Molecular physiology of vision

Visual sensastion results initially from light-induced isomerization of 11-cis-retinal in rhodopsin and cone pigments of photoreceptor cells. This transformation triggers cascades of events, i. e., activation of transducin and cGMP photodiesterase, decrease of cGMP, closure of cGMP-gated channels, and generation of active potential. Activated rhodopsin is then inactivated and uncouples all-trans-retinal, which is metabolized to all-trans-retinol and transferred to the retinal pigment epithelium, where it is re-isomerzed to form 11-cis-retinal. The 11-cis-retinal returns to the photoreceptor outer segments and regenerates rhodopsin. Many of the players in these two pathways are also essential for survival and maintenance of photoreceptors. Mutations in their genes cause retinitis pigmentosa and macular dystrophies. This article aims to summarize current understanding of the molecular mechanisms underlying these reactions and their relevance to pathophysiology of the retinal diseases.