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Neurobiology of the circadian clock and its role in cardiovascular disease: Mechanisms, biomarkers, and chronotherapy 生物钟的神经生物学及其在心血管疾病中的作用：机制、生物标志物和时间疗法

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-06-03 DOI: 10.1016/j.nbscr.2025.100131

Abhimanyu Thakur , Raj Kishore

Cardiovascular diseases are paramount cause of morbidity in aging population and aging disrupts normal circadian rhythm cycle. Circadian rhythms, regulated by the suprachiasmatic nucleus in the brain, profoundly influence cardiovascular health through intricate neurobiological mechanisms. These rhythms regulate gene expression in cardiomyocytes, modulate autonomic nervous system (ANS) activity, and synchronize cardiovascular functions with environmental cues, ultimately impacting heart rate, blood pressure, and susceptibility to cardiac events. The intricate relationship between circadian rhythms and cardiovascular health emphasizes the critical role of brain-heart communication in physiological processes.

This review explores the neurobiology of circadian clock in cardiovascular disease, exploring how peripheral clocks in cardiovascular tissues influence organ physiology and how their disruption contributes to pathogenesis. The examination of neurobiological pathways linking circadian clock to cardiovascular disease, including ANS function, neuroendocrine signaling, and inflammatory responses, highlights the interplay between brain and heart. By probing environmental and lifestyle factors that modulate the circadian clock, as well as sex-specific variations in circadian rhythms, the review provides a comprehensive understanding of how these factors impact cardiovascular health. The discussion of emerging concepts, such as exosome-mediated intracellular communication in circadian physiology, offers new insights into the molecular mechanisms underlying brain-heart interactions. Furthermore, the exploration of diagnostic potential and therapeutic strategies, particularly chronotherapy, emphasizes the importance of targeting the circadian clock for disease prevention and treatment in cardiovascular medicine. This comprehensive assessment not only advances our understanding about circadian clock's role in cardiovascular health but also paves the way for innovative approaches in theranostic, ultimately improving patient outcomes.

心血管疾病是老年人发病的首要原因，老龄化破坏了正常的昼夜节律周期。昼夜节律由大脑视交叉上核调节，通过复杂的神经生物学机制深刻影响心血管健康。这些节律调节心肌细胞的基因表达，调节自主神经系统（ANS）的活动，并使心血管功能与环境信号同步，最终影响心率、血压和对心脏事件的易感性。昼夜节律与心血管健康之间的复杂关系强调了脑-心通讯在生理过程中的关键作用。本文综述了心血管疾病中生物钟的神经生物学，探讨了心血管组织中的外周时钟如何影响器官生理以及它们的破坏如何导致发病。研究将生物钟与心血管疾病联系起来的神经生物学途径，包括ANS功能、神经内分泌信号和炎症反应，强调了大脑和心脏之间的相互作用。通过探索调节生物钟的环境和生活方式因素，以及昼夜节律的性别差异，该综述提供了对这些因素如何影响心血管健康的全面理解。对新兴概念的讨论，如昼夜生理学中外泌体介导的细胞内通讯，为脑-心相互作用的分子机制提供了新的见解。此外，对诊断潜力和治疗策略的探索，特别是时间疗法，强调了在心血管医学中以生物钟为目标预防和治疗疾病的重要性。这项全面的评估不仅促进了我们对生物钟在心血管健康中的作用的理解，而且为创新的治疗方法铺平了道路，最终改善了患者的预后。

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引用次数: 0

Sleep and immune health: How dogs, goats and ‘factor S’ shaped a field 睡眠和免疫健康：狗、山羊和“S因素”如何塑造一个领域

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Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100118

Mark R. Opp , Luca Imeri

Chronic insufficient sleep kills! Although this statement has high ‘face validity’, it is only recently that empirical evidence existed to support it. There are now sufficient data for numerous meta-analyses and systematic reviews to demonstrate that chronic insufficient sleep is associated with many inflammatory pathologies that are a public health burden. As a result, it is now well accepted that sleep is important for physical and mental health. This awareness derives from research that began in the late 19th and early 20th centuries and continues to the present day. In this narrative review we trace this rich history within the context of the research contributions of Professor James Krueger and his colleagues. The historic and current research by Professor Krueger and colleagues is fundamental to the many ongoing pre-clinical and clinical research programs focused on all aspects of sleep and immune health.

长期睡眠不足会致命！虽然这种说法具有很高的“表面效度”，但直到最近才有经验证据支持它。现在有足够的数据进行大量的荟萃分析和系统综述，以证明慢性睡眠不足与许多炎症病理有关，这些炎症病理是公共卫生负担。因此，人们普遍认为睡眠对身心健康都很重要。这种意识源于始于19世纪末和20世纪初并持续至今的研究。在这篇叙述性评论中，我们在詹姆斯·克鲁格教授和他的同事的研究贡献的背景下追溯了这段丰富的历史。克鲁格教授及其同事的历史和当前研究是许多正在进行的临床前和临床研究项目的基础，这些研究项目专注于睡眠和免疫健康的各个方面。

引用次数: 0

Sleep and circadian disorders as risk factors for autoimmune disease: A population-based study 睡眠和昼夜节律紊乱是自身免疫性疾病的危险因素：一项基于人群的研究

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100129

Amber R. Li , Bhaavyaa Shah , Michael L. Thomas , Michael J. McCarthy , Alejandro D. Meruelo

Background

Sleep and circadian disruption have been increasingly linked to immune dysregulation, yet population-level associations with autoimmune disease remain underexplored. We examined whether delayed sleep phase disorder (DSPD), obstructive sleep apnea (OSA), primary insomnia, and hypersomnia were associated with autoimmune conditions in a large, diverse U.S. cohort.

Methods

Data were drawn from the All of Us Research Program Registered Tier Dataset v8. Participants were categorized into sleep disorder groups based on clinical diagnoses, with regular sleepers serving as controls. Autoimmune disease was defined using SNOMED-coded records. DSPD and primary insomnia were analyzed using rare disease logistic regression; OSA and hypersomnia were analyzed using 1:5 propensity score matching. Adjusted logistic regression models included age, sex at birth, race, ethnicity, income, BMI, and chronic inflammatory diagnosis. E-values assessed robustness to unmeasured confounding.

Results

All four sleep disorder groups showed significantly higher odds of autoimmune diagnosis relative to regular sleepers (p < 2.2 × 10⁻¹⁶). Adjusted odds ratios were: DSPD (OR = 0.26; 95 % CI: 0.15–0.45), OSA (OR = 0.46; 95 % CI: 0.41–0.52), primary insomnia (OR = 0.46; 95 % CI: 0.41–0.52), and hypersomnia (OR = 0.48; 95 % CI: 0.46–0.50). Older age, female sex, and chronic inflammation were associated with higher autoimmune prevalence. Asian race and BMI were inversely associated with autoimmune risk; higher income was unexpectedly associated with greater autoimmune diagnosis.

Conclusions

Distinct sleep phenotypes were associated with autoimmune conditions. These associations may reflect shared or bidirectional links between sleep disruption and immune dysregulation.

背景：睡眠和昼夜节律紊乱与免疫失调的联系越来越紧密，但在人群水平上与自身免疫性疾病的关联仍未得到充分探讨。我们研究了延迟睡眠阶段障碍（DSPD）、阻塞性睡眠呼吸暂停（OSA）、原发性失眠和嗜睡是否与自身免疫性疾病有关。方法数据来自All of Us Research Program注册Tier Dataset v8。根据临床诊断，参与者被分为睡眠障碍组，正常睡眠者作为对照组。自身免疫性疾病的定义使用snomed编码记录。采用罕见病logistic回归分析DSPD与原发性失眠症；采用1:5倾向评分匹配法对OSA和嗜睡症进行分析。调整后的logistic回归模型包括年龄、出生性别、种族、民族、收入、BMI和慢性炎症诊断。e值评估了对未测量混杂的稳健性。结果4个睡眠障碍组的自身免疫诊断率均高于正常睡眠组(p <；2.2 × 10−16)。调整后的优势比为：DSPD (OR = 0.26；95% ci: 0.15-0.45), osa (or = 0.46；95% CI: 0.41-0.52)，原发性失眠(OR = 0.46；95% CI: 0.41-0.52)和嗜睡症(OR = 0.48；95% ci: 0.46-0.50)。年龄较大、女性和慢性炎症与较高的自身免疫性患病率相关。亚洲人种和BMI与自身免疫风险呈负相关；高收入出乎意料地与更高的自身免疫诊断相关。结论不同的睡眠表型与自身免疫性疾病相关。这些关联可能反映了睡眠中断和免疫失调之间的共享或双向联系。

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引用次数: 0

The cell-intrinsic circadian clock is dispensable for lateral posterior clock neuron regulation of Drosophila rest-activity rhythms 果蝇休息-活动节律的外侧后时钟神经元调节，离不开细胞内的生物钟

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100124

Charlene Y.P. Guerrero, Madelyn R. Cusick, Amanda J. Samaras, Natalie S. Shamon, Daniel J. Cavanaugh

Circadian control of behavior arises from intercommunication among a distributed network of circadian clock neurons in the brain. Single-cell sequencing and brain connectome data support the division of the ∼240 brain clock neurons in Drosophila into ∼20 subclusters, and functional studies demonstrate that these populations differentially contribute to behavioral outputs. Here, we have used genetic tools that enable highly selective, cell-specific manipulations to investigate the role of molecular clock function and neuronal activity within the lateral posterior clock neurons (LPNs) in the regulation of rest-activity rhythms. We find that genetic silencing of these neurons, which compromises signaling with downstream neuronal targets, substantially reduces the strength of free-running rest-activity rhythms. In contrast, locomotor activity patterns are robust to CRISPR-mediated disruption of molecular clock cycling within the LPNs. We conclude that the LPNs act as driven oscillators that retain the capacity to transmit circadian information in the absence of cell-intrinsic molecular clocks.

行为的昼夜节律控制源于大脑中分布的昼夜节律时钟神经元网络之间的相互交流。单细胞测序和脑连接组数据支持果蝇约240个脑时钟神经元分为约20个亚簇，功能研究表明，这些群体对行为输出的贡献是不同的。在这里，我们使用了遗传工具，使高选择性，细胞特异性操作，以研究分子钟功能和神经元活动在外侧后时钟神经元（lpn）内调节休息-活动节律中的作用。我们发现，这些神经元的基因沉默会损害下游神经元目标的信号，从而大大降低自由运行的休息-活动节律的强度。相反，运动活动模式对crispr介导的lpn内分子时钟循环的破坏是稳健的。我们得出结论，lpn作为驱动振荡器，在缺乏细胞固有分子钟的情况下保留了传递昼夜节律信息的能力。

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引用次数: 0

Synergies from a distance: Inspirations from the struggles of Dr James M Krueger 远距离协同效应：来自詹姆斯·克鲁格博士奋斗的启示

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100114

William A. Banks

In this article for Dr Krueger's Festschrift, I trace how his early career influenced many aspects in the fields of sleep, neuroimmunology, and the microbiome. Mostly, however, I trace how his career and interests intertwined with those of Abba J. Kastin and mine and how he exerted a profound influence on the direction of our studies. Dr. Krueger, while developing his career as a sleep researcher, encountered resistance to his work that required two major paradigm shifts: 1) that bacterial products could affect sleep and 2) that small peptides can cross the blood-brain barrier (BBB) in sufficient amounts to affect brain functioning. Dr Kastin had also shown that small peptides administered peripherally could affect brain function and postulated that this was because they could cross the BBB. Our efforts to determine whether peptides could or could not cross the BBB were bolstered by Dr Krueger's exemplary struggles.

在这篇为克鲁格博士撰写的文章中，我追溯了他早期的职业生涯如何影响了睡眠、神经免疫学和微生物组等领域的许多方面。然而，我主要是追溯他的事业和兴趣是如何与阿巴·j·卡斯汀和我的事业和兴趣交织在一起的，以及他是如何对我们的研究方向产生深远影响的。克鲁格博士在发展自己的睡眠研究事业时，遇到了对他的工作的阻力，这需要他进行两个主要的范式转变：1)细菌产物可能影响睡眠；2)小肽可以通过血脑屏障（BBB），数量足够多，从而影响大脑功能。卡斯汀博士还指出，在外围注射小肽可以影响大脑功能，并推测这是因为它们可以穿过血脑屏障。我们努力确定肽是否能或不能通过血脑屏障是由克鲁格博士的示范斗争支持。

引用次数: 0

Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection 感染的先天免疫机制：我们所知道的和感染期间影响睡眠的潜在保守机制

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Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100121

Mark R. Zielinski , Sean D. Carey , John A. Craig

Evidence indicates relationships between sleep and the innate immune system during homeostatic sleep and sleep responses after infection. The innate immune system and sleep-like states are highly conserved between simple species and more complex species such as humans. A wide variety of bacteria, viruses, and parasites change sleep patterns in the host during infection. The effects of infection on sleep can occur, in part, due to the bolus and route of infection, prior exposure, immune status of the individual/organism, and the type of pathogen. In addition, elements of circadian patterns and sleep prior to and after infection can modulate the infection pathology and resolution. Innate immune molecules, such as the cytokines interleukin-1 beta and tumor necrosis factor-alpha, fluctuate with the time of day of increased activity and sleep propensity, increase in response to increased waking activity from sleep loss, and are altered from infection by bacteria and viruses to alter sleep and the electroencephalogram. This review focuses innate immune mechanisms of how pathogen recognition receptors, pathogen-associated molecular patterns and danger-associated molecular patterns, energy-related molecules, oxidative stress, and inflammasomes are activated with infection to potentially affect sleep.

有证据表明，在体内平衡睡眠和感染后的睡眠反应期间，睡眠与先天免疫系统之间存在关系。先天免疫系统和睡眠状态在简单物种和更复杂的物种（如人类）之间是高度保守的。在感染期间，各种各样的细菌、病毒和寄生虫会改变宿主的睡眠模式。感染对睡眠的影响部分是由于感染的剂量和途径、先前的暴露、个体/生物体的免疫状态以及病原体的类型。此外，感染前后的昼夜节律模式和睡眠因素可以调节感染的病理和解决。先天免疫分子，如细胞因子白细胞介素-1 β和肿瘤坏死因子α，随着一天中活动增加和睡眠倾向的时间而波动，对睡眠不足引起的清醒活动增加的反应增加，并因细菌和病毒感染而改变，从而改变睡眠和脑电图。本文综述了病原体识别受体、病原体相关分子模式和危险相关分子模式、能量相关分子、氧化应激和炎症小体在感染时激活的先天免疫机制，以潜在地影响睡眠。

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引用次数: 0

No association between chronotype and cardiovascular response to a cognitive challenge in the morning using a Bayesian approach 使用贝叶斯方法，睡眠类型与心血管对早晨认知挑战的反应之间没有关联

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Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100125

Larissa N. Wüst , Christian Cajochen , Ruta Lasauskaite

A chronotype is defined as a preference for certain behaviours (e.g., sleep and wake) to occur at specific times of day. It is therefore also temporally linked with cognitive performance across the day. In an exploratory analysis, we sought to find associations between chronotypes determined from self-reported habitual sleep timing and from salivary melatonin onset with mental effort during a 2-back working memory task. Mental effort was operationalized as sympathetic beta-adrenergic impact on the heart, which is best reflected by the cardiac pre-ejection period (PEP) and also influences systolic blood pressure (SBP). Each participant underwent two experimental sessions in the morning: once after sleeping for 8 h and once after sleeping for 5 h the night before. To determine the timing of evening melatonin onset, participants took saliva samples at hourly intervals at home in the evening, prior to their experimental sessions. Chronotypes were determined using reported sleep times from the Munich Chronotype Questionnaire and average melatonin onset during both sleep conditions. Based on this, participants were grouped into early, intermediate, or late types. Neither alertness (BF₁₀ = 0.019), perceived task demand (BF₁₀ = 0.008), nor SBP response (BF₁₀ = 0.268) were credibly impacted by sleep-time derived chronotype, while the association with PEP response (BF₁₀ = 0.631) during a cognitive challenge in the morning was inconclusive. Similarly, the timing of evening melatonin onset did not affect alertness (BF₁₀ = 0.003), perceived task demand (BF₁₀ = 0.006), or PEP or SBP response (PEP: BF₁₀ = 0.232, SBP: BF₁₀ = 0.263) during the cognitive challenge. Our data shows no impact of chronotypes on effort-related cardiovascular response during a cognitive challenge in the morning, which was scheduled according to habitual sleep times.

时间类型被定义为对特定行为（例如，睡眠和醒来）在一天中特定时间发生的偏好。因此，它也与一天中的认知表现有暂时的联系。在一项探索性分析中，我们试图发现自我报告的习惯性睡眠时间和唾液褪黑素在两回工作记忆任务中与精神努力之间的联系。精神努力被运作为对心脏的交感-肾上腺素能影响，这在心脏射血前期（PEP）中得到最好的反映，也影响收缩压（SBP）。每个参与者在早上进行两次实验：一次是在睡了8小时后，一次是在前一天晚上睡了5小时后。为了确定褪黑素在晚上起作用的时间，参与者在实验开始之前，每隔一小时在家里采集一次唾液样本。根据慕尼黑睡眠类型问卷报告的睡眠时间和两种睡眠状态下褪黑素的平均分泌量来确定睡眠类型。在此基础上，参与者被分为早期、中期和晚期。警觉性（BF10 = 0.019）、感知任务需求（BF10 = 0.008）和收缩压反应（BF10 = 0.268）均不受睡眠时间衍生时型的影响，而与早晨认知挑战时PEP反应（BF10 = 0.631）的关系尚无定论。同样，在认知挑战期间，夜间褪黑激素的发作时间并不影响警觉性（BF10 = 0.003）、感知任务需求（BF10 = 0.006）或PEP或SBP反应（PEP: BF10 = 0.232, SBP: BF10 = 0.263）。我们的数据显示，在早晨的认知挑战中，生物钟类型对与努力相关的心血管反应没有影响，这是根据习惯睡眠时间安排的。

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引用次数: 0

Sleep in disease: inflammation and chronic rhinosinusitis 睡眠中的疾病：炎症和慢性鼻窦炎

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100120

Vivek C. Pandrangi , Jeremiah A. Alt

Chronic rhinosinusitis (CRS) is a common inflammatory disorder that is associated with significant quality of life (QOL) impairment, including sleep dysfunction. There are multiple factors that have been independently associated with poor sleep among this population including alterations in inflammatory mediators, rhinologic symptom interference such as nasal discharge, obstruction, and facial pain, and co-morbid conditions including asthma. While there is a high prevalence of sleep dysfunction among this population, treatment with both medical and surgical options may lead to sustained improvements in sleep. This review aims to highlight the burden of sleep dysfunction, discuss common theories regarding the etiology, and evaluate strategies that may facilitate improvement in sleep dysfunction among patients with CRS.

慢性鼻窦炎（CRS）是一种常见的炎症性疾病，与显著的生活质量（QOL）损害相关，包括睡眠障碍。在这一人群中，有多种因素与睡眠不良独立相关，包括炎症介质的改变、鼻症状的干扰，如鼻溢液、梗阻和面部疼痛，以及包括哮喘在内的合并症。虽然这一人群中睡眠障碍的患病率很高，但药物和手术治疗可能会导致睡眠的持续改善。本综述旨在强调睡眠功能障碍的负担，讨论有关病因的常见理论，并评估可能有助于改善CRS患者睡眠功能障碍的策略。

引用次数: 0

Metabolic signals in sleep regulation: the role of brown adipose tissue 代谢信号在睡眠调节中的作用：棕色脂肪组织

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100122

Éva Szentirmai , Levente Kapás

The regulation of sleep, while primarily attributed to the interplay between circadian and homeostatic processes, is significantly influenced by a multitude of additional factors that profoundly impact sleep quantity and quality. These factors encompass both external environmental stimuli, such as ambient temperature and somatosensory inputs, and internal physiological changes. The intricate relationship between metabolism and sleep has been a subject of extensive research, with particular attention given to the role of metabolic signals in sleep regulation. Among these, the brown adipose tissue (BAT) has emerged as a key player, studied from various perspectives including its physiological responses to sleep deprivation, its effects on sleep when activated, the consequences of impaired BAT thermogenesis on sleep patterns, and its metabolic activity across different sleep states. The cumulative evidence from these investigations suggests that BAT plays a crucial role in maintaining an optimal metabolic environment conducive to sleep, a function that becomes particularly significant in contexts of prior sleep loss, inflammatory conditions, and fluctuations in ambient temperature.

睡眠的调节，虽然主要归因于昼夜节律和体内平衡过程之间的相互作用，但也受到许多其他因素的显著影响，这些因素深刻地影响着睡眠的数量和质量。这些因素既包括外部环境刺激，如环境温度和体感输入，也包括内部生理变化。新陈代谢和睡眠之间的复杂关系一直是广泛研究的主题，特别关注代谢信号在睡眠调节中的作用。其中，棕色脂肪组织（BAT）已成为一个关键角色，从多个角度进行了研究，包括其对睡眠剥夺的生理反应、激活时对睡眠的影响、BAT产热功能受损对睡眠模式的影响，以及它在不同睡眠状态下的代谢活动。这些研究的累积证据表明，BAT在维持有利于睡眠的最佳代谢环境中起着至关重要的作用，这一功能在先前睡眠不足、炎症条件和环境温度波动的情况下变得尤为重要。

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引用次数: 0

Microglial depletion and repopulation differentially modulate sleep and inflammation in a mouse model of traumatic brain injury 在创伤性脑损伤小鼠模型中，小胶质细胞耗竭和再生差异调节睡眠和炎症

Q2 Medicine

Neurobiology of Sleep and Circadian Rhythms

Pub Date : 2025-05-01 DOI: 10.1016/j.nbscr.2025.100115

Katherine R. Giordano , Tabitha R.F. Green , Mark R. Opp , Rachel K. Rowe

Traumatic brain injury (TBI) causes persistent sleep disturbances, leading to long-term neurological consequences and reduced quality of life. We hypothesized that microglial depletion via PLX5622 (PLX), a colony-stimulating factor 1 receptor (CSFR1R) inhibitor, would exacerbate sleep disturbances and alter inflammatory profiles after TBI, and that microglial repopulation would ameliorate these effects. Male mice received PLX or control diets (21 days) followed by a midline fluid percussion injury (mFPI) or sham surgery. Physiological parameters were recorded non-invasively to determine sleep for 7 days post-injury. Subsequently, PLX was withdrawn to allow microglial repopulation, and sleep was assessed during the 7-day repopulation period. In a subset of mice, repeated blood draws were taken to quantify sleep regulatory cytokine concentrations (interleukin [IL]-6, IL-1β, tumor necrosis factor [TNF]-α). TBI significantly reduced sleep in mice on a control diet during the light period (3, 5, and 7 days post-injury), but not the dark period. In PLX-treated mice, TBI did not alter sleep in the light period, however, sleep in the dark period was increased at 3 days post-injury. During the microglial repopulation period, PLX-treated TBI mice slept significantly more in the dark period compared to PLX sham mice and sleep was similar in control TBI vs PLX TBI mice. Analyses revealed that elimination of microglia did not alter baseline cytokine levels. IL-6 was elevated in PLX TBI mice at 1 and 7 days post-injury compared to TBI mice on control diet, while IL-1β and TNF-α remained unchanged. This study highlights the critical role of microglia in modulating post-TBI sleep and inflammation. Findings suggest differential effects of TBI on sleep depending on microglial depletion or repopulation status, with IL-6 serving as a marker of the inflammatory response in microglia-depleted conditions.

创伤性脑损伤（TBI）引起持续的睡眠障碍，导致长期的神经系统后果和生活质量下降。我们假设，通过集落刺激因子1受体（CSFR1R）抑制剂PLX5622 （PLX）消耗小胶质细胞会加剧TBI后的睡眠障碍并改变炎症特征，而小胶质细胞的再生会改善这些影响。雄性小鼠接受PLX或对照饮食（21天），然后进行中线液体撞击损伤（mFPI）或假手术。无创记录生理参数以确定损伤后7天的睡眠情况。随后，停用PLX以允许小胶质细胞再生，并在7天的再生期内评估睡眠。在一组小鼠中，反复抽血以定量睡眠调节细胞因子浓度（白细胞介素[IL]-6， IL-1β，肿瘤坏死因子[TNF]-α）。在光照期（损伤后3、5和7天），TBI显著减少了对照组小鼠的睡眠，但在黑暗期则没有。在plx治疗的小鼠中，TBI没有改变光照期的睡眠，但在损伤后3天，黑暗期的睡眠增加。在小胶质细胞再生期间，与PLX假组相比，PLX治疗的TBI小鼠在黑暗期的睡眠时间明显增加，而对照组TBI小鼠的睡眠时间与PLX治疗的TBI小鼠相似。分析显示，消除小胶质细胞不会改变基线细胞因子水平。与对照组TBI小鼠相比，PLX TBI小鼠损伤后1天和7天IL-6升高，而IL-1β和TNF-α保持不变。这项研究强调了小胶质细胞在脑外伤后睡眠和炎症调节中的关键作用。研究结果表明，脑外伤对睡眠的不同影响取决于小胶质细胞的消耗或再生状态，IL-6是小胶质细胞消耗条件下炎症反应的标志。

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引用次数: 0