Neurobiology of Sleep and Circadian Rhythms最新文献

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The neuron-specific interleukin-1 receptor accessory protein alters emergent network state properties in Vitro 神经元特异性白细胞介素-1受体辅助蛋白在体外改变突现网络状态特性
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2019-01-01 DOI: 10.1016/j.nbscr.2019.01.002
Joseph T. Nguyen , Dinuka Sahabandu , Ping Taishi , Mengran Xue , Kathryn Jewett , Cheryl Dykstra-Aiello , Sandip Roy , James M. Krueger
{"title":"The neuron-specific interleukin-1 receptor accessory protein alters emergent network state properties in Vitro","authors":"Joseph T. Nguyen ,&nbsp;Dinuka Sahabandu ,&nbsp;Ping Taishi ,&nbsp;Mengran Xue ,&nbsp;Kathryn Jewett ,&nbsp;Cheryl Dykstra-Aiello ,&nbsp;Sandip Roy ,&nbsp;James M. Krueger","doi":"10.1016/j.nbscr.2019.01.002","DOIUrl":"https://doi.org/10.1016/j.nbscr.2019.01.002","url":null,"abstract":"<div><p>Small <em>in vitro</em> neuronal/glial networks exhibit sleep-like states. Sleep regulatory substance interleukin-1β (IL1) signals via its type I receptor and a receptor accessory protein (AcP). AcP has a neuron-specific isoform called AcPb. After sleep deprivation, AcPb, but not AcP, upregulates in brain, and mice lacking AcPb lack sleep rebound. Herein we used action potentials (APs), AP burstiness, synchronization of electrical activity (SYN), and delta wave (0.5–3.75 Hz) power to characterize cortical culture network state. Homologous parameters are used <em>in vivo</em> to characterize sleep. Cortical cells from 1–2-day-old pups from AcP knockout (KO, lacking both AcP and AcPb), AcPb KO (lacking only AcPb), and wild type (WT) mice were cultured separately on multi-electrode arrays. Recordings of spontaneous activity were taken each day during days 4–14 <em>in vitro</em>. In addition, cultures were treated with IL1, or in separate experiments, stimulated electrically to determine evoked response potentials (ERPs). In AcP KO cells, the maturation of network properties accelerated compared to those from cells lacking only AcPb. In contrast, the lack of AcPb delayed spontaneous network emergence of sleep-linked properties. The addition of IL1 enhanced delta wave power in WT cells but not in AcP KO or AcPb KO cells. The ontology of electrically-induced ERPs was delayed in AcP KO cells. We conclude IL1 signaling has a critical role in the emergence of sleep-linked network behavior with AcP playing a dominant role in the slowing of development while AcPb enhances development rates of sleep-linked emergent network properties.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"6 ","pages":"Pages 35-43"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2019.01.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72117475","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}
引用次数: 10
Glucocorticoid and inflammatory reactivity to a repeated physiological stressor in insomnia disorder 失眠障碍中糖皮质激素和对重复生理应激源的炎症反应
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2019-01-01 DOI: 10.1016/j.nbscr.2018.06.001
J.K. Devine , S.M. Bertisch , H. Yang , J. Scott-Sutherland , A. Wilkins , V. Molina , K. Henrikson , M. Haack
{"title":"Glucocorticoid and inflammatory reactivity to a repeated physiological stressor in insomnia disorder","authors":"J.K. Devine ,&nbsp;S.M. Bertisch ,&nbsp;H. Yang ,&nbsp;J. Scott-Sutherland ,&nbsp;A. Wilkins ,&nbsp;V. Molina ,&nbsp;K. Henrikson ,&nbsp;M. Haack","doi":"10.1016/j.nbscr.2018.06.001","DOIUrl":"10.1016/j.nbscr.2018.06.001","url":null,"abstract":"<div><p>Despite known associations of insomnia disorder with alterations in cytokine and glucocorticoid (GC) production, neither the sensitivity of immune cells to a GC signal nor the reactivity of the hypothalamus-pituitary-adrenal (HPA) axis and inflammatory system to stress, or adaptation of these systems to repeated stress have been assessed in patients with insomnia. To investigate potential dysregulation in stress reactivity and adaptation to repeated exposure, a physiological stressor (the cold pressor test; CPT) was repeatedly administered to N = 20 participants with insomnia disorder (based on DSM-V, 18 females, age 30 ± 2.5 years) and N = 20 sex-matched healthy controls following an at-home actigraphy and in-laboratory PSG. HPA and inflammatory markers (serum cortisol, plasma interleukin [IL]-6) were measured at baseline/resting levels and following each of the three CPTs. In addition, sensitivity of monocytes to the synthetic GC dexamethasone was assessed in-vitro at baseline levels in order to examine the cortisol-IL-6 interplay at the cell level. Compared to healthy controls, individuals with insomnia disorder exhibited shorter sleep duration as assessed by actigraphy and PSG (p ≤ 0.05). HPA, but not inflammatory reactivity to the repeated CPT challenge was greater in insomnia disorder (p ≤ 0.05 for group effect), due to greater cortisol responses to the initial CPT (p ≤ 0.05). There were no between-group differences in the ability of the HPA to adapt to stress repetition nor in basal/resting levels of cortisol, IL-6, and GC sensitivity. These findings suggest that insomnia disorder potentiates HPA axis reactivity to initial/novel stressors, which may constitute a pathway underlying adverse health consequences in the long term.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"6 ","pages":"Pages 77-84"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.06.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37362397","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}
引用次数: 18
Investigating the relationships between hypothalamic volume and measures of circadian rhythm and habitual sleep in premanifest Huntington's disease 研究先兆亨廷顿病患者下丘脑体积与昼夜节律测量和习惯性睡眠之间的关系
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2019-01-01 DOI: 10.1016/j.nbscr.2018.07.001
Danielle M. Bartlett , Juan F. Domínguez D , Alvaro Reyes , Pauline Zaenker , Kirk W. Feindel , Robert U. Newton , Anthony J. Hannan , James A. Slater , Peter R. Eastwood , Alpar S. Lazar , Mel Ziman , Travis Cruickshank
{"title":"Investigating the relationships between hypothalamic volume and measures of circadian rhythm and habitual sleep in premanifest Huntington's disease","authors":"Danielle M. Bartlett ,&nbsp;Juan F. Domínguez D ,&nbsp;Alvaro Reyes ,&nbsp;Pauline Zaenker ,&nbsp;Kirk W. Feindel ,&nbsp;Robert U. Newton ,&nbsp;Anthony J. Hannan ,&nbsp;James A. Slater ,&nbsp;Peter R. Eastwood ,&nbsp;Alpar S. Lazar ,&nbsp;Mel Ziman ,&nbsp;Travis Cruickshank","doi":"10.1016/j.nbscr.2018.07.001","DOIUrl":"10.1016/j.nbscr.2018.07.001","url":null,"abstract":"<div><h3>Objective</h3><p>Pathological changes within the hypothalamus have been proposed to mediate circadian rhythm and habitual sleep disturbances in individuals with Huntington’s disease (HD). However, investigations examining the relationships between hypothalamic volume and circadian rhythm and habitual sleep in individuals with HD are sparse. This study aimed to comprehensively evaluate the relationships between hypothalamic pathology and circadian rhythm and habitual sleep disturbances in individuals with premanifest HD.</p></div><div><h3>Methods</h3><p>Thirty-two individuals with premanifest HD and twenty-nine healthy age- and gender-matched controls participated in this dual-site, cross-sectional study. Magnetic resonance imaging scans were performed to evaluate hypothalamic volume. Circadian rhythm and habitual sleep were assessed via measurement of morning and evening cortisol and melatonin levels, wrist-worn actigraphy, the Consensus Sleep Diary and sleep questionnaires. Information on mood, physical activity levels and body composition were also collected.</p></div><div><h3>Results</h3><p>Compared to healthy controls, individuals with premanifest HD displayed significantly reduced grey matter volume in the hypothalamus, decreased habitual sleep efficiency and increased awakenings; however, no alterations in morning cortisol or evening melatonin release were noted in individuals with premanifest HD. While differences in the associations between hypothalamic volume and cortisol and melatonin output existed in individuals with premanifest HD compared to healthy controls, no consistent associations were observed between hypothalamic volume and circadian rhythm or habitual sleep outcomes.</p></div><div><h3>Conclusion</h3><p>While significant differences in associations between hypothalamic volume and cortisol and melatonin existed between individuals with premanifest HD and healthy controls, no differences in circadian markers were observed between the groups. This suggests that circadian regulation is maintained despite hypothalamic pathology, perhaps via neural compensation. Longitudinal studies are required to further understand the relationships between the hypothalamus and circadian rhythm and habitual sleep disturbances in HD as the disease course lengthens.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"6 ","pages":"Pages 1-8"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359311","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}
引用次数: 28
Sleep and circadian defects in a Drosophila model of mitochondrial encephalomyopathy 线粒体脑肌病果蝇模型的睡眠和昼夜节律缺陷
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2019-01-01 DOI: 10.1016/j.nbscr.2019.01.003
Keri J. Fogle , Catherina L. Mobini , Abygail S. Paseos , Michael J. Palladino
{"title":"Sleep and circadian defects in a Drosophila model of mitochondrial encephalomyopathy","authors":"Keri J. Fogle ,&nbsp;Catherina L. Mobini ,&nbsp;Abygail S. Paseos ,&nbsp;Michael J. Palladino","doi":"10.1016/j.nbscr.2019.01.003","DOIUrl":"https://doi.org/10.1016/j.nbscr.2019.01.003","url":null,"abstract":"<div><p>Mitochondrial encephalomyopathies (ME) are complex, incurable diseases characterized by severe bioenergetic distress that can affect the function of all major organ systems but is especially taxing to neuromuscular tissues. Animal models of MEs are rare, but the <em>Drosophila ATP6</em><sup><em>1</em></sup> mutant is a stable, well-characterized genetic line that accurately models progressive human mitochondrial diseases such as Maternally-Inherited Leigh Syndrome (MILS), Neuropathy, Ataxia, and Retinitis Pigmentosa (NARP), and Familial Bilateral Striatal Necrosis (FBSN). While it is established that this model exhibits important hallmarks of ME, including excess cellular and mitochondrial reactive oxygen species, shortened lifespan, muscle degeneration, and stress-induced seizures, it is unknown whether it exhibits defects in sleep or circadian function. This is a clinically relevant question, as many neurological and neurodegenerative diseases are characterized by such disturbances, which can exacerbate other symptoms and worsen quality of life. Since <em>Drosophila</em> is highly amenable to sleep and circadian studies, we asked whether we could detect disease phenotypes in the circadian behaviors of <em>ATP6</em><sup><em>1</em></sup>. Indeed, we found that day-time and night-time activity and sleep are altered through disease progression, and that circadian patterns are disrupted at both the behavioral and neuronal levels. These results establish <em>ATP6</em><sup><em>1</em></sup> as an important model of sleep and circadian disruption in ME that can be studied mechanistically at the molecular, cellular, and behavioral level to uncover underlying pathophysiology and test novel therapies.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"6 ","pages":"Pages 44-52"},"PeriodicalIF":0.0,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2019.01.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72082744","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}
引用次数: 7
Circadian phase-shifting by light: Beyond photons 光的昼夜相移:超越光子
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.03.003
Sevag Kaladchibachi , David C. Negelspach , Fabian Fernandez
{"title":"Circadian phase-shifting by light: Beyond photons","authors":"Sevag Kaladchibachi ,&nbsp;David C. Negelspach ,&nbsp;Fabian Fernandez","doi":"10.1016/j.nbscr.2018.03.003","DOIUrl":"10.1016/j.nbscr.2018.03.003","url":null,"abstract":"<div><p>Circadian entrainment to the solar light:dark schedule is thought to be maintained by a simple photon counting method. According to this hypothesis, the pacemaker adjusts the phase of the body’s endogenous rhythms in accordance to the intensity and duration with which it encounters a perceived twilight signal. While previous data have generally supported the hypothesis, more recent analysis has codified other factors besides irradiance that influence the magnitude of resetting responses to light delivered within the same phase of the circadian cycle. In particular, the frequency with which light is alternated with darkness, or whether it’s packaged in millisecond flashes versus continuous blocks, can significantly alter the dose-response relationship. Here, we used a drosophilid model to test whether circadian photon-counting trends can be broken with light administration protocols spanning just 15 minutes. In the early part of the delay zone, a 15-min continuous light pulse was fragmented until it could no longer produce a full-magnitude shift of the flies’ locomotor activity rhythms. The remaining exposure was then reorganized along various fractionation schemes that employed pulses with different widths and interstimulus intervals. Our results suggest that the pacemaker integrates the phase-shifting effects of equiluminous light differently depending on the stimulus pattern with which light is made available. For example, despite having fewer photons, certain ratios of light and darkness could be optimized on a timescale of seconds and minutes so as to achieve pacemaker resetting close to par with steady luminance. These data provide further evidence that the circadian pacemaker’s responses to light entail more than photon counting and motivate continued discussion on how phototherapy can be best optimized in clinical practice to improve conditions linked to circadian impairment.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 8-14"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.03.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358823","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}
引用次数: 12
Dose response of acute cocaine on sleep/waking behavior in mice 急性可卡因对小鼠睡眠/清醒行为的剂量反应
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.02.001
Theresa E. Bjorness , Robert W. Greene
{"title":"Dose response of acute cocaine on sleep/waking behavior in mice","authors":"Theresa E. Bjorness ,&nbsp;Robert W. Greene","doi":"10.1016/j.nbscr.2018.02.001","DOIUrl":"10.1016/j.nbscr.2018.02.001","url":null,"abstract":"<div><p>Chronic cocaine use has been associated with sleep disturbances, both during active use periods and during withdrawal and abstinence. Acute cocaine also increases waking at the expense of slow wave sleep and Rapid Eye Movement in non-human subjects. However, the effects of acute cocaine on sleep/waking activity in mice, a rodent model commonly used in both sleep and addiction research due to its high genetic tractability, has yet to be investigated. Sleep/waking activity was measured via polysomnography following IP administration of three doses of cocaine (3.6, 9.6, 18 mg/kg) and vehicle control in male C57BL/6 mice. Cocaine dose-dependently increased sleep latency, increased waking time and increased fast EEG activity within waking. Increases in waking occurred primarily during the first hour following injection, followed by rebound SWS sleep. Sleep/waking activity normalized within a 24-hour period. As with humans and other rodents, cocaine dose dependently reduces sleep in a wildtype strain of mice commonly used in reward and addiction research.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 84-93"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.02.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359309","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}
引用次数: 5
Chronic social defeat stress suppresses locomotor activity but does not affect the free-running circadian period of the activity rhythm in mice 慢性社会失败应激抑制小鼠的运动活动,但不影响活动节律的自由运行昼夜周期
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.03.002
S.M. Ota , D. Suchecki , P. Meerlo
{"title":"Chronic social defeat stress suppresses locomotor activity but does not affect the free-running circadian period of the activity rhythm in mice","authors":"S.M. Ota ,&nbsp;D. Suchecki ,&nbsp;P. Meerlo","doi":"10.1016/j.nbscr.2018.03.002","DOIUrl":"10.1016/j.nbscr.2018.03.002","url":null,"abstract":"<div><p>In mammals, daily rhythms in behavior and physiology are under control of an endogenous clock or pacemaker located in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN assures an optimal temporal organization of internal physiological process and also synchronizes rhythms in physiology and behavior to the cyclic environment. The SCN receives direct light input from the retina, which is capable of resetting the master clock and thereby synchronizes internally driven rhythms to the external light-dark cycle. In keeping with its function as a clock and pacemaker, the SCN appears to be well buffered against influences by other stimuli and conditions that contain no relevant timing information, such as acute stressors. On the other hand, it has been suggested that chronic forms of stress may have gradually accumulating effects that can disturb normal clock function and thereby contribute to stress-related disorders. Therefore, in the present study we investigated whether chronic intermittent social stress affects the endogenous period and phase of the free-running activity rhythm in mice. Adult male mice were maintained in constant dim red light conditions and exposed to a daily 20 min social defeat stress session for 10 consecutive days, either during the first half of their activity phase or the first half of their resting phase. The overall amount of running wheel activity was strongly suppressed during the 10 days of social defeat, to about 50% of the activity in non-defeated control mice. Activity levels gradually normalized during post-defeat recovery days. Despite the strong suppression of activity in defeated animals, the endogenous free-running circadian period of the activity rhythm and the phase of activity onset were not affected. These findings are thus in agreement with earlier studies suggesting that the circadian pacemaker in the SCN that is driving the rhythmicity in activity is well-protected against stress. Even severe social defeat stress for 10 consecutive days, which has a major effect on the levels of activity, does not affect the pace of the endogenous clock.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 1-7"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.03.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358822","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}
引用次数: 12
Chronic circadian advance shifts abolish melatonin secretion for days in rats 在大鼠体内,慢性昼夜节律提前变化会使褪黑激素分泌中断数天
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.02.002
Gang Xu , Jon Dean , Tiecheng Liu , Fangyun Tian , Jimo Borjigin
{"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}
引用次数: 3
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 为果蝇时钟的“重大发现”做出贡献的思考:我们与2017年诺贝尔奖得主杰夫·霍尔、迈克尔·罗斯巴什和迈克·杨一起成为博士后的幸运之路
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.02.004
Kathleen K. Siwicki , Paul E. Hardin , Jeffrey L. Price
{"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}
引用次数: 4
Sleep homeostasis and the circadian clock: Do the circadian pacemaker and the sleep homeostat influence each other’s functioning? 睡眠内稳态和生物钟:昼夜节律起搏器和睡眠内稳态器相互影响对方的功能吗?
Neurobiology of Sleep and Circadian Rhythms Pub Date : 2018-06-01 DOI: 10.1016/j.nbscr.2018.02.003
Tom Deboer
{"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}
引用次数: 132
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