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Rodents are integral components of ecosystems as they provide several important ecosystem services. Despite their importance as prey, pollinators and seed distributors, African rodents are largely understudied. The effect of anthropogenic changes such as artificial light at night extends past urban areas to peri-urban and rural habitats, and can have profound effects on entire ecosystems. We investigated the effect of dim light at night (dLAN) on the locomotor activity rhythms of the African pygmy mouse (Mus minutoides). Pygmy mice showed a dramatic, intensity-dependent reduction in their locomotor activity when subjected to dLAN, which was accompanied by a delay in the activity onset. We also considered masking responses with a dark pulse (DP) during the day and a light pulse at night. All animals became inactive in response to a light pulse during the night, whereas approximately half of the animals showed activity during a DP in the day. Our results suggest that the African pygmy mouse is highly sensitive to light and that their activity is strongly masked by light. In their natural environment, vegetation could shield pygmy mice against high light levels; however, other anthropogenic disturbances can alter the behaviour of these animals and could affect their survival.

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Holometabolous insects exhibit complex life cycles in which both morphology and ecological niche change dramatically during development. In the larval stage, many insects have soft, slow-moving bodies and poor vision, limiting their ability to respond to environmental threats. Artificial light at night (ALAN) is an environmental perturbation known to severely impact the fitness of adult insects by disrupting both temporal and spatial orientation. The impact of ALAN on earlier life stages, however, is largely unknown. We conducted a series of laboratory experiments to investigate how two distinct forms of ALAN affect the development and movement of immature Photuris sp. and Photinus obscurellus fireflies. Although long-term exposure to dim light at night (dLAN), akin to urban skyglow, did not impact overall survivorship or duration of egg, larval, and pupal stages in either species, it did accelerate weight gain in early-instar Photuris larvae. Late-instar Photuris exposed to point sources of ALAN at the start of their nightly foraging period were also significantly more likely to burrow beneath the soil surface, rather than disperse across it. ALAN may therefore impede dispersal of firefly larvae away from illuminated areas, which could have downstream consequences for the reproductive fitness of adults.

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Artificial light, despite its widespread and valuable use, has been associated with deterioration of health and well-being, including altered circadian timing and sleep disturbances, particularly in nocturnal exposure. Recent findings from our lab reveal significant sleep and sleep electroencephalogram (EEG) changes owing to three months exposure to dim-light-at-night (DLAN). Aiming to further explore the detrimental effects of DLAN exposure, in the present study, we continuously recorded sleep EEG and the electromyogram for baseline 24-h and following 6-h sleep deprivation in a varied DLAN duration scheme. C57BL/6J mice were exposed to a 12:12 h light:DLAN cycle (75lux:5lux) vs. a 12:12 h light:dark cycle (75lux:0lux) for one day, one week, and one month. Our results show that sleep was already affected by a mere day of DLAN exposure with additional complications emerging with increasing DLAN exposure duration, such as the gradual delay of the daily 24-h vigilance state rhythms. We conducted detrended fluctuation analysis (DFA) on the locomotor activity data following 1-month and 3-month DLAN exposure, and a significantly less healthy rest-activity pattern, based on the decreased alpha values, was found in both conditions compared to the control light-dark. Taking into account the behavioral, sleep and the sleep EEG parameters, our data suggest that DLAN exposure, even in the shortest duration, induces deleterious effects; nevertheless, potential compensatory mechanisms render the organism partly adjustable and able to cope. We think that, for this reason, our data do not always depict linear divergence among groups, as compared with control conditions. Chronic DLAN exposure impacts the sleep regulatory system, but also brain integrity, diminishing its adaptability and reactivity, especially apparent in the sleep EEG alterations and particular low alpha values following DFA.

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The gastrointestinal tract (GIT) hosts a large number of diverse microorganisms, with mutualistic interactions with the host. Here, in two separate experiments, we investigated whether light at night (LAN) would affect GIT microbiota and, in turn, the host physiology in diurnal zebra finches (Taeniopygia guttata). Experiment I assessed the effects of no-night (LL) and dimly illuminated night (dim light at night, dLAN) on fecal microbiota diversity and host physiology of birds born and raised under 12 h photoperiod (LD; 12 h light: 12 h darkness). Under LL and dLAN, compared to LD, we found a significant increase in the body mass, subcutaneous fat deposition and hepatic accumulation of lipids. Although we found no difference in total 24 h food consumption, LL/ dLAN birds ate also at night, suggesting LAN-induced alteration in daily feeding times. Concurrently, there were marked differences in amplicon sequence and bacterial species richness between LD and LAN, with notable decline in Lactobacillus richness in birds under LL and dLAN. We attributed declined Lactobacillus population as causal (at least partially) to negative effects on the host metabolism. Therefore, in experiment II with similar protocol, birds under LL and dLAN were fed on diet with or without Lactobacillus rhamnosus GG (LGG) supplement. Clearly, LGG supplement ameliorated LL- and dLAN-induced negative effects in zebra finches. These results demonstrate adverse effects of unnatural lighting on GIT bacterial diversity and host physiology, and suggest the role of GIT microbiota in the maintenance of metabolic homeostasis in response to LAN environment in diurnal animals.

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Dim-light-at-night (DLAN) exposure is associated with health problems, such as metabolic disruptions, immunological modulations, oxidative stress, sleep problems, and altered circadian timing. Neurophysiological parameters, including sleep patterns, are altered in the course of aging in a similar way. Here, we investigated the effect of chronic (three months) DLAN exposure (12 L:12 Dim-light, 75:5 lux) on sleep and the sleep electroencephalogram (EEG), and rest-activity behavior in young (6-month-old, n = 9) and aged (18- n = 8, 24-month-old, n = 6) C57BL/6J mice and compared with age-matched controls (n = 11, n = 9 and n = 8, respectively). We recorded the EEG and electromyogram continuously for 48-h and conducted a 6-h sleep-deprivation. A delay in the phase angle of entrainment of locomotor activity and daily vigilance state rhythms was apparent in mice following DLAN exposure, throughout the whole age spectrum, rendering sleep characteristics similar among the three age DLAN groups and significantly different from the age-matched controls. Notably, slow-wave-activity in NREM sleep (SWA, EEG power density in 0.5-4.0 Hz) was differentially altered in young and aged DLAN mice. Particularly, SWA increased as a function of age, which was further accentuated following DLAN exposure. However, this was not found in the young DLAN animals, which were characterized by the lowest SWA levels. Concluding, long-term DLAN exposure induced more pronounced alterations in the sleep architecture of young mice, towards an aging phenotype, while it enhanced age-associated sleep changes in the older groups. Our data suggest that irrespective of age, chronic DLAN exposure deteriorates sleep behavior and may consequently impact general health.

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Artificial light at night induces circadian disruptions and causes cognitive impairment and mood disorders; yet very little is known about the neural and molecular correlates of these effects in diurnal animals. We manipulated the night environment and examined cellular and molecular changes in hippocampus, the brain region involved in cognition and mood, of Indian house crows (Corvus splendens) exposed to 12 hr light (150 lux): 12 hr darkness (0 lux). Diurnal corvids are an ideal model species with cognitive abilities at par with mammals. Dim light (6 lux) at night (dLAN) altered daily activity:rest pattern, reduced sleep, and induced depressive-like responses (decreased eating and self-grooming, self-mutilation, and reduced novel object exploration); return to an absolute dark night reversed these negative effects. dLAN suppressed nocturnal melatonin levels; however, diurnal corticosterone levels were unaffected. Concomitant reduction of immunoreactivity for DCX and BDNF suggested dLAN-induced suppression of hippocampal neurogenesis and compromised neuronal health. dLAN also negatively influenced hippocampal expression of genes associated with depressive-like responses (bdnf, il-1ß, tnfr1, nr4a2), but not of those associated with neuronal plasticity (egr1, creb, syngap, syn2, grin2a, grin2b), cellular oxidative stress (gst, sod3, cat1) and neuronal death (caspase2, caspase3, foxo3). Furthermore, we envisaged the role of BDNF and showed epigenetic modification of bdnf gene by decreased histone H3 acetylation and increased hdac4 expression under dLAN. These results demonstrate transcriptional and epigenetic bases of dLAN-induced negative effects in diurnal crows, and provide insights into the risks of exposure to illuminated nights to animals including humans in an urban setting.

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The accumulation and aggregation of phosphorylated tau proteins in the brain are the hallmarks for the onset of Alzheimer's disease (AD). In addition, disruptions in circadian rhythms (CRs) with altered sleep-wake cycles, dysregulation of locomotion, and increased memory defects have been reported in patients with AD. Drosophila flies that have an overexpression of human tau protein in neurons exhibit most of the symptoms of human patients with AD, including locomotion defects and neurodegeneration. Using the fly model for tauopathy/AD, we investigated the effects of an exposure to dim light at night on AD symptoms. We used a light intensity of 10 lux, which is considered the lower limit of light pollution in many countries. After the tauopathy flies were exposed to the dim light at night for 3 days, the flies showed disrupted CRs, altered sleep-wake cycles due to increased pTau proteins and neurodegeneration, in the brains of the AD flies. The results indicate that the nighttime exposure of tauopathy/AD model Drosophila flies to dim light disrupted CR and sleep-wake behavior and promoted neurodegeneration.

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Photoperiodic regulation of physiology, morphology, and behavior is crucial for many animals to survive seasonally variable conditions unfavorable for reproduction and survival. The photoperiodic response in mammals is mediated by nocturnal secretion of melatonin under the control of a circadian clock. However, artificial light at night caused by recent urbanization may disrupt the circadian clock, as well as the photoperiodic response by blunting melatonin secretion. Here we examined the effect of dim light at night (dLAN) (5lux of light during the dark phase) on locomotor activity rhythms and short-day regulation of reproduction, body mass, pelage properties, and immune responses of male Siberian hamsters. Short-day animals reduced gonadal and body mass, decreased spermatid nuclei and sperm numbers, molted to a whiter pelage, and increased pelage density compared to long-day animals. However, animals that experienced short days with dLAN did not show these short-day responses. Moreover, short-day specific immune responses were altered in dLAN conditions. The nocturnal activity pattern was blunted in dLAN hamsters, consistent with the observation that dLAN changed expression of the circadian clock gene, Period1. In addition, we demonstrated that expression levels of genes implicated in the photoperiodic response, Mel-1a melatonin receptor, Eyes absent 3, thyroid stimulating hormone receptor, gonadotropin-releasing hormone, and gonadotropin-inhibitory hormone, were higher in dLAN animals than those in short-day animals. These results suggest that dLAN disturbs the circadian clock function and affects the molecular mechanisms of the photoperiodic response.

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