Abstract
The retina is part of the central nervous system specially adapted to capture light photons and transmit this information to the brain through photosensitive retinal cells involved in visual and non-visual activities. However, excessive light exposure may accelerate genetic retinal diseases or induce photoreceptor cell (PRC) death, finally leading to retinal degeneration (RD). Light pollution (LP) caused by the characteristic use of artificial light in modern day life may accelerate degenerative diseases or promote RD and circadian desynchrony. We have developed a working model to study RD mechanisms in a low light environment using light-emitting diode (LED) sources, at constant or long exposure times under LP conditions. The mechanism of PRC death is still not fully understood. Our main goal is to study the biochemical mechanisms of RD. We have previously demonstrated that constant light (LL) exposure to white LED produces a significant reduction in the outer nuclear layer (ONL) by classical PRC death after 7 days of LL exposure. The PRCs showed TUNEL-positive labeling and a caspase-3-independent mechanism of cell death. Here, we investigate whether constant LED exposure affects the inner-retinal organization and structure, cell survival and the expression of photopigments; in particular we look into whether constant LED exposure causes the death of retinal ganglion cells (RGCs), of intrinsically photosensitive RGCs (ipRGCs), or of other inner-retinal cells. Wistar rats exposed to 200 lx of LED for 2 to 8 days (LL 2 and LL 8) were processed for histological and protein. The results show no differences in the number of nucleus or TUNEL positive RGCs nor inner structural damage in any of LL groups studied, indicating that LL exposure affects ONL but does not produce RGC death. However, the photopigments melanopsin (OPN4) and neuropsin (OPN5) expressed in the inner retina were seen to modify their localization and expression during LL exposure. Our findings suggest that constant light during several days produces retinal remodeling and ONL cell death as well as significant changes in opsin expression in the inner nuclear layer.
Highlights
The retina is the neural portion of the eye adapted to capturing light photons and transmitting this information to other structures in the brain
We showed positive transferase dUTP nick end labeling (TUNEL) outer nuclear layer (ONL) staining in the retinas of rats exposed to 4 days of light stimulation (LL) [28], whereas no staining was detected after 4 days in retinas in the light dark cycle (LD) conditions, indicating that the thinning of the retina induced by light exposure was caused by photoreceptor cell (PRC) death
There are no TUNEL-positive cells labeled in the ganglion cell layer (GCL) and inner nuclear layer (INL) at any time of light exposure studied, clearly indicating no cell death in these regions (Figures 2A–C, 2, 4, and 8 of LL, respectively)
Summary
The retina is the neural portion of the eye adapted to capturing light photons and transmitting this information to other structures in the brain. Light acts directly in the retina to fulfill two important roles: the visual function through rods and cones photoreceptor cells (PRCs) and the so-called “non-image forming tasks” such as the photoentrainment of circadian rhythms, pupilary light response, melatonin secretion, sleep regulation, and light-dependent relaxation of the retinal vasculature. These tasks are carried out by intrinsically photosensitive RGCs (ipRGCs), a subset of RGC that project to the suprachiasmatic nucleus in the hypothalamus and other non-visual areas [1,2,3]. It is known that OPN4-expressing ipRGCs are dysfunctional in various retinal and optic nerve diseases [11] and that they may be more resistant to injury than the general RGC population [12]
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