By its action on rhodopsin, light t

By its action on rhodopsin, light triggers the well-known visual transduction cascade, but can also
induce cell damage and death through phototoxic mechanisms -- a comprehensive understanding of
which is still elusive despite more than 40 years of research. Herein, we integrate recent experimental
findings to address several hypotheses of retinal light damage, premised in part on the close
anatomical and metabolic relationships between the photoreceptors and the retinal pigment
epithelium. We begin by reviewing the salient features of light damage, recently joined by evidence
for retinal remodeling which has implications for the prognosis of recovery of function in retinal
degenerations. We then consider select factors that influence the progression of the damage process
and the extent of visual cell loss. Traditional, genetically-modified, and emerging animal models are
discussed, with particular emphasis on cone visual cells. Exogenous and endogenous retinal
protective factors are explored, with implications for light damage mechanisms and some suggested
avenues for future research. Synergies are known to exist between our long term light environment
and photoreceptor cell death in retinal disease. Understanding the molecular mechanisms of light
damage in a variety of animal models can provide valuable insights into the effects of light in clinical
disorders and may form the basis of future therapies to prevent or delay visual cell loss.