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Author |
Ulgezen, Z.N.; Kapyla, T.; Meerlo, P.; Spoelstra, K.; Visser, M.E.; Dominoni, D.M. |
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Title |
The preference and costs of sleeping under light at night in forest and urban great tits |
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Journal Article |
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Year |
2019 |
Publication |
Proceedings. Biological Sciences |
Abbreviated Journal |
Proc Biol Sci |
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Volume  |
286 |
Issue |
1905 |
Pages |
20190872 |
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Keywords |
Animals |
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Abstract |
Artificial light at night (ALAN) is an increasing phenomenon associated with worldwide urbanization. In birds, broad-spectrum white ALAN can have disruptive effects on activity patterns, metabolism, stress response and immune function. There has been growing research on whether the use of alternative light spectra can reduce these negative effects, but surprisingly, there has been no study to determine which light spectrum birds prefer. To test such a preference, we gave urban and forest great tits (Parus major) the choice where to roost using pairwise combinations of darkness, white light or green dim light at night (1.5 lux). Birds preferred to sleep under artificial light instead of darkness, and green was preferred over white light. In a subsequent experiment, we investigated the consequence of sleeping under a particular light condition, and measured birds' daily activity levels, daily energy expenditure (DEE), oxalic acid as a biomarker for sleep debt and cognitive abilities. White light affected activity patterns more than green light. Moreover, there was an origin-dependent response to spectral composition: in urban birds, the total daily activity and night activity did not differ between white and green light, while forest birds were more active under white than green light. We also found that individuals who slept under white and green light had higher DEE. However, there were no differences in oxalic acid levels or cognitive abilities between light treatments. Thus, we argue that in naive birds that had never encountered light at night, white light might disrupt circadian rhythms more than green light. However, it is possible that the negative effects of ALAN on sleep and cognition might be observed only under intensities higher than 1.5 lux. These results suggest that reducing the intensity of light pollution as well as tuning the spectrum towards long wavelengths may considerably reduce its impact. |
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5 Institute of Biodiversity, Animal Health and Comparative Medicine, University of Glasgow , Glasgow , UK |
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0962-8452 |
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PMID:31213184; PMCID:PMC6599990 |
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GFZ @ kyba @ |
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2557 |
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Kernbach, M.E.; Newhouse, D.J.; Miller, J.M.; Hall, R.J.; Gibbons, J.; Oberstaller, J.; Selechnik, D.; Jiang, R.H.Y.; Unnasch, T.R.; Balakrishnan, C.N.; Martin, L.B. |
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Title |
Light pollution increases West Nile virus competence of a ubiquitous passerine reservoir species |
Type |
Journal Article |
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Year |
2019 |
Publication |
Proceedings. Biological Sciences |
Abbreviated Journal |
Proc Biol Sci |
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Volume |
286 |
Issue |
1907 |
Pages |
20191051 |
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Keywords |
Animals; Human Health; anthropogenic; ecoimmunology; host competence; light pollution; reservoir host |
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Abstract |
Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow (Passer domesticus), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas. |
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Center for Global Health Infectious Disease Research, University of South Florida, Tampa, FL 33620, USA |
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0962-8452 |
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PMID:31337318; PMCID:PMC6661335 |
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GFZ @ kyba @ |
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2611 |
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Dananay, K.L.; Benard, M.F. |
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Title |
Artificial light at night decreases metamorphic duration and juvenile growth in a widespread amphibian |
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Journal Article |
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Year |
2018 |
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Proceedings of the Royal Society B: Biological Sciences |
Abbreviated Journal |
Proc. R. Soc. B |
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285 |
Issue |
1882 |
Pages |
20180367 |
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Animals |
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Artificial light at night (ALAN) affects over 20% of the earth's surface and is estimated to increase 6% per year. Most studies of ALAN have focused on a single mechanism or life stage. We tested for indirect and direct ALAN effects that occurred by altering American toads' (Anaxyrus americanus) ecological interactions or by altering toad development and growth, respectively. We conducted an experiment over two life stages using outdoor mesocosms and indoor terraria. In the first phase, the presence of ALAN reduced metamorphic duration and periphyton biomass. The effects of ALAN appeared to be mediated through direct effects on toad development, and we found no evidence for indirect effects of ALAN acting through altered ecological interactions or colonization. In the second phase, post-metamorphic toad growth was reduced by 15% in the ALAN treatment. Juvenile-stage ALAN also affected toad activity: in natural light, toads retreated into leaf litter at night whereas ALAN toads did not change behaviour. Carry-over effects of ALAN were also present; juvenile toads that had been exposed to larval ALAN exhibited marginally increased activity. In this time frame and system, our experiments suggested ALAN's effects act primarily through direct effects, rather than indirect effects, and can persist across life stages. |
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0962-8452 |
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GFZ @ kyba @ |
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1951 |
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Bullock, B.; McGlashan, E.M.; Burns, A.C.; Lu, B.S.; Cain, S.W. |
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Title |
Traits related to bipolar disorder are associated with an increased post-illumination pupil response |
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Journal Article |
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Year |
2019 |
Publication |
Psychiatry Research |
Abbreviated Journal |
Psychiatry Res |
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278 |
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35-41 |
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Human Health |
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Mood states in bipolar disorder appear to be closely linked to changes in sleep and circadian function. It has been suggested that hypersensitivity of the circadian system to light may be a trait vulnerability for bipolar disorder. Healthy persons with emotional-behavioural traits associated with bipolar disorder also appear to exhibit problems with circadian rhythms, which may be associated with individual differences in light sensitivity. This study investigated the melanopsin-driven post-illumination pupil response (PIPR) in relation to emotional-behavioural traits associated with bipolar disorder (measured with the General Behavior Inventory) in a non-clinical group (n=61). An increased PIPR was associated with increased bipolar disorder-related traits. Specifically, the hypomania scale of the General Behavior Inventory was associated with an increased post-blue PIPR. Further, both the full hypomania and shortened '7 Up' scales were significantly predicted by PIPR, after age, sex and depressive traits were controlled. These findings suggest that increased sensitivity to light may be a risk factor for mood problems in the general population, and support the idea that hypersensitivity to light is a trait vulnerability for, rather than symptom of, bipolar disorder. |
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School of Psychological Sciences and Turner Institute for Brain and Mental Health, Monash University, Melbourne, VIC, Australia. Electronic address: sean.cain@monash.edu |
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0165-1781 |
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PMID:31136914 |
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GFZ @ kyba @ |
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2510 |
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Author |
Arendt, J.; Middleton, B. |
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Title |
Human seasonal and circadian studies in Antarctica (Halley, 75 degrees S) |
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Journal Article |
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Year |
2018 |
Publication |
General and Comparative Endocrinology |
Abbreviated Journal |
Gen Comp Endocrinol |
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258 |
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250-258 |
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Keywords |
Human Activities; Acclimatization/*physiology; Actigraphy; Adult; Antarctic Regions; Behavior/*physiology; Circadian Rhythm/*physiology; Darkness; Female; Heart Rate/physiology; Humans; Libido; Light; Male; Melatonin/blood; Photoperiod; *Seasons; Sleep/physiology; Young Adult; *Antarctica; *Circadian; *Light; *Melatonin; *Seasonal |
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Living for extended periods in Antarctica exposes base personnel to extremes of daylength (photoperiod) and temperature. At the British Antarctic Survey base of Halley, 75 degrees S, the sun does not rise for 110 d in the winter and does not set for 100 d in summer. Photoperiod is the major time cue governing the timing of seasonal events such as reproduction in many species. The neuroendocrine signal providing photoperiodic information to body physiology is the duration of melatonin secretion which reflects the length of the night: longer in the short days of winter and shorter in summer. Light of sufficient intensity and spectral composition serves to suppress production of melatonin and to set the circadian timing and the duration of the rhythm. In humans early observations suggested that bright (>2000 lux) white light was needed to suppress melatonin completely. Shortly thereafter winter depression (Seasonal Affective Disorder or SAD) was described, and its successful treatment by an artificial summer photoperiod of bright white light, sufficient to shorten melatonin production. At Halley dim artificial light intensity during winter was measured, until 2003, at a maximum of approximately 500 lux in winter. Thus a strong seasonal and circadian time cue was absent. It seemed likely that winter depression would be common in the extended period of winter darkness and could be treated with an artificial summer photoperiod. These observations, and predictions, inspired a long series of studies regarding human seasonal and circadian status, and the effects of light treatment, in a small overwintering, isolated community, living in the same conditions for many months at Halley. We found little evidence of SAD, or change in duration of melatonin production with season. However the timing of the melatonin rhythm itself, and/or that of its metabolite 6-sulphatoxymelatonin (aMT6s), was used as a primary marker of seasonal, circadian and treatment changes. A substantial phase delay of melatonin in winter was advanced to summer phase by a two pulse 'skeleton' bright white light treatment. Subsequently a single morning pulse of bright white light was effective with regard to circadian phase and improved daytime performance. The circadian delay evidenced by melatonin was accompanied by delayed sleep (logs and actigraphy): poor sleep is a common complaint in Polar regions. Appropriate extra artificial light, both standard white, and blue enriched, present throughout the day, effectively countered delay in sleep timing and the aMT6s rhythm. The most important factor appeared to be the maximum light experienced. Another manifestation of the winter was a decline in self-rated libido (men only on base at this time). Women on the base showed lower aspects of physical and mental health compared to men. Free-running rhythms were seen in some subjects following night shift, but were rarely found at other times, probably because this base has strongly scheduled activity and leisure time. Complete circadian adaptation during a week of night shift, also seen in a similar situation on North Sea oil rigs, led to problems readapting back to day shift in winter, compared to summer. Here again timed light treatment was used to address the problem. Sleep, alertness and waking performance are critically dependent on optimum circadian phase. Circadian desynchrony is associated with increased risk of major disease in shift workers. These studies provide some groundwork for countering/avoiding circadian desynchrony in rather extreme conditions. |
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Biochemistry and Physiology, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7XH, UK. Electronic address: b.middleton@surrey.ac.uk |
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0016-6480 |
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PMID:28526480 |
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IDA @ john @ |
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2248 |
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