Effects of light exposure on the calretinin and calbindin expression in zebrafish retina

The incidence rates of light-induced retinopathies increased significantly in the last decades because of continuous exposure to the harmful effects of light from different electronic devices. Recent studies show that exposure to short-wavelength visible light in blue has been related to the pathogenesis of light-induced retinopathies. However, the biological effects of long-term exposure are not fully known yet. Calbindin and calretinin, two homologous cytosolic calcium-binding proteins implicated in the regulation of important processes in central neurons and peripheral nervous systems [1,2,3] were investigated to elucidate the potential role of these proteins in maintaining retinal homeostasis. The effects of exposure to light at different wavelengths with emission peaks in the blue light range (400-500 nm) on the expression of calretinin and calbindin, using double immunofluorescence with confocal laser microscopy, were studied. 20 adult zebrafish (Danio rerio), 3 months old were obtained from previous studies [4], divided into 5 groups, exposed to different lighting conditions (white light, blue-white light, blue light, darkness and control group) for ten days. 4 fish from each group were sacrificed and decapitated [4] and the heads processed for histological and immunohistochemical analysis. The localization of calretinin and calbindin in the retina of zebrafish was analyzed using immunofluorescence method. The results show a different expression of calbindin and calretinin in the zebrafish retina after various lighting conditions. In control group, calretinin immunoreactivity was observed only in a subpopulation of amacrine cells in the inner nuclear and ganglion cells layers while an exposure to white light, white-blue and blue light causes a decrease of immunostaining. No immunostaining was observed after exposition to darkness. Therefore, the results suggest that these calcium binding proteins may be involved in the maintenance of retinal homeostasis.