In the first experiment, the astrocyte morphology and distribution were observed. As shown in figure 1, there were significant increase in astrocyte cell number in the P23H rate compared to the control rates in all retinal regions. In addition, P23H rats were associated with hypertrophy, of astrocytes which also saw an increased GFAP immunoreactivity (figure 2,3). In P23H rats, there also showed a disrupted vessel that was significantly regressed. There is the formation of blood vessel tangles at 12 and at 18 months. (figure 4).
In the second experiment, the result is that there is a relationship between the Cx43 and the hyperplasia and hypertrophy of the P23H astrocytes (figure5). There were also higher expression fold charges in the P23H compared to the control. In the experiment that indicates the tissue stress, P23H the diseased retinas showed GFAP immunoactivity in the muller cells, indicating that the tissue is under significant stress and that photoreceptors were significantly reduced in the mutant rat compared to the control (figure 6,7)l. In addition, from the staining it can be seen that the glial component of the retina expanded, filling the space that was left by the photoreceptors. In the experiment, it has been shown that in the mutant cells, the muller cells were hypertrophied, assumed to be due to the retina. There were also altered the distribution and orientation of cone cells(figure9). In general, the GFAP labeling indicated early retinal gliosis. The number of astrocytes was also higher in the mutant cells as compared to the controls. The astrocytes also degenerated as the rats aged.
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