Neurobiology of Sleep and Circadian Rhythms最新文献

{"title":"Chronic circadian advance shifts abolish melatonin secretion for days in rats","authors":"Gang Xu ,&nbsp;Jon Dean ,&nbsp;Tiecheng Liu ,&nbsp;Fangyun Tian ,&nbsp;Jimo Borjigin","doi":"10.1016/j.nbscr.2018.02.002","DOIUrl":"10.1016/j.nbscr.2018.02.002","url":null,"abstract":"<div><p>Melatonin deficiency has been proposed to underlie higher risks for cardiovascular and several other diseases in humans experiencing prolonged shiftwork. However, melatonin secretion has not been monitored longitudinally during consecutive shifts of the light:dark (LD) cycles in the same individuals (animals or humans) and the extent of melatonin deficiency is unknown in individuals experiencing consecutive LD shifts. We investigated the effect of consecutive LD shifts on melatonin secretion in adult F344 rats using continuous online pineal-microdialysis. The rats were entrained to the 12 h:12 h LD cycle before the shifts. The LD cycle was then advanced (n=5) or delayed (n=4) for six hours every four days for four consecutive times. The rats exhibited marked asymmetry in response to delay or advance LD shifts. While rats exposed to the repeated LD delay shifts always exhibited melatonin secretion throughout the entire periods, repeated LD advance shifts suppressed nocturnal melatonin secretion for several consecutive days in the middle of the 3-week period. Moreover, melatonin offset after LD delay and melatonin onset after LD advance determined the rate of circadian pacemaker reentrainment. Additionally, melatonin offset was phase locked at the new dark/light junctions for days following LD advance. These data demonstrate that chronic LD shifts are deleterious to melatonin rhythms, and that this effect is much more pronounced during advance shifts. These data may enhance our understanding of impact of LD shifts on our circadian timing system and benefit better design of shiftwork schedules to avoid melatonin disruption.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 78-83"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.02.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reflections on contributing to “big discoveries” about the fly clock: Our fortunate paths as post-docs with 2017 Nobel laureates Jeff Hall, Michael Rosbash, and Mike Young","authors":"Kathleen K. Siwicki ,&nbsp;Paul E. Hardin ,&nbsp;Jeffrey L. Price","doi":"10.1016/j.nbscr.2018.02.004","DOIUrl":"10.1016/j.nbscr.2018.02.004","url":null,"abstract":"<div><p>In the early 1980s Jeff Hall and Michael Rosbash at Brandeis University and Mike Young at Rockefeller University set out to isolate the <em>period</em> (<em>per</em>) gene, which was recovered in a revolutionary genetic screen by Ron Konopka and Seymour Benzer for mutants that altered circadian behavioral rhythms. Over the next 15 years the Hall, Rosbash and Young labs made a series of groundbreaking discoveries that defined the molecular timekeeping mechanism and formed the basis for them being awarded the 2017 Nobel Prize in Physiology or Medicine. Here the authors recount their experiences as post-docs in the Hall, Rosbash and Young labs from the mid-1980s to the mid-1990s, and provide a perspective of how basic research conducted on a simple model system during that era profoundly influenced the direction of the clocks field and established novel approaches that are now standard operating procedure for studying complex behavior.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 58-67"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.02.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep homeostasis and the circadian clock: Do the circadian pacemaker and the sleep homeostat influence each other’s functioning?","authors":"Tom Deboer","doi":"10.1016/j.nbscr.2018.02.003","DOIUrl":"10.1016/j.nbscr.2018.02.003","url":null,"abstract":"<div><p>Sleep is regulated by a homeostatic and a circadian process. Together these two processes determine most aspects of sleep and related variables like sleepiness and alertness. The two processes are known to be able to work independently, but also to both influence sleep and sleep related variables in an additive or more complex manner. The question remains whether the two processes are directly influencing each other.</p><p>The present review summarizes evidence from behavioural and electroencephalographic determined sleep, electrophysiology, gene knock out mouse models, and mathematical modelling to explore whether sleep homeostasis can influence circadian clock functioning and <em>vice versa</em>.</p><p>There is a multitude of data available showing parallel action or influence of sleep homeostatic mechanisms and the circadian clock on several objective and subjective variables related to sleep and alertness. However, the evidence of a direct influence of the circadian clock on sleep homeostatic mechanisms is sparse and more research is needed, particularly applying longer sleep deprivations that include a second night.</p><p>The strongest evidence of an influence of sleep homeostatic mechanisms on clock functioning comes from sleep deprivation experiments, demonstrating an attenuation of phase shifts of the circadian rhythm to light pulses when sleep homeostatic pressure is increased. The data suggest that the circadian clock is less susceptible to light when sleep pressure is high.</p><p>The available data indicate that a strong central clock will induce periods of deep sleep, which in turn will strengthen clock function. Both are therefore important for health and wellbeing. Weakening of one will also hamper functioning of the other. Shift work and jet lag are situations where one tries to adapt to zeitgebers in a condition where sleep is compromised. Adaptation to zeitgebers may be improved by introducing nap schedules to reduce sleep pressure, and through that increasing clock susceptibility to light.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 68-77"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.02.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex hormones play a role in vulnerability to sleep loss on emotion processing tasks","authors":"K.A. Lustig,&nbsp;E.M. Stoakley,&nbsp;K.J. MacDonald,&nbsp;S.N. Geniole,&nbsp;C.M. McCormick,&nbsp;K.A. Cote","doi":"10.1016/j.nbscr.2017.10.001","DOIUrl":"10.1016/j.nbscr.2017.10.001","url":null,"abstract":"<div><p>The central aim of this study was to investigate hormones as a predictor of individual vulnerability or resiliency on emotion processing tasks following one night of sleep restriction. The restriction group was instructed to sleep 3<!--> <!-->a.m.–7<!--> <!-->a.m. (13 men, 13 women in follicular phase, 10 women in luteal phase of menstrual cycle), and a control group slept 11<!--> <!-->p.m.–7<!--> <!-->a.m. (12 men, 12 follicular women, 12 luteal women). Sleep from home was verified with actigraphy. Saliva samples were collected on the evening prior to restriction, and in the morning and afternoon following restriction, to measure testosterone, estradiol, and progesterone. In the laboratory, event-related potentials (ERPs) were recorded during presentation of images and faces to index neural processing of emotional stimuli. Compared to controls, sleep-restricted participants had a larger amplitude Late Positive Potential (LPP) ERP to positive vs neutral images, reflecting greater motivated attention towards positive stimuli. Sleep-restricted participants were also less accurate categorizing sad faces and exhibited a larger N170 to sad faces, reflecting greater neural reactivity. Sleep-restricted luteal women were less accurate categorizing all images compared to control luteal women, and progesterone was related to several outcomes. Morning testosterone in men was lower in the sleep-restricted group compared to controls; lower testosterone was associated with lower accuracy to positive images, a greater difference between positive vs neutral LPP amplitude, and lower accuracy to sad and fearful faces. In summary, women higher in progesterone and men lower in testosterone were more vulnerable to the effects of sleep restriction on emotion processing tasks. This study highlights a role for sex and sex hormones in understanding individual differences in vulnerability to sleep loss.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 94-104"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.10.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparing the cardiac autonomic activity profile of daytime naps and nighttime sleep","authors":"Lauren N. Whitehurst ,&nbsp;Mohsen Naji ,&nbsp;Sara C. Mednick","doi":"10.1016/j.nbscr.2018.03.001","DOIUrl":"10.1016/j.nbscr.2018.03.001","url":null,"abstract":"<div><p>Heart rate variability (HRV) is a reliable technique to evaluate autonomic activity and shows marked changes across a night of sleep. Previous nighttime sleep findings report changes in HRV during non-rapid eye movement sleep (NREM), which have been associated with cardiovascular health benefits. Daytime sleep, however, has been linked with both positive and negative cardiovascular outcomes. Yet, no studies have directly compared HRV profiles during an ecologically-valid daytime nap in healthy, well-rested adults to that of nighttime sleep. Using a within-subjects design, 32 people took a daytime nap and slept overnight in the lab at least one week apart; both sleep sessions had polysomnography, including electrocardiography (ECG), recorded. We measured inter-beat intervals (RR), total power (TP), low frequency power (LF; .04–.15 Hz), and high frequency power (HF; .15–.40 Hz) components of HRV during NREM and rapid eye movement (REM) sleep. Compared to the nap, we found longer RR intervals and decreased heart rate during the night for both Stage 2 and SWS and increased TP, LF and HF power during nighttime Stage 2 sleep only; however, no differences in the LFHF ratio or normalized HF power were found between the nap and the night. Also, no differences in REM sleep between the nap and night were detected. Similar relationships emerged when comparing the nap to one cycle of nighttime sleep. These findings suggest that longer daytime naps, with both SWS and REM, may provide similar cardiovascular benefits as nocturnal sleep. In light of the on-going debate surrounding the health benefits and/or risks associated with napping, these results suggest that longer daytime naps in young, healthy adults may support cardiac down-regulation similar to nighttime sleep. In addition, napping paradigms may serve as tools to explore sleep-related changes in autonomic activity in both healthy and at-risk populations.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 52-57"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.03.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian rhythm and sleep-wake systems share the dynamic extracellular synaptic milieu","authors":"Joanna M. Cooper,&nbsp;Kathryn A. Halter,&nbsp;Rebecca A. Prosser","doi":"10.1016/j.nbscr.2018.04.001","DOIUrl":"10.1016/j.nbscr.2018.04.001","url":null,"abstract":"<div><p>The mammalian circadian and sleep-wake systems are closely aligned through their coordinated regulation of daily activity patterns. Although they differ in their anatomical organization and physiological processes, they utilize overlapping regulatory mechanisms that include an assortment of proteins and molecules interacting within the extracellular space. These extracellular factors include proteases that interact with soluble proteins, membrane-attached receptors and the extracellular matrix; and cell adhesion molecules that can form complex scaffolds connecting adjacent neurons, astrocytes and their respective intracellular cytoskeletal elements. Astrocytes also participate in the dynamic regulation of both systems through modulating neuronal appositions, the extracellular space and/or through release of gliotransmitters that can further contribute to the extracellular signaling processes. Together, these extracellular elements create a system that integrates rapid neurotransmitter signaling across longer time scales and thereby adjust neuronal signaling to reflect the daily fluctuations fundamental to both systems. Here we review what is known about these extracellular processes, focusing specifically on areas of overlap between the two systems. We also highlight questions that still need to be addressed. Although we know many of the extracellular players, far more research is needed to understand the mechanisms through which they modulate the circadian and sleep-wake systems.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 15-36"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.04.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mathematical modeling of sleep state dynamics in a rodent model of shift work","authors":"Michael J. Rempe ,&nbsp;Janne Grønli ,&nbsp;Torhild Thue Pedersen ,&nbsp;Jelena Mrdalj ,&nbsp;Andrea Marti ,&nbsp;Peter Meerlo ,&nbsp;Jonathan P. Wisor","doi":"10.1016/j.nbscr.2018.04.002","DOIUrl":"10.1016/j.nbscr.2018.04.002","url":null,"abstract":"<div><p>Millions of people worldwide are required to work when their physiology is tuned for sleep. By forcing wakefulness out of the body’s normal schedule, shift workers face numerous adverse health consequences, including gastrointestinal problems, sleep problems, and higher rates of some diseases, including cancers. Recent studies have developed protocols to simulate shift work in rodents with the intention of assessing the effects of night-shift work on subsequent sleep (Grønli et al., 2017). These studies have already provided important contributions to the understanding of the metabolic consequences of shift work (<span>Arble et al., 2015</span>; <span>Marti et al., 2016</span>; <span>Opperhuizen et al., 2015</span>) and sleep-wake-specific impacts of night-shift work (Grønli et al., 2017). However, our understanding of the causal mechanisms underlying night-shift-related sleep disturbances is limited. In order to advance toward a mechanistic understanding of sleep disruption in shift work, we model these data with two different approaches. First we apply a simple homeostatic model to quantify differences in the rates at which sleep need, as measured by slow wave activity during slow wave sleep (SWS) rises and falls. Second, we develop a simple and novel mathematical model of rodent sleep and use it to investigate the timing of sleep in a simulated shift work protocol (Grønli et al., 2017). This mathematical framework includes the circadian and homeostatic processes of the two-process model, but additionally incorporates a stochastic process to model the polyphasic nature of rodent sleep. By changing only the time at which the rodents are forced to be awake, the model reproduces some key experimental results from the previous study, including correct proportions of time spent in each stage of sleep as a function of circadian time and the differences in total wake time and SWS bout durations in the rodents representing night-shift workers and those representing day-shift workers. Importantly, the model allows for deeper insight into circadian and homeostatic influences on sleep timing, as it demonstrates that the differences in SWS bout duration between rodents in the two shifts is largely a circadian effect. Our study shows the importance of mathematical modeling in uncovering mechanisms behind shift work sleep disturbances and it begins to lay a foundation for future mathematical modeling of sleep in rodents.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 37-51"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.04.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of sleep duration and sleep disordered breathing in gestational diabetes mellitus","authors":"Joshua J. Gooley,&nbsp;Litali Mohapatra,&nbsp;Derek Chao Kuan Twan","doi":"10.1016/j.nbscr.2017.11.001","DOIUrl":"10.1016/j.nbscr.2017.11.001","url":null,"abstract":"<div><p>Many women experience sleep problems during pregnancy. This includes difficulty initiating and maintaining sleep due to physiologic changes that occur as pregnancy progresses, as well as increased symptoms of sleep-disordered breathing (SDB). Growing evidence indicates that sleep deficiency alters glucose metabolism and increases risk of diabetes. Poor sleep may exacerbate the progressive increase in insulin resistance that normally occurs during pregnancy, thus contributing to the development of maternal hyperglycemia. Here, we critically review evidence that exposure to short sleep duration or SDB during pregnancy is associated with gestational diabetes mellitus (GDM). Several studies have found that the frequency of GDM is higher in women exposed to short sleep compared with longer sleep durations. Despite mixed evidence regarding whether symptoms of SDB (e.g., frequent snoring) are associated with GDM after adjusting for BMI or obesity, it has been shown that clinically-diagnosed SDB is prospectively associated with GDM. There are multiple mechanisms that may link sleep deprivation and SDB with insulin resistance, including increased levels of oxidative stress, inflammation, sympathetic activity, and cortisol. Despite emerging evidence that sleep deficiency and SDB are associated with increased risk of GDM, it has yet to be demonstrated that improving sleep in pregnant women (e.g., by extending sleep duration or treating SDB) protects against the development of hyperglycemia. If a causal relationship can be established, behavioral therapies for improving sleep can potentially be used to reduce the risk and burden of GDM.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 34-43"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.11.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential effects of diet composition and timing of feeding behavior on rat brown adipose tissue and skeletal muscle peripheral clocks","authors":"Paul de Goede ,&nbsp;Satish Sen ,&nbsp;Johanneke E. Oosterman ,&nbsp;Ewout Foppen ,&nbsp;Remi Jansen ,&nbsp;Susanne E. la Fleur ,&nbsp;Etienne Challet ,&nbsp;Andries Kalsbeek","doi":"10.1016/j.nbscr.2017.09.002","DOIUrl":"10.1016/j.nbscr.2017.09.002","url":null,"abstract":"<div><p>The effects of feeding behavior and diet composition, as well as their possible interactions, on daily (clock) gene expression rhythms have mainly been studied in the liver, and to a lesser degree in white adipose tissue (WAT), but hardly in other metabolic tissues such as skeletal muscle (SM) and brown adipose tissues (BAT). We therefore subjected male Wistar rats to a regular chow or free choice high-fat-high sugar (fcHFHS) diet in combination with time restricted feeding (TRF) to either the light or dark phase. In SM, all tested clock genes lost their rhythmic expression in the chow light fed group. In the fcHFHS light fed group rhythmic expression for some, but not all, clock genes was maintained, but shifted by several hours. In BAT the daily rhythmicity of clock genes was maintained for the light fed groups, but expression patterns were shifted as compared with <em>ad libitum</em> and dark fed groups, whilst the fcHFHS diet made the rhythmicity of clock genes become more pronounced. Most of the metabolic genes in BAT tissue tested did not show any rhythmic expression in either the chow or fcHFHS groups. In SM <em>Pdk4</em> and <em>Ucp3</em> were phase-shifted, but remained rhythmically expressed in the chow light fed groups. Rhythmic expression was lost for <em>Ucp3</em> whilst on the fcHFHS diet during the light phase. In summary, both feeding at the wrong time of day and diet composition disturb the peripheral clocks in SM and BAT, but to different degrees and thereby result in a further desynchronization between metabolically active tissues such as SM, BAT, WAT and liver.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 24-33"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.09.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute sleep disruption- and high-fat diet-induced hypothalamic inflammation are not related to glucose tolerance in mice","authors":"Jacqueline M. Ho ,&nbsp;Nicole H. Ducich ,&nbsp;Nhat-Quynh K. Nguyen ,&nbsp;Mark R. Opp","doi":"10.1016/j.nbscr.2017.09.003","DOIUrl":"10.1016/j.nbscr.2017.09.003","url":null,"abstract":"<div><p>Chronic insufficient sleep is a major societal problem and is associated with increased risk of metabolic disease. Hypothalamic inflammation contributes to hyperphagia and weight gain in diet-induced obesity, but insufficient sleep-induced neuroinflammation has yet to be examined in relation to metabolic function. We therefore fragmented sleep of adult male C57BL/6<!--> <!-->J mice for 18<!--> <!-->h daily for 9 days to determine whether sleep disruption elicits inflammatory responses in brain regions that regulate energy balance and whether this relates to glycemic control. To additionally test the hypothesis that exposure to multiple inflammatory factors exacerbates metabolic outcomes, responses were compared in mice exposed to sleep fragmentation (SF), high-fat diet (HFD), both SF and HFD, or control conditions. Three or 9 days of high-fat feeding reduced glucose tolerance but SF alone did not. Transient loss of body mass in SF mice may have affected outcomes. Comparisons of pro-inflammatory cytokine concentrations among central and peripheral metabolic tissues indicate that patterns of liver interleukin-1β concentrations best reflects observed changes in glucose tolerance. However, we demonstrate that SF rapidly and potently increases Iba1 immunoreactivity (-ir), a marker of microglia. After 9 days of manipulations, Iba1-ir remains elevated only in mice exposed to both SF and HFD, indicating a novel interaction between sleep and diet on microglial activation that warrants further investigation.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 1-9"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.09.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36074087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}