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Author (up) Buijs, F.N.; Leon-Mercado, L.; Guzman-Ruiz, M.; Guerrero-Vargas, N.N.; Romo-Nava, F.; Buijs, R.M. url  doi
openurl 
  Title The Circadian System: A Regulatory Feedback Network of Periphery and Brain Type Journal Article
  Year 2016 Publication Physiology (Bethesda, Md.) Abbreviated Journal Physiology (Bethesda)  
  Volume 31 Issue 3 Pages 170-181  
  Keywords Human health; circadian rhythm; suprachiasmatic nucleus; brain; clock genes; SCN; review; circadian desynchronization; shiftwork  
  Abstract Circadian rhythms are generated by the autonomous circadian clock, the suprachiasmatic nucleus (SCN), and clock genes that are present in all tissues. The SCN times these peripheral clocks, as well as behavioral and physiological processes. Recent studies show that frequent violations of conditions set by our biological clock, such as shift work, jet lag, sleep deprivation, or simply eating at the wrong time of the day, may have deleterious effects on health. This infringement, also known as circadian desynchronization, is associated with chronic diseases like diabetes, hypertension, cancer, and psychiatric disorders. In this review, we will evaluate evidence that these diseases stem from the need of the SCN for peripheral feedback to fine-tune its output and adjust physiological processes to the requirements of the moment. This feedback can vary from neuronal or hormonal signals from the liver to changes in blood pressure. Desynchronization renders the circadian network dysfunctional, resulting in a breakdown of many functions driven by the SCN, disrupting core clock rhythms in the periphery and disorganizing cellular processes that are normally driven by the synchrony between behavior and peripheral signals with neuronal and humoral output of the hypothalamus. Consequently, we propose that the loss of synchrony between the different elements of this circadian network as may occur during shiftwork and jet lag is the reason for the occurrence of health problems.  
  Address Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, Ciudad Universitaria, Mexico; ruudbuijs(at)gmail.com  
  Corporate Author Thesis  
  Publisher American Physiological Society Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1548-9221 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:27053731 Approved no  
  Call Number IDA @ john @ Serial 1429  
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Author (up) Dominoni, D. url  doi
openurl 
  Title The effects of light pollution on biological rhythms of birds: an integrated, mechanistic perspective Type Journal Article
  Year 2015 Publication Journal of Ornithology Abbreviated Journal J. of Ornith.  
  Volume 156 Issue 1 Pages 409-418  
  Keywords Animals; Birds; Light pollution; Circadian rhythms; Annual rhythms; Chronodisruption; Melatonin; Deep brain photoreceptors; ipRGCs  
  Abstract Light pollution is considered a threat for biodiversity given the extent to which it can affect a vast number of behavioral and physiological processes in several species. This comes as no surprise as light is a fundamental, environmental cue through which organisms time their daily and seasonal activities, and alterations in the light environment have been found to affect profoundly the synchronization of the circadian clock, the endogenous mechanism that tracks and predicts variation in the external light/dark cycles. In this context, birds have been one of the most studied animal taxa, but our understanding of the effects of light pollution on the biological rhythms of avian species is mostly limited to behavioral responses. In order to understand which proximate mechanisms may be affected by artificial lights, we need an integrated perspective that focuses on light as a physiological signal, and especially on how photic information is perceived, decoded, and transmitted through the whole body. The aim of this review is to summarize the effects of light pollution on physiological and biochemical mechanisms that underlie changes in birds’ behavior, highlighting the current gaps in our knowledge and proposing future research avenues.  
  Address Institute of Biodiversity, Animal Health and Comparative Medicine, University of Glasgow, Glasgow, UK; davide.dominoni@glasgow.ac.uk  
  Corporate Author Thesis  
  Publisher Springer Place of Publication Editor  
  Language English Summary Language English Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN ISBN Medium  
  Area Expedition Conference  
  Notes Approved no  
  Call Number IDA @ john @ Serial 1167  
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Author (up) Leung, S.T.; McKinney, R.A.; Watt, A.J. url  doi
openurl 
  Title The impact of light during the night Type Journal Article
  Year 2019 Publication eLife Abbreviated Journal eLife  
  Volume 8 Issue Pages in press  
  Keywords Commentary; *brain development; *chicken; *light-at-night; *neuroscience; *pineal gland; *steroid  
  Abstract Exposing chicks to one hour of light during the night disrupts the release of a hormone that is needed by cells in the developing brain to survive.  
  Address Department of Biology, McGill University, Montreal, Canada  
  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 2050-084X ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31714876; PMCID:PMC6850772 Approved no  
  Call Number GFZ @ kyba @ Serial 2795  
Permanent link to this record
 

 
Author (up) Vandewalle, G.; Maquet, P.; Dijk, D.-J. url  doi
openurl 
  Title Light as a modulator of cognitive brain function Type Journal Article
  Year 2009 Publication Trends in Cognitive Sciences Abbreviated Journal Trends Cogn Sci  
  Volume 13 Issue 10 Pages 429-438  
  Keywords Human Health; Animals; Brain/anatomy & histology/*physiology; Brain Mapping; Circadian Rhythm/*physiology; Cognition/*physiology; Diagnostic Imaging/methods; Humans; *Light; Melatonin/metabolism; Retina/anatomy & histology/physiology; Visual Pathways/anatomy & histology/physiology  
  Abstract Humans are a diurnal species usually exposed to light while engaged in cognitive tasks. Light not only guides performance on these tasks through vision but also exerts non-visual effects that are mediated in part by recently discovered retinal ganglion cells maximally sensitive to blue light. We review recent neuroimaging studies which demonstrate that the wavelength, duration and intensity of light exposure modulate brain responses to (non-visual) cognitive tasks. These responses to light are initially observed in alertness-related subcortical structures (hypothalamus, brainstem, thalamus) and limbic areas (amygdala and hippocampus), followed by modulations of activity in cortical areas, which can ultimately affect behaviour. Light emerges as an important modulator of brain function and cognition.  
  Address Cyclotron Research Centre, University of Liege, 8 Allee du 6 Aout, Batiment B30, B-4000 Liege, Belgium. gilles.vandewalle@umontreal.ca  
  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 1364-6613 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:19748817 Approved no  
  Call Number LoNNe @ kagoburian @ Serial 830  
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Author (up) Walker, W.H. 2nd; Borniger, J.C.; Gaudier-Diaz, M.M.; Hecmarie Melendez-Fernandez, O.; Pascoe, J.L.; Courtney DeVries, A.; Nelson, R.J. url  doi
openurl 
  Title Acute exposure to low-level light at night is sufficient to induce neurological changes and depressive-like behavior Type Journal Article
  Year 2019 Publication Molecular Psychiatry Abbreviated Journal Mol Psychiatry  
  Volume Issue Pages s41380-019-0430-4  
  Keywords Human health; physiology; brain  
  Abstract The advent and wide-spread adoption of electric lighting over the past century has profoundly affected the circadian organization of physiology and behavior for many individuals in industrialized nations; electric lighting in homes, work environments, and public areas have extended daytime activities into the evening, thus, increasing night-time exposure to light. Although initially assumed to be innocuous, chronic exposure to light at night (LAN) is now associated with increased incidence of cancer, metabolic disorders, and affective problems in humans. However, little is known about potential acute effects of LAN. To determine whether acute exposure to low-level LAN alters brain function, adult male, and female mice were housed in either light days and dark nights (LD; 14 h of 150 lux:10 h of 0 lux) or light days and low level light at night (LAN; 14 h of 150 lux:10 h of 5 lux). Mice exposed to LAN on three consecutive nights increased depressive-like responses compared to mice housed in dark nights. In addition, female mice exposed to LAN increased central tendency in the open field. LAN was associated with reduced hippocampal vascular endothelial growth factor-A (VEGF-A) in both male and female mice, as well as increased VEGFR1 and interleukin-1beta mRNA expression in females, and reduced brain derived neurotrophic factor mRNA in males. Further, LAN significantly altered circadian rhythms (activity and temperature) and circadian gene expression in female and male mice, respectively. Altogether, this study demonstrates that acute exposure to LAN alters brain physiology and can be detrimental to well-being in otherwise healthy individuals.  
  Address Department of Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, 26506, USA  
  Corporate Author Thesis  
  Publisher Nature Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 1359-4184 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:31138889 Approved no  
  Call Number IDA @ john @ Serial 2509  
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