial sleep restriction usually exhibit detrimental physiological responses, while total and prolonged sleep loss could lead to death. The perturbation of sleep homeostasis is usually accompanied by an increase in hypothalamic-pituitary-adrenal (HPA) axis activity, leading to a rise in circulating levels of stress hormones (e.g. cortisol in huma ...[more]

PMID: 32382403

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Project description:BackgroundSleep deprivation (SD)-induced cognitive impairment is highly prevalent worldwide and has attracted widespread attention. The temporal and spatial oscillations of circadian genes are severely disturbed after SD, leading to a progressive loss of their physiological rhythms, which in turn affects memory function. However, there is a lack of research on the role of circadian genes and memory function after SD. Therefore, the present study aims to investigate the relationship between circadian genes and memory function and provide potential therapeutic insights into the mechanism of SD-induced memory impairment.MethodsGene expression profiles of GSE33302 and GSE9442 from the Gene Expression Omnibus (GEO) were applied to identify differentially expressed genes (DEGs). Subsequently, both datasets were subjected to Gene Set Enrichment Analysis (GSEA) to determine the overall gene changes in the hippocampus and brain after SD. A Gene Oncology (GO) analysis and Protein-Protein Interaction (PPI) analysis were employed to explore the genes related to circadian rhythm, with their relationship and importance determined through a correlation analysis and a receiver operating characteristic curve (ROC), respectively. The water maze experiments detected behavioral changes related to memory function in SD rats. The expression of circadian genes in several critical organs such as the brain, heart, liver, and lungs and their correlation with memory function was investigated using several microarrays. Finally, changes in the hippocampal immune environment after SD were analyzed using the CIBERSORT in R software.ResultsThe quality of the two datasets was very good. After SD, changes were seen primarily in genes related to memory impairment and immune function. Genes related to circadian rhythm were highly correlated with engagement in muscle structure development and circadian rhythm. Seven circadian genes showed their potential therapeutic value in SD. Water maze experiments confirmed that SD exacerbates memory impairment-related behaviors, including prolonged escape latencies and reduced numbers of rats crossing the platform. The expression of circadian genes was verified, while some genes were also significant in the heart, liver, and lungs. All seven circadian genes were also associated with memory markers in SD. The contents of four immune cells in the hippocampal immune environment changed after SD. Seven circadian genes were related to multiple immune cells.ConclusionsIn the present study, we found that SD leads to memory impairment accompanied by changes in circadian rhythm-related genes. Seven circadian genes play crucial roles in memory impairment after SD. Naïve B cells and follicular helper T cells are closely related to SD. These findings provide new insights into the treatment of memory impairment caused by SD.

Project description:ObjectivesInsufficient sleep affects circadian hormonal profiles and inflammatory markers and may modulate attention, executive functioning and decision-making. Medical professionals and specifically resident physicians, who are involved in long-term nightshift schedules during their post-graduate training, are prone to acute and chronic sleep deprivation and disruption, putting them at risk for making medical errors. The aim of the study was to evaluate the impact of chronic and acute-on-chronic sleep deprivation and disruption among residents on selected physiological and cognitive measures.MethodsThirty-three medical and surgical residents were evaluated twice - at baseline and after a 26-hour shift. Eighteen young attending physicians who did not engage in nightshift schedules served as controls and were evaluated once. Measures included morning cortisol and high-sensitivity C-reactive protein (hs-CRP), computerised tests of attention and behaviour, the Behaviour Rating Inventory of Executive Function, a risk-taking questionnaire and the Pittsburgh Sleep Quality Index.ResultsResidents, but not attendings, reported chronic sleep disruption and deprivation. Residents at baseline exhibited reduced morning cortisol levels and elevated hs-CRP levels, compared to attendings. Residents at baseline had impaired global executive function compared to attendings. A nightshift with acute sleep deprivation further reduced residents' executive function. Residents at baseline and after a nightshift demonstrated increased impulsivity and slower processing time than attendings. Residents and attendings did not differ in risk-taking tendencies which were assessed in a separate cohort.ConclusionsIn a real-life setting, resident physicians exhibit increased low-grade systemic inflammation (hs-CRP) and impaired HPA-axis function. Their chronic sleep curtailment is associated with greater impulsivity, slower cognitive processing, and impaired executive function. Future research is warranted to understand how improving working schedule by increasing sleep duration may minimise the short-term and potential long-term risks to physicians in training.

Project description:BackgroundMany aging changes seem similar to those elicited by sleep-deprivation and psychosocial stress. Further, sleep architecture changes with age suggest an age-related loss of sleep. Here, we hypothesized that sleep deprivation in young subjects would elicit both stress and aging-like transcriptional responses.Methodology/principal findingsF344 rats were divided into control and sleep deprivation groups. Body weight, adrenal weight, corticosterone level and hippocampal CA1 transcriptional profiles were measured. A second group of animals was exposed to novel environment stress (NES), and their hippocampal transcriptional profiles measured. A third cohort exposed to control or SD was used to validate transcriptional results with Western blots. Microarray results were statistically contrasted with prior transcriptional studies. Microarray results pointed to sleep pressure signaling and macromolecular synthesis disruptions in the hippocampal CA1 region. Animals exposed to NES recapitulated nearly one third of the SD transcriptional profile. However, the SD-aging relationship was more complex. Compared to aging, SD profiles influenced a significant subset of genes. mRNA associated with neurogenesis and energy pathways showed agreement between aging and SD, while immune, glial, and macromolecular synthesis pathways showed SD profiles that opposed those seen in aging.Conclusions/significanceWe conclude that although NES and SD exert similar transcriptional changes, selective presynaptic release machinery and Homer1 expression changes are seen in SD. Among other changes, the marked decrease in Homer1 expression with age may represent an important divergence between young and aged brain response to SD. Based on this, it seems reasonable to conclude that therapeutic strategies designed to promote sleep in young subjects may have off-target effects in the aged. Finally, this work identifies presynaptic vesicular release and intercellular adhesion molecular signatures as novel therapeutic targets to counter effects of SD in young subjects.

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Sleep deprivation and stress: a reciprocal relationship.

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Sleep deprivation and stress: a reciprocal relationship.

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