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Journal articles on the topic 'Melanopsin'

Author: Grafiati

Published: 4 June 2021

Last updated: 24 January 2023

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1

Spitschan, Manuel, Andrew S. Bock, Jack Ryan, Giulia Frazzetta, David H. Brainard, and Geoffrey K. Aguirre. "The human visual cortex response to melanopsin-directed stimulation is accompanied by a distinct perceptual experience." Proceedings of the National Academy of Sciences 114, no. 46 (October 31, 2017): 12291–96. http://dx.doi.org/10.1073/pnas.1711522114.

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The photopigment melanopsin supports reflexive visual functions in people, such as pupil constriction and circadian photoentrainment. What contribution melanopsin makes to conscious visual perception is less studied. We devised a stimulus that targeted melanopsin separately from the cones using pulsed (3-s) spectral modulations around a photopic background. Pupillometry confirmed that the melanopsin stimulus evokes a response different from that produced by cone stimulation. In each of four subjects, a functional MRI response in area V1 was found. This response scaled with melanopic contrast and was not easily explained by imprecision in the silencing of the cones. Twenty additional subjects then observed melanopsin pulses and provided a structured rating of the perceptual experience. Melanopsin stimulation was described as an unpleasant, blurry, minimal brightening that quickly faded. We conclude that isolated stimulation of melanopsin is likely associated with a response within the cortical visual pathway and with an evoked conscious percept.

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2

Somasundaram, Preethi, Glenn R. Wyrick, Diego Carlos Fernandez, Alireza Ghahari, Cindy M. Pinhal, Melissa Simmonds Richardson, Alan C. Rupp, et al. "C-terminal phosphorylation regulates the kinetics of a subset of melanopsin-mediated behaviors in mice." Proceedings of the National Academy of Sciences 114, no. 10 (February 21, 2017): 2741–46. http://dx.doi.org/10.1073/pnas.1611893114.

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Intrinsically photosensitive retinal ganglion cells (ipRGCs) express the photopigment melanopsin and mediate several non–image-forming visual functions, including circadian photoentrainment and the pupillary light reflex (PLR). ipRGCs act as autonomous photoreceptors via the intrinsic melanopsin-based phototransduction pathway and as a relay for rod/cone input via synaptically driven responses. Under low light intensities, where only synaptically driven rod/cone input activates ipRGCs, the duration of the ipRGC response will be determined by the termination kinetics of the rod/cone circuits. Little is known, however, about the termination kinetics of the intrinsic melanopsin-based phototransduction pathway and its contribution to several melanopsin-mediated behaviors. Here, we show that C-terminal phosphorylation of melanopsin determines the recovery kinetics of the intrinsic melanopsin-based photoresponse in ipRGCs, the duration of the PLR, and the speed of reentrainment. In contrast, circadian phase alignment and direct effects of light on activity (masking) are not influenced by C-terminal phosphorylation of melanopsin. Electrophysiological measurements demonstrate that expression of a virally encoded melanopsin lacking all C-terminal phosphorylation sites (C terminus phosphonull) leads to a prolonged intrinsic light response. In addition, mice expressing the C terminus phosphonull in ipRGCs reentrain faster to a delayed light/dark cycle compared with mice expressing virally encoded WT melanopsin; however, the phase angle of entrainment and masking were indistinguishable. Importantly, a sustained PLR in the phosphonull animals is only observed at brighter light intensities that activate melanopsin phototransduction, but not at dimmer light intensities that activate only the rod/cone pathway. Taken together, our results highlight how the kinetics of the melanopsin photoresponse differentially regulate distinct light-mediated behaviors.

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3

Woelders, Tom, Thomas Leenheers, Marijke C. M. Gordijn, Roelof A. Hut, Domien G. M. Beersma, and Emma J. Wams. "Melanopsin- and L-cone–induced pupil constriction is inhibited by S- and M-cones in humans." Proceedings of the National Academy of Sciences 115, no. 4 (January 8, 2018): 792–97. http://dx.doi.org/10.1073/pnas.1716281115.

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The human retina contains five photoreceptor types: rods; short (S)-, mid (M)-, and long (L)-wavelength–sensitive cones; and melanopsin-expressing ganglion cells. Recently, it has been shown that selective increments in M-cone activation are paradoxically perceived as brightness decrements, as opposed to L-cone increments. Here we show that similar effects are also observed in the pupillary light response, whereby M-cone or S-cone increments lead to pupil dilation whereas L-cone or melanopic illuminance increments resulted in pupil constriction. Additionally, intermittent photoreceptor activation increased pupil constriction over a 30-min interval. Modulation of L-cone or melanopic illuminance within the 0.25–4-Hz frequency range resulted in more sustained pupillary constriction than light of constant intensity. Opposite results were found for S-cone and M-cone modulations (2 Hz), mirroring the dichotomy observed in the transient responses. The transient and sustained pupillary light responses therefore suggest that S- and M-cones provide inhibitory input to the pupillary control system when selectively activated, whereas L-cones and melanopsin response fulfill an excitatory role. These findings provide insight into functional networks in the human retina and the effect of color-coding in nonvisual responses to light, and imply that nonvisual and visual brightness discrimination may share a common pathway that starts in the retina.

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4

McGregor, K. M., C. Bécamel, P. Marin, and R. Andrade. "Using melanopsin to study G protein signaling in cortical neurons." Journal of Neurophysiology 116, no. 3 (September 1, 2016): 1082–92. http://dx.doi.org/10.1152/jn.00406.2016.

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Our understanding of G protein-coupled receptors (GPCRs) in the central nervous system (CNS) has been hampered by the limited availability of tools allowing for the study of their signaling with precise temporal control. To overcome this, we tested the utility of the bistable mammalian opsin melanopsin to examine G protein signaling in CNS neurons. Specifically, we used biolistic (gene gun) approaches to transfect melanopsin into cortical pyramidal cells maintained in organotypic slice culture. Whole cell recordings from transfected neurons indicated that application of blue light effectively activated the transfected melanopsin to elicit the canonical biphasic modulation of membrane excitability previously associated with the activation of GPCRs coupling to Gαq-11. Remarkably, full mimicry of exogenous agonist concentration could be obtained with pulses as short as a few milliseconds, suggesting that their triggering required a single melanopsin activation-deactivation cycle. The resulting temporal control over melanopsin activation allowed us to compare the activation kinetics of different components of the electrophysiological response. We also replaced the intracellular loops of melanopsin with those of the 5-HT2A receptor to create a light-activated GPCR capable of interacting with the 5-HT2A receptor interacting proteins. The resulting chimera expressed weak activity but validated the potential usefulness of melanopsin as a tool for the study of G protein signaling in CNS neurons.

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5

Berman, SM, and RD Clear. "A practical metric for melanopic metrology." Lighting Research & Technology 51, no. 8 (January 29, 2019): 1178–91. http://dx.doi.org/10.1177/1477153518824147.

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Over the past decade, there has been a growing interest in lighting research on the effects of the recently discovered melanopsin receptor (also referred to as the intrinsically photosensitive retinal ganglion cell) and its impacts on health and vision. Presently, there is not a generally accepted metrology for dealing with the spectral response of the melanopsin receptor as applied to both lighting and vision research. A proposition to handle this issue from a vision science perspective has been presented in 2014 in the journal Trends in Neurosciences and from a more lighting perspective in 2017 in Lighting Research and Technology. These propositions are complex, and do not retain the CIE standard definition of a lumen. In this paper, we propose an approach based on effective watts and melanopic/photopic ratios that is both simpler and more closely aligned with CIE standard unit definitions. In addition, we include some practical examples of how such ratios are accessible now, and can be used for both lighting and vision research as well as applications.

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6

SOLLARS, PATRICIA J., CYNTHIA A. SMERASKI, JESSICA D. KAUFMAN, MALCOLM D. OGILVIE, IGNACIO PROVENCIO, and GARY E. PICKARD. "Melanopsin and non-melanopsin expressing retinal ganglion cells innervate the hypothalamic suprachiasmatic nucleus." Visual Neuroscience 20, no. 6 (November 2003): 601–10. http://dx.doi.org/10.1017/s0952523803206027.

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Retinal input to the hypothalamic suprachiasmatic nucleus (SCN) synchronizes the SCN circadian oscillator to the external day/night cycle. Retinal ganglion cells that innervate the SCN via the retinohypothalamic tract are intrinsically light sensitive and express melanopsin. In this study, we provide data indicating that not all SCN-projecting retinal ganglion cells express melanopsin. To determine the proportion of ganglion cells afferent to the SCN that express melanopsin, ganglion cells were labeled following transsynaptic retrograde transport of a recombinant of the Bartha strain of pseudorabies virus (PRV152) constructed to express the enhanced green fluorescent protein (EGFP). PRV152 injected into the anterior chamber of the eye retrogradely infects four retinorecipient nuclei in the brain via autonomic circuits to the eye, resulting in transneuronally labeled ganglion cells in the contralateral retina 96 h after intraocular infection. In animals with large bilateral lesions of the lateral geniculate body/optic tract, ganglion cells labeled with PRV152 are retrogradely infected from only the SCN. In these animals, most PRV152-infected ganglion cells were immunoreactive for melanopsin. However, a significant percentage (10–20%) of EGFP-labeled ganglion cells did not express melanopsin. These data suggest that in addition to the intrinsically light-sensitive melanopsin-expressing ganglion cells, conventional ganglion cells also innervate the SCN. Thus, it appears that the rod/cone system of photoreceptors may provide signals to the SCN circadian system independent of intrinsically light-sensitive melanopsin ganglion cells.

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VUGLER, ANTHONY A., MA'AYAN SEMO, ANNA JOSEPH, and GLEN JEFFERY. "Survival and remodeling of melanopsin cells during retinal dystrophy." Visual Neuroscience 25, no. 2 (March 2008): 125–38. http://dx.doi.org/10.1017/s0952523808080309.

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AbstractThe melanopsin positive, intrinsically photosensitive retinal ganglion cells (ipRGCs) of the inner retina have been shown to send wide-ranging projections throughout the brain. To investigate the response of this important cell type during retinal dystrophy, we use the Royal College of Surgeons (RCS) dystrophic rat, a major model of retinal degeneration. We find that ipRGCs exhibit a distinctive molecular profile that remains unaltered during early stages of outer retinal pathology (15 weeks of age). In particular, these cells express βIII tubulin, α-acetylated tubulin, and microtubule-associated proteins (MAPs), while remaining negative for other RGC markers such as neurofilaments, calretinin, and parvalbumin. By 14 months of age, melanopsin positive fibers invade ectopic locations in the dystrophic retina and ipRGC axons/dendrites become distorted (a process that may involve vascular remodeling). The morphological abnormalities in melanopsin processes are associated with elevated immunoreactivity for MAP1b and a reduction in α-acetylated tubulin. Quantification of ipRGCs in whole mounts reveals reduced melanopsin cell number with increasing age. Focusing on the retinal periphery, we find a significant decline in melanopsin cell density contrasted by a stability of melanopsin positive processes. In addition to these findings, we describe for the first time, a distinct plexus of melanopsin processes in the far peripheral retina, a structure that is coincident with a short wavelength opsin cone-enriched rim. We conclude that some ipRGCs are lost in RCS dystrophic rats as the disease progresses and that this loss may involve vascular remodeling. However, a significant number of melanopsin positive cells survive into advanced stages of retinal degeneration and show indications of remodeling in response to pathology. Our findings underline the importance of early intervention in human retinal disease in order to preserve integrity of the inner retinal photoreceptive network.

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8

Lucas, Robert J., Annette E. Allen, Nina Milosavljevic, Riccardo Storchi, and Tom Woelders. "Can We See with Melanopsin?" Annual Review of Vision Science 6, no. 1 (September 15, 2020): 453–68. http://dx.doi.org/10.1146/annurev-vision-030320-041239.

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A small fraction of mammalian retinal ganglion cells are directly photoreceptive thanks to their expression of the photopigment melanopsin. These intrinsically photosensitive retinal ganglion cells (ipRGCs) have well-established roles in a variety of reflex responses to changes in ambient light intensity, including circadian photoentrainment. In this article, we review the growing evidence, obtained primarily from laboratory mice and humans, that the ability to sense light via melanopsin is also an important component of perceptual and form vision. Melanopsin photoreception has low temporal resolution, making it fundamentally biased toward detecting changes in ambient light and coarse patterns rather than fine details. Nevertheless, melanopsin can indirectly impact high-acuity vision by driving aspects of light adaptation ranging from pupil constriction to changes in visual circuit performance. Melanopsin also contributes directly to perceptions of brightness, and recent data suggest that this influences the appearance not only of overall scene brightness, but also of low-frequency patterns.

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9

SEMO, MA'AYAN, MARTA MUÑOZ LLAMOSAS, RUSSELL G. FOSTER, and GLEN JEFFERY. "Melanopsin (Opn4) positive cells in the cat retina are randomly distributed across the ganglion cell layer." Visual Neuroscience 22, no. 1 (January 2005): 111–16. http://dx.doi.org/10.1017/s0952523805001069.

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A rare type of rodent retinal ganglion cell expresses melanopsin (Opn4), the majority of which project to the suprachiasmatic nuclei. Many of these cells are directly light sensitive and appear to regulate the circadian system in the absence of rod and cone photoreceptors. However, the rodent retina contains no overt regions of specialization, and the different ganglion cell types are hard to distinguish. Consequently, attempts to distinguish the distribution of melanopsin ganglion cells in relation to regions of retinal specialization or subtype have proved problematic. Retinal cells with a common function tend to be regularly distributed. In this study, we isolate cat melanopsin and label melanopsin expressing cells usingin situhybridization. The labelled cells were all confined to the ganglion cell layer, their density was low, and their distribution was random. Melanopsin containing cells showed no clear center-to-periphery gradient in their distribution and were comprised of a relatively uniform cellular population.

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10

Conus, Vincent, and Martial Geiser. "A Review of Silent Substitution Devices for Melanopsin Stimulation in Humans." Photonics 7, no. 4 (November 30, 2020): 121. http://dx.doi.org/10.3390/photonics7040121.

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One way to study the specific response of the non-visual melanopsin photoreceptors of the human eye is to silence the response of cones and rods. Melanopsin photoreceptors (ipRGC), highlighted in the early 2000s, are intimately linked to the circadian rhythm and therefore to our sleep and wakefulness. Rest and sleep regulation, health and cognitive functions are all linked to ipRGC and play an important role in work and human relationships. Thus, we believe that the study of ipRGC responses is important.We searched and reviewed scientific articles describing instrumentation dedicated to these studies. PubMed lists more than 90,000 articles created since the year 2000 that contain the word circadian but only 252 with silent substitution. In relation to melanopsin, we found 39 relevant articles from which only 11 give a device description for humans, which is incomplete in most cases. We did not find any consensus for light intensity description, melanopsin contrast, sequences of melanopsin light stimulation and optical setup to expose the retina to the light.

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11

Fasick, Jeffry I., Haya Algrain, Courtland Samuels, Padmanabhan Mahadevan, Lorian E. Schweikert, Zaid J. Naffaa, and Phyllis R. Robinson. "Spectral tuning and deactivation kinetics of marine mammal melanopsins." PLOS ONE 16, no. 10 (October 15, 2021): e0257436. http://dx.doi.org/10.1371/journal.pone.0257436.

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In mammals, the photopigment melanopsin (Opn4) is found in a subset of retinal ganglion cells that serve light detection for circadian photoentrainment and pupil constriction (i.e., mydriasis). For a given species, the efficiency of photoentrainment and length of time that mydriasis occurs is determined by the spectral sensitivity and deactivation kinetics of melanopsin, respectively, and to date, neither of these properties have been described in marine mammals. Previous work has indicated that the absorbance maxima (λmax) of marine mammal rhodopsins (Rh1) have diversified to match the available light spectra at foraging depths. However, similar to the melanopsin λmax of terrestrial mammals (~480 nm), the melanopsins of marine mammals may be conserved, with λmax values tuned to the spectrum of solar irradiance at the water’s surface. Here, we investigated the Opn4 pigments of 17 marine mammal species inhabiting diverse photic environments including the Infraorder Cetacea, as well as the Orders Sirenia and Carnivora. Both genomic and cDNA sequences were used to deduce amino acid sequences to identify substitutions most likely involved in spectral tuning and deactivation kinetics of the Opn4 pigments. Our results show that there appears to be no amino acid substitutions in marine mammal Opn4 opsins that would result in any significant change in λmax values relative to their terrestrial counterparts. We also found some marine mammal species to lack several phosphorylation sites in the carboxyl terminal domain of their Opn4 pigments that result in significantly slower deactivation kinetics, and thus longer mydriasis, compared to terrestrial controls. This finding was restricted to cetacean species previously found to lack cone photoreceptor opsins, a condition known as rod monochromacy. These results suggest that the rod monochromat whales rely on extended pupillary constriction to prevent photobleaching of the highly photosensitive all-rod retina when moving between photopic and scotopic conditions.

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12

Li, Songshan, Chao Yang, Li Zhang, Xin Gao, Xuejie Wang, Wen Liu, Yuqi Wang, et al. "Promoting axon regeneration in the adult CNS by modulation of the melanopsin/GPCR signaling." Proceedings of the National Academy of Sciences 113, no. 7 (February 1, 2016): 1937–42. http://dx.doi.org/10.1073/pnas.1523645113.

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Cell-type–specific G protein-coupled receptor (GPCR) signaling regulates distinct neuronal responses to various stimuli and is essential for axon guidance and targeting during development. However, its function in axonal regeneration in the mature CNS remains elusive. We found that subtypes of intrinsically photosensitive retinal ganglion cells (ipRGCs) in mice maintained high mammalian target of rapamycin (mTOR) levels after axotomy and that the light-sensitive GPCR melanopsin mediated this sustained expression. Melanopsin overexpression in the RGCs stimulated axonal regeneration after optic nerve crush by up-regulating mTOR complex 1 (mTORC1). The extent of the regeneration was comparable to that observed after phosphatase and tensin homolog (Pten) knockdown. Both the axon regeneration and mTOR activity that were enhanced by melanopsin required light stimulation and Gq/11 signaling. Specifically, activating Gq in RGCs elevated mTOR activation and promoted axonal regeneration. Melanopsin overexpression in RGCs enhanced the amplitude and duration of their light response, and silencing them with Kir2.1 significantly suppressed the increased mTOR signaling and axon regeneration that were induced by melanopsin. Thus, our results provide a strategy to promote axon regeneration after CNS injury by modulating neuronal activity through GPCR signaling.

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Lax, Pedro, Isabel Ortuño-Lizarán, Victoria Maneu, Manuel Vidal-Sanz, and Nicolás Cuenca. "Photosensitive Melanopsin-Containing Retinal Ganglion Cells in Health and Disease: Implications for Circadian Rhythms." International Journal of Molecular Sciences 20, no. 13 (June 28, 2019): 3164. http://dx.doi.org/10.3390/ijms20133164.

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Melanopsin-containing retinal ganglion cells (mRGCs) represent a third class of retinal photoreceptors involved in regulating the pupillary light reflex and circadian photoentrainment, among other things. The functional integrity of the circadian system and melanopsin cells is an essential component of well-being and health, being both impaired in aging and disease. Here we review evidence of melanopsin-expressing cell alterations in aging and neurodegenerative diseases and their correlation with the development of circadian rhythm disorders. In healthy humans, the average density of melanopsin-positive cells falls after age 70, accompanied by age-dependent atrophy of dendritic arborization. In addition to aging, inner and outer retinal diseases also involve progressive deterioration and loss of mRGCs that positively correlates with progressive alterations in circadian rhythms. Among others, mRGC number and plexus complexity are impaired in Parkinson’s disease patients; changes that may explain sleep and circadian rhythm disorders in this pathology. The key role of mRGCs in circadian photoentrainment and their loss in age and disease endorse the importance of eye care, even if vision is lost, to preserve melanopsin ganglion cells and their essential functions in the maintenance of an adequate quality of life.

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Feigl, Beatrix, Sunila Dumpala, Graham K. Kerr, and Andrew J. Zele. "Melanopsin Cell Dysfunction is Involved in Sleep Disruption in Parkinson’s Disease." Journal of Parkinson's Disease 10, no. 4 (October 27, 2020): 1467–76. http://dx.doi.org/10.3233/jpd-202178.

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Background: Melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) signal the environmental light to mediate circadian photoentrainment and sleep-wake cycles. There is high prevalence of circadian and sleep disruption in people with Parkinson’s disease, however the underlying mechanisms of these symptoms are not clear. Objective: Based on recent evidence of anatomical and functional loss of melanopsin ganglion cells in Parkinson’s disease, we evaluate the link between melanopsin function, circadian, and sleep behavior. Methods: The pupil light reflex and melanopsin-mediated post-illumination pupil response were measured using chromatic pupillometry in 30 optimally medicated people with Parkinson’s disease and 29 age-matched healthy controls. Circadian health was determined using dim light melatonin onset, sleep questionnaires, and actigraphy. Ophthalmic examination quantified eye health and optical coherence tomography measured retinal thickness. Results: The melanopsin-mediated post-illumination pupil response amplitudes were significantly reduced in Parkinson’s disease (p < 0.0001) and correlated with poor sleep quality (r2 = 33; p < 0.001) and nerve fiber layer thinning (r2 = 0.40; p < 0.001). People with Parkinson’s disease had significantly poorer sleep quality with higher subjective sleep scores (p < 0.05) and earlier melatonin onset (p = 0.01). Pupil light (outer retinal) response metrics, daily light exposure and outer retinal thickness were similar between the groups (p > 0.05). Conclusion: Our evidence-based data identify a mechanism through which inner retinal ipRGC dysfunction contributes to sleep disruption in Parkinson’s disease in the presence of normal outer retinal (rod-cone photoreceptor) function. Our findings provide a rationale for designing new treatment approaches in Parkinson’s disease through melanopsin photoreceptor-targeted light therapies for improving sleep-wake cycles.

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GRÜNERT, ULRIKE, PATRICIA R. JUSUF, SAMMY C. S. LEE, and DUNG THAN NGUYEN. "Bipolar input to melanopsin containing ganglion cells in primate retina." Visual Neuroscience 28, no. 1 (October 18, 2010): 39–50. http://dx.doi.org/10.1017/s095252381000026x.

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AbstractTwo morphological types of melanopsin-expressing ganglion cells have been described in primate retina. Both types show intrinsic light responses as well as rod- and cone-driven ON-type responses. Outer stratifying cells have their dendrites close to the inner nuclear layer (OFF sublamina); inner stratifying cells have their dendrites close to the ganglion cell layer (ON sublamina). Both inner and outer stratifying cells receive synaptic input via ribbon synapses, but the bipolar cell types providing this input have not been identified. Here, we addressed the question whether the diffuse (ON) cone bipolar type DB6 and/or rod bipolar cells contact melanopsin-expressing ganglion cells. Melanopsin containing ganglion cells in marmoset (Callithrix jacchus) and macaque (Macaca fascicularis) retinas were identified immunohistochemically; DB6 cells were labeled with antibodies against the carbohydrate epitope CD15, rod bipolar cells were labeled with antibodies against protein kinase C, and putative synapses between the two cells types were identified with antibodies against piccolo. For one inner cell, nearly all of the DB6 axon terminals that overlap with its dendrites in the two-dimensional space show areas of close contact. In vertical sections, the large majority of the areas of close contact also contain a synaptic punctum, suggesting that DB6 cells contact inner melanopsin cells. The output from DB6 cells accounts for about 30% of synapses onto inner melanopsin cells. Synaptic contacts between rod bipolar axons and inner dendrites were not observed. In the OFF sublamina, about 10% of the DB6 axons are closely associated with dendrites of outer cells, and in about a third of these areas, axonal en passant synapses are detected. This result suggests that DB6 cells may also provide input to outer melanopsin cells.

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Walch, Olivia J., L. Samantha Zhang, Aaron N. Reifler, Michael E. Dolikian, Daniel B. Forger, and Kwoon Y. Wong. "Characterizing and modeling the intrinsic light response of rat ganglion-cell photoreceptors." Journal of Neurophysiology 114, no. 5 (November 1, 2015): 2955–66. http://dx.doi.org/10.1152/jn.00544.2015.

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Intrinsically photosensitive retinal ganglion cells (ipRGCs) mediate both image-forming vision and non-image-forming visual responses such as pupillary constriction and circadian photoentrainment. Five types of ipRGCs, named M1–M5, have been discovered in rodents. To further investigate their photoresponse properties, we made multielectrode array spike recordings from rat ipRGCs, classified them into M1, M2/M4, and M3/M5 clusters, and measured their intrinsic, melanopsin-based responses to single and flickering light pulses. Results showed that ipRGC spiking can track flickers up to ∼0.2 Hz in frequency and that flicker intervals between 5 and 14 s evoke the most spikes. We also learned that melanopsin’s integration time is intensity and cluster dependent. Using these data, we constructed a mathematical model for each cluster’s intrinsic photoresponse. We found that the data for the M1 cluster are best fit by a model that assumes a large photoresponse, causing the cell to enter depolarization block. Our models also led us to hypothesize that the M2/M4 and M3/M5 clusters experience comparable photoexcitation but that the M3/M5 cascade decays significantly faster than the M2/M4 cascade, resulting in different response waveforms between these clusters. These mathematical models will help predict how each ipRGC cluster might respond to stimuli of any waveform and could inform the invention of lighting technologies that promote health through melanopsin stimulation.

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Hankins, Mark W., Stuart N. Peirson, and Russell G. Foster. "Melanopsin: an exciting photopigment." Trends in Neurosciences 31, no. 1 (January 2008): 27–36. http://dx.doi.org/10.1016/j.tins.2007.11.002.

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Davies, Wayne L., Russell G. Foster, and Mark W. Hankins. "Focus on Molecules: Melanopsin." Experimental Eye Research 97, no. 1 (April 2012): 161–62. http://dx.doi.org/10.1016/j.exer.2010.07.020.

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Hannibal, Jens. "Regulation of Melanopsin Expression." Chronobiology International 23, no. 1-2 (January 2006): 159–66. http://dx.doi.org/10.1080/07420520500464544.

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McAdams, Harrison, Eric A. Kaiser, Aleksandra Igdalova, Edda B. Haggerty, Brett Cucchiara, David H. Brainard, and Geoffrey K. Aguirre. "Selective amplification of ipRGC signals accounts for interictal photophobia in migraine." Proceedings of the National Academy of Sciences 117, no. 29 (July 6, 2020): 17320–29. http://dx.doi.org/10.1073/pnas.2007402117.

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Second only to headache, photophobia is the most debilitating symptom reported by people with migraine. While the melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs) are thought to play a role, how cone and melanopsin signals are integrated in this pathway to produce visual discomfort is poorly understood. We studied 60 people: 20 without headache and 20 each with interictal photophobia from migraine with or without visual aura. Participants viewed pulses of spectral change that selectively targeted melanopsin, the cones, or both and rated the degree of visual discomfort produced by these stimuli while we recorded pupil responses. We examined the data within a model that describes how cone and melanopsin signals are weighted and combined at the level of the retina and how this combined signal is transformed into a rating of discomfort or pupil response. Our results indicate that people with migraine do not differ from headache-free controls in the manner in which melanopsin and cone signals are combined. Instead, people with migraine demonstrate an enhanced response to integrated ipRGC signals for discomfort. This effect of migraine is selective for ratings of visual discomfort, in that an enhancement of pupil responses was not seen in the migraine group, nor were group differences found in surveys of other behaviors putatively linked to ipRGC function (chronotype, seasonal sensitivity, presence of a photic sneeze reflex). By revealing a dissociation in the amplification of discomfort vs. pupil response, our findings suggest a postretinal alteration in processing of ipRGC signals for photophobia in migraine.

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Schmidt, Tiffany M., Kenichiro Taniguchi, and Paulo Kofuji. "Intrinsic and Extrinsic Light Responses in Melanopsin-Expressing Ganglion Cells During Mouse Development." Journal of Neurophysiology 100, no. 1 (July 2008): 371–84. http://dx.doi.org/10.1152/jn.00062.2008.

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Melanopsin (Opn4) is a photopigment found in a subset of retinal ganglion cells (RGCs) that project to various brain areas. These neurons are intrinsically photosensitive (ipRGCs) and are implicated in nonimage-forming responses to environmental light such as the pupillary light reflex and circadian entrainment. Recent evidence indicates that ipRGCs respond to light at birth, but questions remain as to whether and when they undergo significant functional changes. We used bacterial artificial chromosome transgenesis to engineer a mouse line in which enhanced green fluorescent protein (EGFP) is expressed under the control of the melanopsin promoter. Double immunolabeling for EGFP and melanopsin demonstrates their colocalization in ganglion cells of mutant mouse retinas. Electrophysiological recordings of ipRGCs in neonatal mice (postnatal day 0 [P0] to P7) demonstrated that these cells responded to light with small and sluggish depolarization. However, starting at P11 we observed ipRGCs that responded to light with a larger and faster onset (<1 s) and offset (<1 s) depolarization. These faster, larger depolarizations were observed in most ipRGCs by early adult ages. However, on application of a cocktail of synaptic blockers, we found that all cells responded to light with slow onset (>2.5 s) and offset (>10 s) depolarization, revealing the intrinsic, melanopsin-mediated light responses. The extrinsic, cone/rod influence on ipRGCs correlates with their extensive dendritic stratification in the inner plexiform layer. Collectively, these results demonstrate that ipRGCs make use of melanopsin for phototransduction before eye opening and that these cells further integrate signals derived from the outer retina as the retina matures.

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JOO, HANNAH R., BETH B. PETERSON, DENNIS M. DACEY, SAMER HATTAR, and SHIH-KUO CHEN. "Recurrent axon collaterals of intrinsically photosensitive retinal ganglion cells." Visual Neuroscience 30, no. 4 (July 2013): 175–82. http://dx.doi.org/10.1017/s0952523813000199.

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AbstractRetinal ganglion cells (RGCs), the output neurons of the retina, have axons that project via the optic nerve to diverse targets in the brain. Typically, RGC axons do not branch before exiting the retina and thus do not provide it with synaptic feedback. Although a small subset of RGCs with intraretinal axon collaterals has been previously observed in human, monkey, cat, and turtle, their function remains unknown. A small, more recently identified population of RGCs expresses the photopigment melanopsin. These intrinsically photosensitive retinal ganglion cells (ipRGCs) transmit an irradiance-coding signal to visual nuclei in the brain, contributing both to image-forming vision and to several nonimage-forming functions, including circadian photoentrainment and the pupillary light reflex. In this study, using melanopsin immunolabeling in monkey and a genetic method to sparsely label the melanopsin cells in mouse, we show that a subgroup of ipRGCs have axons that branch en route to the optic disc, forming intraretinal axon collaterals that terminate in the inner plexiform layer of the retina. The previously described collateral-bearing population identified by intracellular dye injection is anatomically indistinguishable from the collateral-bearing melanopsin cells identified here, suggesting they are a subset of the melanopsin-expressing RGC type and may therefore share its functional properties. Identification of an anatomically distinct subpopulation in mouse, monkey, and human suggests this pathway may be conserved in these and other species (turtle and cat) with intraretinal axon collaterals. We speculate that ipRGC axon collaterals constitute a likely synaptic pathway for feedback of an irradiance signal to modulate retinal light responses.

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23

Peinado, Gabriel, Tomás Osorno, María del Pilar Gomez, and Enrico Nasi. "Calcium activates the light-dependent conductance in melanopsin-expressing photoreceptors of amphioxus." Proceedings of the National Academy of Sciences 112, no. 25 (June 8, 2015): 7845–50. http://dx.doi.org/10.1073/pnas.1420265112.

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Melanopsin, the photopigment of the “circadian” receptors that regulate the biological clock and the pupillary reflex in mammals, is homologous to invertebrate rhodopsins. Evidence supporting the involvement of phosphoinositides in light-signaling has been garnered, but the downstream effectors that control the light-dependent conductance remain unknown. Microvillar photoreceptors of the primitive chordate amphioxus also express melanopsin and transduce light via phospholipase-C, apparently not acting through diacylglycerol. We therefore examined the role of calcium in activating the photoconductance, using simultaneous, high time-resolution measurements of membrane current and Ca2+ fluorescence. The light-induced calcium rise precedes the onset of the photocurrent, making it a candidate in the activation chain. Moreover, photolysis of caged Ca elicits an inward current of similar size, time course and pharmacology as the physiological photoresponse, but with a much shorter latency. Internally released calcium thus emerges as a key messenger to trigger the opening of light-dependent channels in melanopsin-expressing microvillar photoreceptors of early chordates.

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24

Pant, Mukund, Andrew J. Zele, Beatrix Feigl, and Prakash Adhikari. "Light adaptation characteristics of melanopsin." Vision Research 188 (November 2021): 126–38. http://dx.doi.org/10.1016/j.visres.2021.07.005.

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25

Spitschan, Manuel. "Measuring melanopsin function in people." Journal of Vision 17, no. 15 (December 1, 2017): 2. http://dx.doi.org/10.1167/17.15.2.

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26

Panda, S., M. Hatori, S. R. Keding, and H. Le. "Cellular circuitry of melanopsin function." Journal of Vision 9, no. 14 (December 1, 2009): 24–249. http://dx.doi.org/10.1167/9.14.24.

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27

Matsuyama, Take, Takahiro Yamashita, Yasushi Imamoto, and Yoshinori Shichida. "Photochemical Properties of Mammalian Melanopsin." Biochemistry 51, no. 27 (June 25, 2012): 5454–62. http://dx.doi.org/10.1021/bi3004999.

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28

Spitschan, Manuel, and Geoffrey K. Aguirre. "Vision: Melanopsin as a Raumgeber." Current Biology 27, no. 13 (July 2017): R644—R646. http://dx.doi.org/10.1016/j.cub.2017.05.052.

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29

Do, Michael Tri H. "Mixed Palettes of Melanopsin Phototransduction." Cell 175, no. 3 (October 2018): 637–39. http://dx.doi.org/10.1016/j.cell.2018.09.046.

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30

Bailes, Helena J., and Robert J. Lucas. "Melanopsin and inner retinal photoreception." Cellular and Molecular Life Sciences 67, no. 1 (October 29, 2009): 99–111. http://dx.doi.org/10.1007/s00018-009-0155-7.

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31

Palumaa, Teele, Michael J. Gilhooley, Aarti Jagannath, Mark W. Hankins, Steven Hughes, and Stuart N. Peirson. "Melanopsin: photoreceptors, physiology and potential." Current Opinion in Physiology 5 (October 2018): 68–74. http://dx.doi.org/10.1016/j.cophys.2018.08.001.

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32

White, Owen B., and Fiona Costello. "Melanopsin Effects on Pupil Responses." JAMA Neurology 74, no. 5 (May 1, 2017): 506. http://dx.doi.org/10.1001/jamaneurol.2016.5385.

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33

Bellingham, James, Shyam S. Chaurasia, Zara Melyan, Cuimei Liu, Morven A. Cameron, Emma E. Tarttelin, P. Michael Iuvone, Mark W. Hankins, Gianluca Tosini, and Robert J. Lucas. "Evolution of Melanopsin Photoreceptors: Discovery and Characterization of a New Melanopsin in Nonmammalian Vertebrates." PLoS Biology 4, no. 8 (July 25, 2006): e254. http://dx.doi.org/10.1371/journal.pbio.0040254.

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34

Vidal-Villegas, Beatriz, Johnny Di Pierdomenico, Juan A. Miralles de Imperial-Ollero, Arturo Ortín-Martínez, Francisco M. Nadal-Nicolás, Jose M. Bernal-Garro, Nicolás Cuenca Navarro, María P. Villegas-Pérez, and Manuel Vidal-Sanz. "Melanopsin+RGCs Are fully Resistant to NMDA-Induced Excitotoxicity." International Journal of Molecular Sciences 20, no. 12 (June 20, 2019): 3012. http://dx.doi.org/10.3390/ijms20123012.

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We studied short- and long-term effects of intravitreal injection of N-methyl-d-aspartate (NMDA) on melanopsin-containing (m+) and non-melanopsin-containing (Brn3a+) retinal ganglion cells (RGCs). In adult SD-rats, the left eye received a single intravitreal injection of 5µL of 100nM NMDA. At 3 and 15 months, retinal thickness was measured in vivo using Spectral Domain-Optical Coherence Tomography (SD-OCT). Ex vivo analyses were done at 3, 7, or 14 days or 15 months after damage. Whole-mounted retinas were immunolabelled for brain-specific homeobox/POU domain protein 3A (Brn3a) and melanopsin (m), the total number of Brn3a+RGCs and m+RGCs were quantified, and their topography represented. In control retinas, the mean total numbers of Brn3a+RGCs and m+RGCs were 78,903 ± 3572 and 2358 ± 144 (mean ± SD; n = 10), respectively. In the NMDA injected retinas, Brn3a+RGCs numbers diminished to 49%, 28%, 24%, and 19%, at 3, 7, 14 days, and 15 months, respectively. There was no further loss between 7 days and 15 months. The number of immunoidentified m+RGCs decreased significantly at 3 days, recovered between 3 and 7 days, and were back to normal thereafter. OCT measurements revealed a significant thinning of the left retinas at 3 and 15 months. Intravitreal injections of NMDA induced within a week a rapid loss of 72% of Brn3a+RGCs, a transient downregulation of melanopsin expression (but not m+RGC death), and a thinning of the inner retinal layers.

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35

Enezi, Jazi al, Victoria Revell, Timothy Brown, Jonathan Wynne, Luc Schlangen, and Robert Lucas. "A “Melanopic” Spectral Efficiency Function Predicts the Sensitivity of Melanopsin Photoreceptors to Polychromatic Lights." Journal of Biological Rhythms 26, no. 4 (July 19, 2011): 314–23. http://dx.doi.org/10.1177/0748730411409719.

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36

Bellingham, James, Shyam S. Chaurasia, Zara Melyan, Cuimei Liu, Morven A. Cameron, Emma E. Tarttelin, P. Michael Iuvone, Mark W. Hankins, Gianluca Tosini, and Robert J. Lucas. "Correction: Evolution of Melanopsin Photoreceptors: Discovery and Characterization of a New Melanopsin in Nonmammalian Vertebrates." PLoS Biology 4, no. 10 (October 17, 2006): e320. http://dx.doi.org/10.1371/journal.pbio.0040320.

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37

Nasi, Enrico, and María del Pilar Gomez. "Melanopsin-mediated light-sensing in amphioxus." Communicative & Integrative Biology 2, no. 5 (September 2009): 441–43. http://dx.doi.org/10.4161/cib.2.5.9244.

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38

Chakraborty, Ranjay, Erica G. Landis, Reece Mazade, Victoria Yang, Ryan Strickland, Samer Hattar, Richard A. Stone, P. Michael Iuvone, and Machelle T. Pardue. "Melanopsin modulates refractive development and myopia." Experimental Eye Research 214 (January 2022): 108866. http://dx.doi.org/10.1016/j.exer.2021.108866.

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39

KARDON, RANDY. "Melanopsin and its role in photophobia." Acta Ophthalmologica 90 (August 6, 2012): 0. http://dx.doi.org/10.1111/j.1755-3768.2012.3865.x.

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40

Rollag, Mark D. "Does Melanopsin Bistability Have Physiological Consequences?" Journal of Biological Rhythms 23, no. 5 (October 2008): 396–99. http://dx.doi.org/10.1177/0748730408323067.

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41

Beaulé, Christian, Barry Robinson, Elaine Waddington Lamont, and Shimon Amir. "Melanopsin in the Circadian Timing System." Journal of Molecular Neuroscience 21, no. 1 (2003): 73–90. http://dx.doi.org/10.1385/jmn:21:1:73.

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42

Van Gelder, R. N., T. Lamprecht, K. Mawad, T. Sexton, and X. Qiu. "Mechanisms of murine melanopsin-mediated photoreception." Journal of Vision 9, no. 14 (December 1, 2009): 25. http://dx.doi.org/10.1167/9.14.25.

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43

Panda, S. "Illumination of the Melanopsin Signaling Pathway." Science 307, no. 5709 (January 28, 2005): 600–604. http://dx.doi.org/10.1126/science.1105121.

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44

Van Gelder, Russell N., and Ethan D. Buhr. "Melanopsin: The Tale of the Tail." Neuron 90, no. 5 (June 2016): 909–11. http://dx.doi.org/10.1016/j.neuron.2016.05.033.

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45

Pottackal, Joseph, and Jonathan B. Demb. "Melanopsin Shows Its (Contrast-)Sensitive Side." Neuron 99, no. 4 (August 2018): 630–32. http://dx.doi.org/10.1016/j.neuron.2018.08.007.

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46

Peirson, Stuart, and Russell G. Foster. "Melanopsin: Another Way of Signaling Light." Neuron 49, no. 3 (February 2006): 331–39. http://dx.doi.org/10.1016/j.neuron.2006.01.006.

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47

Kumbalasiri, Tida, and Ignacio Provencio. "Melanopsin and other novel mammalian opsins." Experimental Eye Research 81, no. 4 (October 2005): 368–75. http://dx.doi.org/10.1016/j.exer.2005.05.004.

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48

Lima, Leonardo H. R. G., Ana C. Scarparo, Mauro C. Isoldi, Maria A. Visconti, and Ana M. L. Castrucci. "Melanopsin in chicken melanocytes and retina." Biological Rhythm Research 37, no. 5 (October 2006): 393–404. http://dx.doi.org/10.1080/09291010600870230.

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49

Lucas, R., A. Allen, T. Brown, R. Storchi, K. Davis, and F. Martial. "Visual functions for melanopsin in mice." Journal of Vision 13, no. 15 (December 27, 2013): T6. http://dx.doi.org/10.1167/13.15.6.

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50

Jackson, Abigail C., and Jessica Ortega. "A Mathematical Model of Melanopsin Phototransduction." Biophysical Journal 108, no. 2 (January 2015): 151a. http://dx.doi.org/10.1016/j.bpj.2014.11.831.

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