Melanopsin Vision

Joyce, Daniel S.; Houser, Kevin W.; Peirson, Stuart N.; Zeitzer, Jamie M.; Zele, Andrew J.

doi:10.1017/9781009029865

Cited by 13 publications

(3 citation statements)

References 335 publications

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“…In addition to their effect on photoreceptor [88] and bipolar cell function [40], the amplification may involve excitatory glutamatergic amacrine cell feedback from ipRGCs to ganglion cells [86,89], through ipRGC axon collaterals to the inner plexiform layer [90] and/or via gap junctions to other ganglion cells [91,92]. At least 15 brain areas receive direct ipRGC projections to mediate the effects of light on visual and non-visual functions [93]. In macaques, a higher order cortico-geniculate feedback pathway could amplify the signal via excitatory glutamatergic feedback from cortical layer VI to the LGN in as little as 37 ms [94].…”

Section: Discussionmentioning

confidence: 99%

“…Spectrally tuning all five photoreceptor excitations [27] might itself provide a more practical experimental paradigm to evaluate time-of-day circadian effects systematically and efficiently in a laboratory setting, and to study afferent pathway modulation of higher order processes. It will be interesting to determine how the retinal and cortical melanopsin pathways modulate light-dependent effects on visual function and other electrophysiological signals, such as the electroencephalogram [93,98]. Although photometric luminance is the primary metric used in industry to specify the visual effectiveness of a light [99], we show that cone-mediated vision is also dependent on the ambient spectral and irradiance content of the light that drives the luxotonic melanopsin signal [38], independent of the photometric luminance and rod excitation, which is critical because melanopsin-rod-cone interactions have non-complementary effects on visual contrast sensitivity.…”

Section: Discussionmentioning

confidence: 99%

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Melanopsin-mediated amplification of cone signals in the human visual cortex

Adhikari,

Uprety,

Feigl

et al. 2024

Proc. R. Soc. B.

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The ambient daylight variation is coded by melanopsin photoreceptors and their luxotonic activity increases towards midday when colour temperatures are cooler, and irradiances are higher. Although melanopsin and cone photoresponses can be mediated via separate pathways, the connectivity of melanopsin cells across all levels of the retina enables them to modify cone signals. The downstream effects of melanopsin-cone interactions on human vision are however, incompletely understood. Here, we determined how the change in daytime melanopsin activation affects the human cone pathway signals in the visual cortex. A 5-primary silent-substitution method was developed to evaluate the dependence of cone-mediated signals on melanopsin activation by spectrally tuning the lights and stabilizing the rhodopsin activation under a constant cone photometric luminance. The retinal (white noise electroretinogram) and cortical responses (visual evoked potential) were simultaneously recorded with the photoreceptor-directed lights in 10 observers. By increasing the melanopsin activation, a reverse response pattern was observed with cone signals being supressed in the retina by 27% ( p = 0.03) and subsequently amplified by 16% ( p = 0.01) as they reach the cortex. We infer that melanopsin activity can amplify cone signals at sites distal to retinal bipolar cells to cause a decrease in the psychophysical Weber fraction for cone vision.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Melanopsin-mediated amplification of cone signals in the human visual cortex

Adhikari,

Uprety,

Feigl

et al. 2024

Proc. R. Soc. B.

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“…“Human-centric lighting” or “circadian lighting” represents a major recent push of the LED lighting industry toward products that in some way incorporate the recent knowledge on the NIF effects of light on human physiology. These claims can exceed the current state of knowledge ( Houser et al, 2021 ; Joyce et al, 2023 ), and to the consumer, it may not be obvious to what extent lighting solutions that are available on the market are indeed conducive to health. There are also subtleties of messaging that may not be understood by the consumer (e.g., that blue-enriched light is potentially harmful to circadian rhythms during the evening but potentially helpful during the day).…”

Section: Effects Of Light On Circadian Neuroendocrine and Sleep Physi...mentioning

confidence: 92%

Human-Centric Lighting Research and Policy in the Melanopsin Age

Spitschan,

Joyce

2023

Policy Insights from the Behavioral and Brain Sciences

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Beyond visual function, specialized light-sensitive retinal circuits involving the photopigment melanopsin drive critical aspects of human physiology and behavior, including sleep–wake rhythms, hormone production, mood, and cognition. Fundamental discoveries of visual neurobiology dating back to the 1990s have given rise to strong interest from the lighting industry in optimizing lighting to benefit health. Consequently, evidence-based recommendations, regulations, and policies need to translate current knowledge of neurobiology into practice. Here, reviewing recent advances in understanding of NIF circuits in humans leads to proposed strategies to optimize electric lighting. Highlighted knowledge gaps must be addressed urgently, as well as the challenge of developing personalized, adaptive NIF lighting interventions accounting for complex individual differences in physiology, behavior, and environment. Finally, lighting equity issues appear in the context of marginalized groups, who have traditionally been underserved in research on both fundamental visual processes and applied lighting. Biologically optimal light is a fundamental environmental right.

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Targeting sleep and the circadian system as a novel treatment strategy for Parkinson’s disease

Feigl,

Lewis,

Rawashdeh

2023

J Neurol

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There is a growing appreciation of the wide range of sleep–wake disturbances that occur frequently in Parkinson’s disease. These are known to be associated with a range of motor and non-motor symptoms and significantly impact not only on the quality of life of the patient, but also on their bed partner. The underlying causes for fragmented sleep and daytime somnolence are no doubt multifactorial but there is clear evidence for circadian disruption in Parkinson’s disease. This appears to be occurring not only as a result of the neuropathological changes that occur across a distributed neural network, but even down to the cellular level. Such observations indicate that circadian changes may in fact be a driver of neurodegeneration, as well as a cause for some of the sleep–wake symptoms observed in Parkinson’s disease. Thus, efforts are now required to evaluate approaches including the prescription of precision medicine to modulate photoreceptor activation ratios that reflect daylight inputs to the circadian pacemaker, the use of small molecules to target clock genes, the manipulation of orexin pathways that could help restore the circadian system, to offer novel symptomatic and novel disease modifying strategies.

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Melanopsin Vision

Cited by 13 publications

References 335 publications

Melanopsin-mediated amplification of cone signals in the human visual cortex

Melanopsin-mediated amplification of cone signals in the human visual cortex

Human-Centric Lighting Research and Policy in the Melanopsin Age

Targeting sleep and the circadian system as a novel treatment strategy for Parkinson’s disease

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