The retina is the part of the central nervous system adapted to initial capture and processing of visual signals. However, its organization makes it vulnerable to dysfunction. Retinitis pigmentosa (RP) is a group of dystrophies that leads retinal degeneration and therefore blindness. In most typical cases the rods are the predominantly affected cells in the retina which generate symptoms including night blindness, bilateral symmetric loss of the mind-peripheral visual field, or/and electroretinographic (EGR) abnormalities. Some forms of RP kill the photoreceptor cells causing visual damages ranging from mild (in night blindness) to severe visual impairment due to a high rate and constitutive activation of the phototransduction process. If so, the question arising is: why phototransduction kills?

A powerful approach to the understanding of etiologies of visual impairment at the cellular and molecular levels has been the obtaining and characterization of diverse experimental animal models. They consist of animals carrying specific retinal gene mutations or wild type animals exposed to continuous light treatment to cause a damage mimicking the human pathologies for a number of inherited retinal diseases.

The death of photoreceptor cells induced by lower-intensity of light required the activation of the photopigments and a consequent downstream signal transduction cascade. For that light exposure has served as a model for human retinal degeneration arising from environmental insults and genetic diseases. In this chapter we will discuss the different retinal degenerations related to retinitis pigmentosa (RP) disease, emphasizing those caused by genetic defects, vitamin A deficiency or a prolonged light exposure producing the constitutive activation of the phototransduction pathway. Moreover, we will examine the mechanisms of apoptotic death occurring after retinal light damage, as well as the positive and negative insights of retinal degeneration models. We considerer that the molecular mechanism taking place at low light intensity damage can provide valuable experimental models for the effects of clinical genetic disorders related to phototransduction mechanism defects.