Acute exposure to evening blue-enriched light impacts on human sleep.

Light in the short wavelength range (blue light: 446-483 nm) elicits direct effects on human melatonin secretion, alertness and cognitive performance via non-image-forming photoreceptors. However, the impact of blue-enriched polychromatic light on human sleep architecture and sleep electroencephalographic activity remains fairly unknown. In this study we investigated sleep structure and sleep electroencephalographic characteristics of 30 healthy young participants (16 men, 14 women; age range 20-31 years) following 2 h of evening light exposure to polychromatic light at 6500 K, 2500 K and 3000 K. Sleep structure across the first three non-rapid eye movement non-rapid eye movement - rapid eye movement sleep cycles did not differ significantly with respect to the light conditions. All-night non-rapid eye movement sleep electroencephalographic power density indicated that exposure to light at 6500 K resulted in a tendency for less frontal non-rapid eye movement electroencephalographic power density, compared to light at 2500 K and 3000 K. The dynamics of non-rapid eye movement electroencephalographic slow wave activity (2.0-4.0 Hz), a functional index of homeostatic sleep pressure, were such that slow wave activity was reduced significantly during the first sleep cycle after light at 6500 K compared to light at 2500 K and 3000 K, particularly in the frontal derivation. Our data suggest that exposure to blue-enriched polychromatic light at relatively low room light levels impacts upon homeostatic sleep regulation, as indexed by reduction in frontal slow wave activity during the first non-rapid eye movement episode.

Retinorecipient areas in the common marmoset (Callithrix jacchus): An image-forming and non-image forming circuitry.

The mammalian retina captures a multitude of diverse features from the external environment and conveys them via the optic nerve to a myriad of retinorecipient nuclei. Understanding how retinal signals act in distinct brain functions is one of the most central and established goals of neuroscience. Using the common marmoset (Callithrix jacchus), a monkey from Northeastern Brazil, as an animal model for parsing how retinal innervation works in the brain, started decades ago due to their marmoset's small bodies, rapid reproduction rate, and brain features. In the course of that research, a large amount of new and sophisticated neuroanatomical techniques was developed and employed to explain retinal connectivity. As a consequence, image and non-image-forming regions, functions, and pathways, as well as retinal cell types were described. Image-forming circuits give rise directly to vision, while the non-image-forming territories support circadian physiological processes, although part of their functional significance is uncertain. Here, we reviewed the current state of knowledge concerning retinal circuitry in marmosets from neuroanatomical investigations. We have also highlighted the aspects of marmoset retinal circuitry that remain obscure, in addition, to identify what further research is needed to better understand the connections and functions of retinorecipient structures.

In a Heartbeat: Light and Cardiovascular Physiology.

Light impinging on the retina fulfils a dual function: it serves for vision and it is required for proper entrainment of the endogenous circadian timing system to the 24-h day, thus influencing behaviors that promote health and optimal quality of life but are independent of image formation. The circadian pacemaker located in the suprachiasmatic nuclei modulates the cardiovascular system with an intrinsic ability to anticipate morning solar time and with a circadian nature of adverse cardiovascular events. Here, we infer that light exposure might affect cardiovascular function and provide evidence from existing research. Findings show a time-of-day dependent increase in relative sympathetic tone associated with bright light in the morning but not in the evening hours. Furthermore, dynamic light in the early morning hours can reduce the deleterious sleep-to-wake evoked transition on cardiac modulation. On the contrary, effects of numerous light parameters, such as illuminance level and wavelength of monochromatic light, on cardiac function are mixed. Therefore, in future research studies, light modalities, such as timing, duration, and its wavelength composition, should be taken in to account when testing the potential of light as a non-invasive countermeasure for adverse cardiovascular events.

Light modulation of human sleep depends on a polymorphism in the clock gene Period3.

Non-image-forming (NIF) responses to light powerfully modulate human physiology. However, it remains scarcely understood how NIF responses to light modulate human sleep and its EEG hallmarks, and if there are differences across individuals. Here we investigated NIF responses to light on sleep in individuals genotyped for the PERIOD3 (PER3) variable-number tandem-repeat (VNTR) polymorphism. Eighteen healthy young men (20-28 years; mean ± SEM: 25.9 ± 1.2) homozygous for the PER3 polymorphism were matched by age, body-mass index, and ethnicity. The study protocol comprised a balanced cross-over design during the winter, during which participants were exposed to either light of 40 lx at 6,500 K (blue-enriched) or light at 2,500 K (non-blue enriched), during 2h in the evening. Compared to light at 2,500 K, light at 6,500 K induced a significant increase in all-night NREM sleep slow-wave activity (SWA: 1.0-4.5 Hz) in the occipital cortex for PER3(5/5) individuals, but not for PER3(4/4) volunteers. Dynamics of SWA across sleep cycles revealed increased occipital NREM sleep SWA for virtually all sleep episode only for PER3(5/5) individuals. Furthermore, they experienced light at 6,500 K as significantly brighter. Intriguingly, this subjective perception of brightness significantly predicted their increased occipital SWA throughout the sleep episode. Our data indicate that humans homozygous for the PER3(5/5) allele are more sensitive to NIF light effects, as indexed by specific changes in sleep EEG activity. Ultimately, individual differences in NIF light responses on sleep may depend on a clock gene polymorphism involved in sleep-wake regulation.