Abstract
Abstract: :
Purpose: Mice with the pcd (Purkinje Cell Degeneration) mutation undergo a slow progressive degeneration of the photoreceptors comparable to human retinitis pigmentosa; moreover, as in this illness, the symptoms become apparent in the second half of the animal’s life. Although the spatial and temporal patterns of this degeneration have already been described, it is not known whether the remainder of the retinal cells, both glia and neurons, are affected by this degeneration, an indispensable requisite for the use of this animal model as a recipient of retinal transplants.Methods: We used C57/BL6 mice carriers of the pcd mutation in homocygosis and C57/BL6 mice without mutation, which served as reference animals. The technique employed in this work was that of immunohistochemistry by the avidin–biotin peroxidase method in sections. S100, glutamin syntethase And GFAP for the Müller cells; different biotinylated lectins in the case of the microglial cells; calbindin D 28K for horizontal cells; parvalbumin for type II amacrine cells; protein kinase C for bipolar cell; calretinin for ganglion cells and collagen type IV for the basal membrane of the blood vessels. Furthermore, antibodies against synapsin and syntaxin were used to obtain information about the synaptic vesicles and RT97 for the study of the neurofilaments. Results: The most acute change was the increase in the elements positive to GFAP on the periphery of the retina of the animals who were carriers of the mutation. Regarding the remainder of the labels, the changes in number and distribution of the positive elements were less striking, although changes were detected in the neurochemical patterns. No significant modifications were found in the population of microglial cells. In relation to the blood vessels, labelled elements were detected in the most scleral portion of the retina, probably of choroid origin. Conclusions: The most acute change was the increase in the elements positive to GFAP on the periphery of the retina of the animals who were carriers of the mutation. Regarding the remainder of the labels, the changes in number and distribution of the positive elements were less striking, although changes were detected in the neurochemical patterns. No significant modifications were found in the population of microglial cells. In relation to the blood vessels, labelled elements were detected in the most scleral portion of the retina, probably of choroid origin.
Keywords: retinal degenerations: cell biology • microscopy: light/fluorescence/immunohistochemistry • Muller cells