scholarly journals Fundamentals of circadian entrainment by light

2021 ◽  
Vol 53 (5) ◽  
pp. 377-393
Author(s):  
RG Foster

Light at dawn and dusk is the key signal for the entrainment of the circadian clock. Light at dusk delays the clock. Light at dawn advances the clock. The threshold for human entrainment requires relatively bright light for a long duration, but the precise irradiance/duration relationships for photoentrainment have yet to be fully defined. Photoentrainment is achieved by a network of photosensitive retinal ganglion cells (pRGCs) which utilise the short-wavelength light-sensitive photopigment, melanopsin. Although rods and cones are not required, they do play a role in photoentrainment, by projecting to and modulating the endogenous photosensitivity of the pRGCs, but in a manner that remains poorly understood. It is also important to emphasise that the age and prior light exposure of an individual will modify the efficacy of entrainment stimuli. Because of the complexity of photoreceptor interactions, attempts to develop evidence-based human centric lighting are not straightforward. We need to study how humans respond to dynamic light exposure in the ‘real world’ where light intensity, duration, spectral quality and the time of exposure vary greatly. Defining these parameters will allow the development of electric lighting systems that will enhance human circadian entrainment.

2019 ◽  
Author(s):  
Manuel Spitschan ◽  
Rafael Lazar ◽  
Ebru Yetik ◽  
Christian Cajochen

Exposure to even moderately bright, short-wavelength light in the evening can strongly suppress the production of melatonin and can delay our circadian rhythm. These effects are mediated by the retinohypothalamic pathway, connecting a subset of retinal ganglion cells to the circadian pacemaker in the suprachiasmatic nucleus (SCN) in the brain. These retinal ganglion cells directly express the photosensitive protein melanopsin, rendering them intrinsically photosensitive (ipRGCs). But ipRGCs also receive input from the classical photoreceptors — the cones and rods. Here, we examined whether the short-wavelength-sensitive (S) cones contribute to circadian photoreception by using lights which differed exclusively in the amount of S cone excitation by almost two orders of magnitude (ratio 1:83), but not in the excitation of long-wavelength-sensitive (L) and medium-wavelength-sensitive (M) cones, rods, and melanopsin. We find no evidence for a role of S cones in the acute alerting and melatonin supressing response to evening light exposure, pointing to an exclusive role of melanopsin in driving circadian responses.


Biology ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 180
Author(s):  
Russell G. Foster ◽  
Steven Hughes ◽  
Stuart N. Peirson

Light around twilight provides the primary entrainment signal for circadian rhythms. Here we review the mechanisms and responses of the mouse and human circadian systems to light. Both utilize a network of photosensitive retinal ganglion cells (pRGCs) expressing the photopigment melanopsin (OPN4). In both species action spectra and functional expression of OPN4 in vitro show that melanopsin has a λmax close to 480 nm. Anatomical findings demonstrate that there are multiple pRGC sub-types, with some evidence in mice, but little in humans, regarding their roles in regulating physiology and behavior. Studies in mice, non-human primates and humans, show that rods and cones project to and can modulate the light responses of pRGCs. Such an integration of signals enables the rods to detect dim light, the cones to detect higher light intensities and the integration of intermittent light exposure, whilst melanopsin measures bright light over extended periods of time. Although photoreceptor mechanisms are similar, sensitivity thresholds differ markedly between mice and humans. Mice can entrain to light at approximately 1 lux for a few minutes, whilst humans require light at high irradiance (>100’s lux) and of a long duration (>30 min). The basis for this difference remains unclear. As our retinal light exposure is highly dynamic, and because photoreceptor interactions are complex and difficult to model, attempts to develop evidence-based lighting to enhance human circadian entrainment are very challenging. A way forward will be to define human circadian responses to artificial and natural light in the “real world” where light intensity, duration, spectral quality, time of day, light history and age can each be assessed.


2003 ◽  
Vol 88 (9) ◽  
pp. 4502-4505 ◽  
Author(s):  
Steven W. Lockley ◽  
George C. Brainard ◽  
Charles A. Czeisler

The endogenous circadian oscillator in mammals, situated in the suprachiasmatic nuclei, receives environmental photic input from specialized subsets of photoreceptive retinal ganglion cells. The human circadian pacemaker is exquisitely sensitive to ocular light exposure, even in some people who are otherwise totally blind. The magnitude of the resetting response to white light depends on the timing, intensity, duration, number and pattern of exposures. We report here that the circadian resetting response in humans, as measured by the pineal melatonin rhythm, is also wavelength dependent. Exposure to 6.5 h of monochromatic light at 460 nm induces a two-fold greater circadian phase delay than 6.5 h of 555 nm monochromatic light of equal photon density. Similarly, 460 nm monochromatic light causes twice the amount of melatonin suppression compared to 555 nm monochromatic light, and is dependent on the duration of exposure in addition to wavelength. These studies demonstrate that the peak of sensitivity of the human circadian pacemaker to light is blue-shifted relative to the three-cone visual photopic system, the sensitivity of which peaks at ∼555 nm. Thus photopic lux, the standard unit of illuminance, is inappropriate when quantifying the photic drive required to reset the human circadian pacemaker.


2019 ◽  
pp. 178-216
Author(s):  
Gordon L. Fain

“Photoreception” is the ninth chapter of the book Sensory Transduction and begins with general mechanisms of light detection, photopigment activation, and the variety of pathways of phototransduction using the scallop eye as an example. There is then a thorough treatment of the photoreceptors of arthropods, particularly those of Limulus and Drosophila. Following a description of photoreceptor anatomy, the chapter describes transduction in these arthropods including photoreceptor channels and the role of Ca2+ in the regulation of gain and turnoff. It then proceeds to vertebrate rods and cones, with individual treatment of the topics of transduction in vertebrate photoreceptors, the ion channels of rods and cones, the description and measurement of the photocurrent, pathways responsible for shutting down the light response, light adaptation, pigment renewal, and the recovery of sensitivity after bright light exposure. It concludes with transduction in intrinsically photosensitive retinal ganglion cells.


2021 ◽  
Vol 11 ◽  
Author(s):  
Aki Kawasaki ◽  
Morgane Udry ◽  
Mohamad El Wardani ◽  
Mirjam Münch

Glaucoma damages retinal ganglion cells, including intrinsically photosensitive retinal ganglion cells (ipRGCs). These cells modulate various non-visual physiological and psychological functions which are modulated by light. In patients with glaucoma, we assessed the effect of daily bright light exposure (LE) on several melanopsin-dependent functions, such as the pupil constriction, circadian rest-activity cycles, sleep and subjective well-being including relaxation, alertness and mood. Twenty patients participated in the study (9 women, 11 men, mean age = 67.6 ± 7.5 y). Pupillometry was performed before the LE weeks and repeated on the last day of LE. The post-illumination pupil response (PIPR) was calculated as a proxy for melanopsin-dependent activation. Participants continuously wore an activity monitor and self-assessed sleep quality, well-being and visual comfort for 7 days before and during 4 weeks of daily bright LE (30 min to 10,000 lux polychromatic bright white light). After the LE, there was a significantly greater PIPR and higher subjective sleep quality when compared to the pre-LE week (p < 0.05), but no significant changes in 24-h rhythms or sleep parameters. A greater PIPR was correlated with an increase in circadian amplitude and higher inter-daily stability (derived from rest-activity cycles; p < 0.05). In a small group of patients with glaucoma, scheduled daily bright light exposure could improve subjective sleep quality. These findings highlight the importance to evaluate and maintain non-visual functions at different levels in patients with progressive loss of ipRGCs.


2010 ◽  
Vol 277 (1693) ◽  
pp. 2485-2492 ◽  
Author(s):  
Sei-ichi Tsujimura ◽  
Kazuhiko Ukai ◽  
Daisuke Ohama ◽  
Atsuo Nuruki ◽  
Kazutomo Yunokuchi

The recent discovery of melanopsin-containing retinal ganglion cells (mRGCs) has led to a fundamental reassessment of non-image forming processing, such as circadian photoentrainment and the pupillary light reflex. In the conventional view of retinal physiology, rods and cones were assumed to be the only photoreceptors in the eye and were, therefore, considered responsible for non-image processing. However, signals from mRGCs contribute to this non-image forming processing along with cone-mediated luminance signals; although both signals contribute, it is unclear how these signals are summed. We designed and built a novel multi-primary stimulation system to stimulate mRGCs independently of other photoreceptors using a silent-substitution technique within a bright steady background. The system allows direct measurements of pupillary functions for mRGCs and cones. We observed a significant change in steady-state pupil diameter when we varied the excitation of mRGC alone, with no change in luminance and colour. Furthermore, the change in pupil diameter induced by mRGCs was larger than that induced by a variation in luminance alone: that is, for a bright steady background, the mRGC signals contribute to the pupillary pathway by a factor of three times more than the L- and M-cone signals.


2020 ◽  
Vol 26 (4) ◽  
pp. 221-228
Author(s):  
Lisa L. Onega ◽  
Thomas W. Pierce

SUMMARYBright light therapy is an accepted and commonly used treatment for seasonal affective and circadian rhythm disorders. In the past 20 years, researchers have examined the effectiveness of bright light therapy in improving depression and agitation in older adults with dementia. This article provides clinicians with a summary of the neurophysiology of bright light therapy, bright light research considerations, an evidence-based bright light protocol, problems related to bright light therapy, and clinical implications for bright light therapy in older adults with dementia. Bright light exposure is a safe, non-pharmacological treatment that is currently underutilised in this population. Clinicians may find bright light therapy beneficial as a primary or adjunctive treatment in reducing depression and agitation in older adults with dementia.


2013 ◽  
Vol 111 ◽  
pp. 17-26 ◽  
Author(s):  
Jie Hong ◽  
Qiang Zeng ◽  
Huaizhou Wang ◽  
Debbie S. Kuo ◽  
William H. Baldridge ◽  
...  

2016 ◽  
Vol 283 (1845) ◽  
pp. 20162275 ◽  
Author(s):  
Shu K. E. Tam ◽  
Sibah Hasan ◽  
Steven Hughes ◽  
Mark W. Hankins ◽  
Russell G. Foster ◽  
...  

Acute light exposure exerts various effects on physiology and behaviour. Although the effects of light on brain network activity in humans are well demonstrated, the effects of light on cognitive performance are inconclusive, with the size, as well as direction, of the effect depending on the nature of the task. Similarly, in nocturnal rodents, bright light can either facilitate or disrupt performance depending on the type of task employed. Crucially, it is unclear whether the effects of light on behavioural performance are mediated via the classical image-forming rods and cones or the melanopsin-expressing photosensitive retinal ganglion cells. Here, we investigate the modulatory effects of light on memory performance in mice using the spontaneous object recognition task. Importantly, we examine which photoreceptors are required to mediate the effects of light on memory performance. By using a cross-over design, we show that object recognition memory is disrupted when the test phase is conducted under a bright light (350 lux), regardless of the light level in the sample phase (10 or 350 lux), demonstrating that exposure to a bright light at the time of test, rather than at the time of encoding, impairs performance. Strikingly, the modulatory effect of light on memory performance is completely abolished in both melanopsin-deficient and rodless–coneless mice. Our findings provide direct evidence that melanopsin-driven and rod/cone-driven photoresponses are integrated in order to mediate the effect of light on memory performance.


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