Deciphering Irradiance Detection in the Mammalian Retina

Publisher Summary This chapter highlights the animal models for irradiance detection in the mammalian retina. Apart from the obvious biological interest, the study of irradiance detection is an excellent illustration of how a set of animal models can enable the cellular and molecular bases of eye function to be deciphered. More specifically, mutant mouse models have allowed researchers to genetically eliminate subsets of retinal cells or disrupt key elements of phototransduction pathways and thus probe the retina for the origin of irradiance detection. Furthermore, comparative studies with other nonmammalian vertebrates as well as invertebrates have proven particularly valuable. As melanopsin loss abolishes ipRGC (intrinsically photosensitive retinal ganglion cells) photosensitivity, the light responses of melanopsin-knockout mice must originate with some other photoreceptors. By studying increasingly sophisticated retinally degenerate and knockout mice, it became clear that irradiance detection can survive loss of rods, cones, or melanopsin, but not all three. This sets the challenge to determine the exact significance of each photoreceptor class for irradiance detection and how their signals are integrated in efferent pathways. Addressing the former issue is a substantial undertaking and will probably require a whole new array of transgenic models. One of the clear consequences of the melanopsin knockout is the loss of photosensitivity in the ipRGCs.