Retinal damage promoted by constant illumination of low intensity resulted in a diminution in classical photoreceptors cells. Glial cells exert profound effects on neurons, vasculature and other glial cells. Macroglia and microglia with specific morphological, physiological, and antigenic characteristics may play an essential role in both the maintenance and control of retinal homeostasis, or to exert mechanisms that promote cell death. The role of glial cells and immune function in the pathogenesis promoted by low light is poorly understood. We performed glial cells characterization along the time-course of retinal degeneration induced by chronic exposure to low intensity of light in Wistar rats. We exposed the animals at constant light from 2 to 8 days and assessed the retinal glia. After 6 days of light exposure, retinas presented increased levels of GFAP, a macroglia marker and microglia markers Iba1 and CD68 displayed increased mRNA levels after 6 days. The number of Iba1 positive cells increased in the outer nuclear layer, showing ameboid morphology with thicker processes characteristic of microglial activated cells. The expression levels of immune mediators TNF-𝜶 and IL-6 were also significantly increased after 6 days. Finally, chemokines analysis showed that CX3CR1 and CCL2 expression levels were significantly elevated after 6 days. Hence, all the events of glial activation occurred after 5-6 days of constant light exposure, when the number of cells of the outer nuclear layer has already decreased significantly. Herein we demonstrated that glial and immune activation are secondary to neurodegeneration; in this scenario, our results suggest that photoreceptor death is an early event that may be induced by phototransduction-dependent mechanisms.
Environmental Modulation of Alcohol Intake in Hamsters: Effects of Wheel Running and Constant Light Exposure