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-1β, 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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Our previous studies have shown that light at night (LAN) impaired cognitive performance and affected neurogenesis and neurochemistry in the cognition‐associated brain regions, particularly the hippocampus (HP) and lateral caudal nidopallium (NCL) of Indian house crows (Corvus splendens). Here, we examined the cytoarchitecture and mapped out the morphology of neurons and glia–neuron density in HP and NCL regions of crows that were first entrained to 12‐hr light (LL): 12‐hr darkness (LD) and then exposed to the light regime in which 12‐hr darkness was either replaced by daytime light (i.e., constant light, LL) or by dim light (i.e., dim light at night, dLAN), with controls continued on LD 12:12. Compared with LD, there was a significant decrease in the soma size, suggesting reduced neuronal plasticity without affecting the neuronal density of both HP and NCL of crows under LL and dLAN conditions. In parallel, we found a reduced number of glia cells and, hence, decreased glia–neuron ratio positively correlated with soma size in both, HP and NCL regions. These results for the first time demonstrate LAN‐induced negative effects on the brain cytoarchitecture of a diurnal species and give insight for possible influence on the brain health and functions in animals including humans that might be inadvertently exposed to LAN in an emerging night‐illuminated urban environment.

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The last 50 years have witnessed extraordinary discoveries in the field of circadian rhythms. However, there are still several mysteries that remain. One of these chronobiological mysteries is the circadian rhythm that is revealed by administration of stimulant drugs to rodents. Herein we describe the discovery of this circadian rhythm and its underlying oscillator, which is frequently called the methamphetamine-sensitive circadian oscillator, or MASCO. This oscillator is distinct from canonical circadian oscillators because it controls robust activity rhythms independently of the suprachiasmatic nucleus and circadian genes are not essential for its timekeeping. We discuss these fundamental properties of MASCO and integrate studies of strain, sex, and circadian gene mutations on MASCO. The anatomical loci of MASCO are not known, so it has not been possible thus far to discover its novel molecular timekeeping mechanism or its functional significance. However, studies in mutant mice suggest that genetic approaches can be used to identify the neural network involved in the rhythm generation of MASCO. We also discuss parallels between human and rodent studies that support our working hypothesis that a function of MASCO may be to regulate sleep-wake cycles.