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Author Bedrosian, T.A. (ed)
Title Circadian Disruption by Light at Night: Implications for Mood Type Book Whole
Year 2013 Publication Abbreviated Journal
Volume Issue Pages
Keywords circadian disruption; sleep; light at night; melanopsin; mood; mental health; Mood Disorders; epigenetics; red light
Abstract Life on Earth has adapted to a consistent 24-h solar cycle. Circadian rhythms in physiology and behavior remain synchronized to the environment using light as the most potent entraining cue. During the past century, however, the widespread adoption of electric light has led to `round-the-clock’ societies. Instead of aligning with the environment, individuals follow artificial and often erratic light cycles created by social and work schedules. In particular, exposure to artificial light at night (LAN), termed “light pollution”, has become pervasive over the past 100 years. Virtually every individual living in the U.S. and Europe experiences this aberrant light exposure, and moreover about 20% of the population performs shift work. LAN may disrupt physiological timekeeping, leading to dysregulation of internal processes and misalignment between behavior and the environment. Recent evidence suggests that individuals exposed to excessive LAN, such as night shift workers, have increased risk for depressive disorders, but the biological mechanism remains unspecified. In mammals, intrinsically photosensitive retinal ganglion cells (ipRGCs) project light information to (1) the suprachiasmatic nucleus (SCN) in the hypothalamus, regulating circadian rhythms, and (2) to limbic regions, putatively regulating mood. Thus, LAN has the potential to affect both circadian timekeeping and mood. In this dissertation, I present evidence from rodent studies supporting the novel hypothesis that night-time exposure to light disrupts circadian organization and contributes to depressed mood. First, I consider the physiological and behavioral consequences associated with unnatural exposure to LAN. The effects of LAN on circadian output are considered in terms of locomotor activity, the diurnal cortisol rhythm, and diurnal clock protein expression in the brain in Chapter 2. The influence of LAN on behavior and brain plasticity is discussed, with particular focus on depressive-like behavior (Chapter 3) and effects of SSRI treatment (Chapter 4). Effects of LAN on structural plasticity and gene expression in the brain are described, with emphasis on potential correlates of the depressive-like behavior observed under LAN in Chapter 5. Given the prevalence of LAN exposure and its importance, strategies for reversing the effects are offered. Specifically, eliminating LAN quickly reverses behavioral and physiological effects of exposure as described in Chapter 5. In Chapter 6 I report that administration of a pharmacological cytokine inhibitor prevents depressive-like behaviors in LAN, implicating brain inflammation in the behavioral effect. Finally, I demonstrate in Chapter 7 that exposure to red wavelength LAN reduces the effects on brain and behavior, suggesting that LAN acts through specific retinal pathways involving melanopsin. Taken together, these studies demonstrate the consequences of LAN, but also outline potential avenues for prevention or intervention.
Address Department of Neuroscience and The Institute for Behavioral Medicine Research The Ohio State University
Corporate Author Thesis Ph.D. thesis
Publisher Place of Publication Editor Bedrosian, T.A.
Language Summary Language 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 323
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Author Benedetto, M.M.; Guido, M.E.; Contin, M.A.
Title Non-Visual Photopigments Effects of Constant Light-Emitting Diode Light Exposure on the Inner Retina of Wistar Rats Type Journal Article
Year 2017 Publication Frontiers in Neurology Abbreviated Journal Front Neurol
Volume 8 Issue Pages 417
Keywords changes in retinal structure; light-emitting diode light; non-visual opsin localization; retinal degeneration models; retinal light damage
Abstract The retina is part of the central nervous system specially adapted to capture light photons and transmit this information to the brain through photosensitive retinal cells involved in visual and non-visual activities. However, excessive light exposure may accelerate genetic retinal diseases or induce photoreceptor cell (PRC) death, finally leading to retinal degeneration (RD). Light pollution (LP) caused by the characteristic use of artificial light in modern day life may accelerate degenerative diseases or promote RD and circadian desynchrony. We have developed a working model to study RD mechanisms in a low light environment using light-emitting diode (LED) sources, at constant or long exposure times under LP conditions. The mechanism of PRC death is still not fully understood. Our main goal is to study the biochemical mechanisms of RD. We have previously demonstrated that constant light (LL) exposure to white LED produces a significant reduction in the outer nuclear layer (ONL) by classical PRC death after 7 days of LL exposure. The PRCs showed TUNEL-positive labeling and a caspase-3-independent mechanism of cell death. Here, we investigate whether constant LED exposure affects the inner-retinal organization and structure, cell survival and the expression of photopigments; in particular we look into whether constant LED exposure causes the death of retinal ganglion cells (RGCs), of intrinsically photosensitive RGCs (ipRGCs), or of other inner-retinal cells. Wistar rats exposed to 200 lx of LED for 2 to 8 days (LL 2 and LL 8) were processed for histological and protein. The results show no differences in the number of nucleus or TUNEL positive RGCs nor inner structural damage in any of LL groups studied, indicating that LL exposure affects ONL but does not produce RGC death. However, the photopigments melanopsin (OPN4) and neuropsin (OPN5) expressed in the inner retina were seen to modify their localization and expression during LL exposure. Our findings suggest that constant light during several days produces retinal remodeling and ONL cell death as well as significant changes in opsin expression in the inner nuclear layer.
Address Centro de Investigaciones en Quimica Biologica de Cordoba (CIQUIBIC), CONICET, Universidad Nacional de Cordoba, Cordoba, Argentina
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 1664-2295 ISBN Medium
Area Expedition Conference
Notes PMID:28871236; PMCID:PMC5566984 Approved no
Call Number LoNNe @ kyba @ Serial 1711
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Author Berson, D.M.; Dunn, F.A.; Takao, M.
Title Phototransduction by retinal ganglion cells that set the circadian clock Type Journal Article
Year 2002 Publication Science (New York, N.Y.) Abbreviated Journal Science
Volume 295 Issue 5557 Pages 1070-1073
Keywords Human Health; Animals; Axons/ultrastructure; *Biological Clocks; *Circadian Rhythm; Dendrites/ultrastructure; Isoquinolines; Kinetics; Light; *Light Signal Transduction; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells/chemistry/cytology/*physiology; Rod Opsins/analysis/physiology; Suprachiasmatic Nucleus/cytology/*physiology
Abstract Light synchronizes mammalian circadian rhythms with environmental time by modulating retinal input to the circadian pacemaker-the suprachiasmatic nucleus (SCN) of the hypothalamus. Such photic entrainment requires neither rods nor cones, the only known retinal photoreceptors. Here, we show that retinal ganglion cells innervating the SCN are intrinsically photosensitive. Unlike other ganglion cells, they depolarized in response to light even when all synaptic input from rods and cones was blocked. The sensitivity, spectral tuning, and slow kinetics of this light response matched those of the photic entrainment mechanism, suggesting that these ganglion cells may be the primary photoreceptors for this system.
Address Department of Neuroscience, Brown University, Providence, RI, 02912 USA. David_Berson@brown.edu
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 0036-8075 ISBN Medium
Area Expedition Conference
Notes PMID:11834835 Approved no
Call Number LoNNe @ kagoburian @ Serial 720
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Author Bonmati-Carrion, M.; Arguelles-Prieto, R.; Martinez-Madrid, M.; Reiter, R.; Hardeland, R.; Rol, M.; Madrid, J.
Title Protecting the Melatonin Rhythm through Circadian Healthy Light Exposure Type Journal Article
Year 2014 Publication International Journal of Molecular Sciences Abbreviated Journal IJMS
Volume 15 Issue 12 Pages 23448-23500
Keywords human health; chronodisruption; circadian; light at night (LAN); melanopsin; melatonin
Abstract Currently, in developed countries, nights are excessively illuminated (light at night), whereas daytime is mainly spent indoors, and thus people are exposed to much lower light intensities than under natural conditions. In spite of the positive impact of artificial light, we pay a price for the easy access to light during the night: disorganization of our circadian system or chronodisruption (CD), including perturbations in melatonin rhythm. Epidemiological studies show that CD is associated with an increased incidence of diabetes, obesity, heart disease, cognitive and affective impairment, premature aging and some types of cancer. Knowledge of retinal photoreceptors and the discovery of melanopsin in some ganglion cells demonstrate that light intensity, timing and spectrum must be considered to keep the biological clock properly entrained. Importantly, not all wavelengths of light are equally chronodisrupting. Blue light, which is particularly beneficial during the daytime, seems to be more disruptive at night, and induces the strongest melatonin inhibition. Nocturnal blue light exposure is currently increasing, due to the proliferation of energy-efficient lighting (LEDs) and electronic devices. Thus, the development of lighting systems that preserve the melatonin rhythm could reduce the health risks induced by chronodisruption. This review addresses the state of the art regarding the crosstalk between light and the circadian system.
Address Department of Physiology, Faculty of Biology, University of Murcia, Murcia 30100, Spain
Corporate Author Thesis
Publisher MDPI Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1422-0067 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 1078
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Author Bullough, J.D.
Title Spectral Sensitivity Modeling and Nighttime Scene Brightness Perception Type Journal Article
Year 2014 Publication Leukos Abbreviated Journal Leukos
Volume 11 Issue 1 Pages 11-17
Keywords Vision; human vision; Melanopsin; Outdoor Lighting; Scene brightness; Spectral sensitivity; visual psychophysics
Abstract Brightness perception under different light sources is an important visual response, because it is related to perceptions of safety. A growing number of studies have been conducted to assess perceptions of scene brightness under light sources differing in spectral content, including results consistent with a role of melanopsin-containing, intrinsically photosensitive retinal ganglion cells in scene brightness. Data from recent studies of scene brightness perception at light levels experienced under nighttime driving conditions are used to compare different models of brightness perception. The data support a role of increased short-wavelength sensitivity for scene brightness perception and a provisional spectral sensitivity model that takes into account the possible influence of melanopsin-containing, intrinsically photoreceptive retinal ganglion cells is suggested as a basis for further investigation. The implications of such a model on brightness perception under several light sources used in transportation lighting are described.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1550-2724 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 1073
Permanent link to this record