Long‐term effects of inherited and acquired retinal degenerations on the retinal ganglion cell population

Abstract

AbstractInherited photoreceptor degenerations cause loss of photoreceptors and retinal remodeling which, when severe, is accompanied of retinal vessel displacements that cause retinal ganglion cell (RGC) axonal compression and death. Light‐induced photoreceptor degenerations cause similar pathologic events and ultimately RGC loss. RGC death is secondary to photoreceptor degeneration and is a delayed event that occurs in retinal sectors where there is maximal photoreceptor degeneration. Other types of acquired retinal diseases, such as taurine deficiency‐induced retinal degeneration, which may be similar to vigabatrine‐induced retinopathy, can also cause photoreceptor degeneration and RGC loss. However, in taurine deficiency, RGC loss may not be secondary to photoreceptor degeneration, but occur as an independent event and thus, RGC loss is diffuse. The combination of two treatments: taurine deficiency and light toxicity increases photoreceptor loss but not RGC loss (García‐Ayuso et al., 2018). The population of intrinsically photosensitive RGCs (ipRGCs) may respond differently than the normal population of RGCs to different types of photoreceptor degeneration because they die in similar proportions to the other RGCs in inherited photoreceptor degenerations (García‐Ayuso et al., 2015), but are selectively affected by taurine‐deficiency and may show only a temporary decrease of melanopsin expression after light‐induced damage. The investigation of RGC loss in different retinal degenerations provides us with information on the mechanisms of cell death in order to plan strategies for its prevention.