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Author Leise, T.L.; Goldberg, A.; Michael, J.; Montoya, G.; Solow, S.; Molyneux, P.; Vetrivelan, R.; Harrington, M.E.
Title Recurring circadian disruption alters circadian clock sensitivity to resetting Type Journal Article
Year 2018 Publication (down) The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages
Keywords Animals
Abstract A single phase advance of the light:dark (LD) cycle can temporarily disrupt synchrony of neural circadian rhythms within the suprachiasmatic nucleus (SCN) and between the SCN and peripheral tissues. Compounding this, modern life can involve repeated disruptive light conditions. To model chronic disruption to the circadian system, we exposed male mice to more than a month of a 20 h light cycle (LD10:10), which mice typically cannot entrain to. Control animals were housed under LD12:12. We measured locomotor activity and body temperature rhythms in vivo, and rhythms of PER2::LUC bioluminescence in SCN and peripheral tissues ex vivo. Unexpectedly, we discovered strong effects of the time of dissection on circadian phase of PER2::LUC bioluminescent rhythms, which varied across tissues. White adipose tissue was strongly reset by dissection, while thymus phase appeared independent of dissection timing. Prior light exposure impacted the SCN, resulting in strong resetting of SCN phase by dissection for mice housed under LD10:10, and weak phase shifts by time of dissection in SCN from control LD12:12 mice. These findings suggest that exposure to circadian disruption may desynchronize SCN neurons, increasing network sensitivity to perturbations. We propose that tissues with a weakened circadian network, such as the SCN under disruptive light conditions, or with little to no coupling, e.g., some peripheral tissues, will show increased resetting effects. In particular, exposure to light at inconsistent circadian times on a recurring weekly basis disrupts circadian rhythms and alters sensitivity of the SCN neural pacemaker to dissection time. This article is protected by copyright. All rights reserved.
Address Neuroscience Program, Smith College, Northampton, MA, 01063, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30269396 Approved no
Call Number GFZ @ kyba @ Serial 2036
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Author Vetter, C.
Title Circadian disruption: What do we actually mean? Type Journal Article
Year 2018 Publication (down) The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages in press
Keywords Human Health; Review
Abstract The circadian system regulates physiology and behavior. Acute challenges to the system, such as those experienced during travel across time zones, will eventually result in re-synchronization to the local environmental time cues, but this re-synchronization is oftentimes accompanied by adverse short-term consequences. When such challenges are experienced chronically, adaptation may not be achieved, as for example in the case of rotating night shift workers. The transient and chronic disturbance of the circadian system is most frequently referred to as “circadian disruption”, but many other terms have been proposed and used to refer to similar situations. It is now beyond doubt that the circadian system contributes to health and disease, emphasizing the need for clear terminology when describing challenges to the circadian system and their consequences. The goal of this review is to provide an overview of the terms used to describe disruption of the circadian system, discuss proposed quantifications of disruption in experimental and observational settings with a focus on human research, and highlight limitations and challenges of currently available tools. For circadian research to advance as a translational science, clear, operationalizable, and scalable quantifications of circadian disruption are key, as they will enable improved assessment and reproducibility of results, ideally ranging from mechanistic settings, including animal research, to large-scale randomized clinical trials. This article is protected by copyright. All rights reserved.
Address Department of Integrative Physiology, University of Colorado Boulder, Boulder, CO, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30402904 Approved no
Call Number GFZ @ kyba @ Serial 2057
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Author Zerbini, G.; Kantermann, T.; Merrow, M.
Title Strategies to decrease social jetlag: Reducing evening blue light advances sleep and melatonin Type Journal Article
Year 2018 Publication (down) The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages
Keywords Human Health
Abstract The timing of sleep is under the control of the circadian clock, which uses light to entrain to the external light-dark cycle. A combination of genetic, physiological and environmental factors produces individual differences in chronotype (entrained phase as manifest in sleep timing). A mismatch between circadian and societal (e.g., work) clocks leads to a condition called social jetlag, which is characterized by changing sleep times over work and free days and accumulation of sleep debt. Social jetlag, which is prevalent in late chronotypes, has been related to several health issues. One way to reduce social jetlag would be to advance the circadian clock via modifications of the light environment. We thus performed two intervention field studies to describe methods for decreasing social jetlag. One study decreased evening light exposure (via blue-light-blocking glasses) and the other used increased morning light (via the use of curtains). We measured behaviour as well as melatonin; the latter in order to validate that behaviour was consistent with this neuroendocrinological phase marker of the circadian clock. We found that a decrease in evening blue light exposure led to an advance in melatonin and sleep onset on workdays. Increased morning light exposure advanced neither melatonin secretion nor sleep timing. Neither protocol led to a significant change in social jetlag. Despite this, our findings show that controlling light exposure at home can be effective in advancing melatonin secretion and sleep, thereby helping late chronotypes to better cope with early social schedules.
Address Institute of Medical Psychology, LMU Munich, Munich, Germany
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30506899 Approved no
Call Number GFZ @ kyba @ Serial 2138
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Author Abbott, S.M.; Malkani, R.G.; Zee, P.C.
Title Circadian disruption and human health: A bidirectional relationship Type Journal Article
Year 2018 Publication (down) The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages
Keywords Human Health; Review
Abstract Circadian rhythm disorders have been classically associated with disorders of abnormal timing of the sleep-wake cycle, however circadian dysfunction can play a role in a wide range of pathology, ranging from the increased risk for cardiometabolic disease and malignancy in shift workers, prompting the need for a new field focused on the larger concept of circadian medicine. The relationship between circadian disruption and human health is bidirectional, with changes in circadian amplitude often preceding the classical symptoms of neurodegenerative disorders. As our understanding of the importance of circadian dysfunction in disease grows, we need to develop better clinical techniques for identifying circadian rhythms and also develop circadian based strategies for disease management. Overall this review highlights the need to bring the concept of time to all aspects of medicine, emphasizing circadian medicine as a prime example of both personalized and precision medicine.
Address Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:30549337 Approved no
Call Number GFZ @ kyba @ Serial 2154
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Author Weil, Z.M.; Fonken, L.K.; Walker, W.H. 2nd; Bumgarner, J.R.; Liu, J.A.; Melendez-Fernandez, O.H.; Zhang, N.; DeVries, A.C.; Nelson, R.J.
Title Dim Light at Night Exacerbates Stroke Outcome Type Journal Article
Year 2020 Publication (down) The European Journal of Neuroscience Abbreviated Journal Eur J Neurosci
Volume in press Issue Pages in press
Keywords Animals; Mcao; circadian rhythms; cytokines; light pollution; neuroinflammation; stroke
Abstract Circadian rhythms are endogenous biological cycles that synchronize physiology and behavior to promote optimal function. These ~24-hour internal rhythms are set to precisely 24 hours daily by exposure to the sun. However, the prevalence of night-time lighting has the potential to dysregulate these biological functions. Hospital patients may be particularly vulnerable to the consequences of light at night because of their compromised physiological state. A mouse model of stroke (middle cerebral artery occlusion; MCAO) was used to test the hypothesis that exposure to dim light at night impairs responses to a major insult. Stroke lesion size was substantially larger among animals housed in dLAN after reperfusion than animals maintained in dark nights. Mice housed in dLAN for three days after the stroke displayed increased post-stroke anxiety-like behavior. Overall, dLAN amplified pro-inflammatory pathways in the CNS, which may have exacerbated neuronal damage. Our results suggest that exposure to LAN is detrimental to stroke recovery.
Address Department of Neuroscience, Rockefeller Neuroscience Institute, West Virginia University School of Medicine, Morgantown, WV, 26506, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0953-816X ISBN Medium
Area Expedition Conference
Notes PMID:32691462 Approved no
Call Number GFZ @ kyba @ Serial 3089
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