[An electron microscopic study of retinal development and pathogenesis in mutant CBA/J mice with hereditary retinal degeneration].

: Electron microscopic study of the neural retina pathogenesis was carried out on mice CBA/J in comparison with corresponding process in substrain CBA/Ki (Caley et al., 1972). A difference in terms of the pathology development was found between substrains CBA/J and CBA/Ki. It was shown that, in CBA/J, the retinal degeneration begins later than in CBA/Ki. As distinct from the latter, CBA/J proceeds to increase the thickness of outer nuclear and plexiform layers as well as the number of membranous discs of rod outer segments (ROS) between P10 and P12. In the retina of mouse CBA/J, pathologic alterations of the outer nuclear layer and the inner segments of photoreceptors precede the ROS destruction. It was found that the pigment epithelium is capable to phagocytize membranous discs of ROS in mouse CBA/J at P10 and P12. In CBA/J, the mitochondria in inner segments of photoreceptors begin to decay at P10; by P12, the amount of such segments reach 40%. At P12, the number of pycnotic nuclei (6%) in the outer nuclear layer coincides with the number of inner segments with dense degenerative cytoplasm. At P15, the state of retina as evaluated by the extent of far advanced degeneration of the outer nuclear layer is equalized in mice of both substrains. From P10 to P15, macrophages which phagocytize membranous discs of ROS are present in the interphotoreceptor space of CBA/J. The administration of PABA solution (7.5 x 10(-3) mg/g) daily from P1 to P9 or from P1 to P11 and with subsequent fixation at P10 and P12 respectively exerted no effect on the rate of retinal pathogenesis in mouse CBA/J. The causes of revealed differences in the development of retinal pathology between CBA/Ki and CBA/J are discussed as well as the causes of the absence of PABA effect on the retina of mutant mouse CBA/J.