You will be presented with the abstract, introduction, and discussion section from a biomedical research article. Your task is to create a summary that a layperson can understand, capturing the essence of the research article. Keep essential scientific terms, but ensure that the language remains clear and the concepts are explained in an uncomplicated manner.

Title: Melanopsin Contributions to Irradiance Coding in the Thalamo-Cortical Visual System}
Article:
Abstract:
Photoreception in the mammalian retina is not restricted to rods and cones but extends to a subset of retinal ganglion cells expressing the photopigment melanopsin( mRGCs). These mRGCs are known to drive such reflex light responses as circadian photoentrainment and pupillomotor movements. By contrast, until now there has been no direct assessment of their contribution to conventional visual pathways. Here, we address this deficit. Using new reporter lines, we show that mRGC projections are much more extensive than previously thought and extend across the dorsal lateral geniculate nucleus( dLGN), origin of thalamo-cortical projection neurons. We continue to show that this input supports extensive physiological light responses in the dLGN and visual cortex in mice lacking rods+cones( a model of advanced retinal degeneration). Moreover, using chromatic stimuli to isolate melanopsin-derived responses in mice with an intact visual system, we reveal strong melanopsin input to the ∼40% of neurons in the LGN that show sustained activation to a light step. We demonstrate that this melanopsin input supports irradiance-dependent increases in the firing rate of these neurons. The implication that melanopsin is required to accurately encode stimulus irradiance is confirmed using melanopsin knockout mice. Our data establish melanopsin-based photoreception as a significant source of sensory input to the thalamo-cortical visual system, providing unique irradiance information and allowing visual responses to be retained even in the absence of rods+cones. These findings identify mRGCs as a potential origin for aspects of visual perception and indicate that they may support vision in people suffering retinal degeneration.
Introduction:
Until 10 years ago it was considered self-evident that all aspects of mammalian vision originate with light detection by either rods or cones. This view has changed with the discovery of a 3rd photoreceptor class[1]—the so-called melanopsin retinal ganglion cells( mRGCs). These mRGCs are able to respond to light even in complete isolation thanks to the presence of melanopsin, an opsin-based photopigment. Until now, the discovery of mRGCs has had the most impact on our understanding of such sub-cortical light responses as circadian entrainment and the pupil light reflex. We now know that mRGCs integrate input from the outer retina with their own intrinsic light response to encode ambient light intensity( irradiance or illuminance) for these and other reflex responses[2]–[11]. By contrast, there has been little consideration of melanopsin's potential to contribute to the physiology or function of conventional visual pathways and little effort to incorporate these newly discovered photoreceptors into models of visual perception. This omission has reflected the balance of published evidence that mRGC axons are largely segregated from the thalamo-cortical visual pathway. Thus, while Dacey et al. reported back-labeling mRGCs from the primate visual thalamus[12], more extensive analysis of the mRGC projection pattern in rodents[13]–[15] suggested that their input to this part of the brain was almost exclusively restricted to the ventral LGN and intergeniculate leaflet, rather than the dLGN which is the site of thalamo-cortical projection neurons. It has since become clear, however, that the Opn4tauLacZ transgenic reporter line employed in the most comprehensive of those rodent studies has incomplete penetrance and labels only around 50% of melanopsin-expressing retinal ganglion cells[11],[13],[16]–[17]. The successfully labeled neurons represent a distinct anatomical subtype( called M1) whose dendrites are restricted to the outer sub-lamina of the inner plexiform layer. The projection pattern of the remaining mRGC classes( which have dendrites in the inner sublamina) has only been very recently addressed[18]. There is thus renewed uncertainty regarding the degree to which mRGCs influence the dLGN and whether they could make a direct contribution to aspects of conventional vision. Here, we employ a Cre-recombinase based reporter line to trace the projection pattern of the full mRGC population. This reveals a substantial innervation of the dLGN. We continue to assess the physiological consequences of this anatomical organization using multichannel extracellular electrophysiology and brain imaging in the visual thalamus and cortex. These experiments reveal an essential role for mRGCs in encoding irradiance for the central pathways of conventional vision.
Discussion:
Using anatomical and physiological experiments we provide here a direct examination of melanopsin contributions to the activity of the thalamo-cortical visual pathway. We find that these rare photoreceptors( <2, 000 per mouse retina compared with many hundreds of thousands of rods and cones) make a disproportionate contribution to visual activity. Thus, our experiments reveal that melanopsin sets the tonic firing rate under steady illumination of around 40% of all light responsive units in the LGN. As mRGCs also provide the major source of light information for accessory visual centers in the hypothalamus and pretectum[6],[7],[11], it seems that, despite their small numbers, these are among the most influential of all ganglion cell classes. Our data suggest that melanopsin contributes a quality of visual information to the thalmo-cortical pathway that is unavailable from rods or cones. The experiments in mice with intact retinas( Opn1mwR) reveal that the “sustained” class of LGN neuron can encode irradiance over a very wide sensitivity range( at least 6 decimal orders). However, this ability is impaired in Opn4−/− mice, which can track irradiance only over a narrow range of dim-moderate intensities. The Opn4−/− LGN shows response saturation at around the threshold for melanopsin phototransduction( ∼1012 photons/cm2/s). These data therefore indicate an irradiance dependent switch from rod/cone to melanopsin phases of irradiance coding in the LGN that is reminiscent of the situation for other melanopsin-influenced responses[4],[42],[50],[51]. In this regard, our data support the view that melanopsin photoreceptors compensate for a fundamental limitation in the ability of cones to encode irradiance over the photopic range. This may be explained by saturation in the “steady-state” level of cone hyperpolarization under extended illumination[52],[53]. Under these conditions photoreceptor adaptation and bleaching desensitization should allow cones to track high frequency modulations in light intensity, without necessarily encoding longer-term changes in illumination. Our data suggest that the visual system relies upon melanopsin to provide this latter information. Insofar as melanopsin enhances the visual system's ability to measure light intensity, our data raise the possibility of an mRGC contribution to any aspect of mammalian vision that requires an accurate assessment of luminance/illuminance. Indeed, the finding that melanopsin influences essentially all thalamic neurons capable of luminance detection( the sustained population) in the mouse represents strong evidence for such a wide-ranging role in that species. If this were true also of humans, then mRGCs may contribute to as yet poorly understood mechanisms of “brightness” and “lightness” perception[54],[55]. For the moment, however, the aspect of human vision most directly addressed by our mouse experiments is spatial brightness perception. Just like our mouse thalamic neurons, human subjects can accurately estimate full field illumination over at least 8 decimal orders[56]. Based on our findings, we predict that melanopsin is responsible for at least the top 3–4 orders of this sensitivity range. In support of this possibility are reports that other features of human brightness perception seem inconsistent with cone physiology[57] and that high color temperature( “bluer”) lights appear brighter to human observers even when matched for photopic luminance[58]–[60]. An important unanswered question is whether mRGC input to the dLGN adopts a retinotopic order allowing it to encode spatial information. The resolution of any such mRGC-dependent spatial map would be low. Thus, if we assume a 90° field of view in mice with a fully constricted pupil and tiling of ∼28×28 for those mRGCs projecting to the dLGN( at most half of the total population of mRGCs), then acuity would be ∼0. 3 cycles/° at best. Behavioral and electrophysiological experiments suggest that mouse visual acuity is not much superior to this[44],[61]–[63]. However, given their anatomy, and the kinetics of melanopsin phototransduction, it is hard to imagine that the selective advantage of retaining mRGC input to the dLGN lies in their ability to provide fine spatial information. It seems much more likely that if mRGCs do provide spatial information it takes the form of a relatively crude map of “brightness” to be used alongside higher acuity information in downstream visual processing. The discovery of widespread melanopsin input to the thalamo-cortical visual pathway could have special relevance for the blind. Millions worldwide suffer varying degrees of blindness thanks to rod/cone degeneration or dysfunction. mRGCs survive even complete rod and cone loss and can support reflex light responses under these conditions. Our demonstration of extensive light driven activation in the LGN and cortex of rd/rd cl mice( an animal model of advanced retinal degeneration) raises the possibility that mRGCs also contribute to aspects of visual perception in these individuals[64]. Crude light perception typically survives in patients with retinal degeneration and there has been a suggestion that this could originate with melanopsin[10],[65]( although note that not all subjects with circadian light responses, and thus functional melanopsin photoreception, retain conscious light perception[66]). If surviving melanopsin photoreceptors might support simple light perception in those with retinal degeneration, could they also provide spatial information? Very recently, Ecker and coworkers reported that Gnat1−/−;Cnga3−/− mice can use visual gratings to navigate a maze[18]. Insofar as these animals are considered to lack critical components of rod and cone phototransduction cascades( but have structurally intact retinae), that finding argues that mRGCs alone can support pattern vision. However, our work in rd/rd cl mice raises doubt over whether this could occur in advanced retinal degeneration. Thus, while melanopsin drives thalamic responses within 200 ms of a change in illumination in mice with an intact retina, responses build up very gradually in rd/rd cl animals, being first apparent at around 2 s after lights on, increasing over subsequent 10 s of seconds, and decaying very slowly at lights off. These kinetics seem incompatible with timeframes of visual fixation and would therefore probably preclude this melanopsin photoreception from providing useful spatial information. In agreement with this prediction, the ability to perceive light typically outlasts spatial discrimination in patients with progressive retinal dystrophy. The discovery of photoreceptive retinal ganglion cells has thus far had little impact on our understanding of the processes of pattern vision and perception. We show here that these mRGCs are in fact influential regulators of electrophysiological activity in the primary visual pathway. Our data suggest that they are responsible for setting the tonic firing rate of 40% of thalamic neurons according to the level of illumination. This unique contribution implicates melanopsin in aspects of spatial brightness perception that have been hard to reconcile with the known capabilities of rods and cones[57]. The fact that these melanopsin signals appear in essentially all LGN neurons with a “sustained” response phenotype further identifies this inner retinal photoreceptor as a potential player in any visual process employing luminance information. These new functions add to the weight of evidence that good practice in architectural lighting should be revised to take account of the specific requirements of melanopsin photoreception.
The ability to convert light into electrical signals in the mammalian retina has traditionally been thought to occur through only two types of photoreceptors , the rods and cones . However , this ability also extends to a small number of neurons expressing the protein melanopsin . To date these melanopsin retinal ganglion cells ( mRGCs ) have been thought to act as photoreceptors primarily for those brain regions regulating subconscious responses to ambient light , such as pupil size . In this study , we provide evidence that mRGCs also contribute extensively to conventional visual pathways . We use a newly developed strategy to characterize the brain regions to which these cells project and then directly monitor visually evoked neural activity in these target regions . We find that mRGCs allow the mouse visual system to faithfully encode ambient illumination over at least a million-fold range and to continue to show light responses even in the absence of all rods and cones . These data reveal a new role for mRGCs during normal vision and suggest that mRGCs could make a significant contribution to assessing brightness and supporting vision even in people with advanced retinal degeneration .