Carter-Dawson L, Burroughs M
Sensory Sciences Center, Graduate School of Biomedical Sciences, University of Texas Health Sciences Center, Houston 77030.
Exp Eye Res. 1989 Nov;49(5):829-41. doi: 10.1016/s0014-4835(89)80042-9.
The distribution of IRBP was examined in postnatal developing retinas of rds (020/A) mutant mice and Balb/c controls by EM immunocytochemistry. Light labeling for IRBP was detected in mutant and control retinas by postnatal day 9 (P9) largely in the interphotoreceptor matrix (IPM). At P14, some photoreceptors in the rds retina showed a higher density of label in the Golgi for IRBP than neighboring cells and those of controls processed simultaneously. This high density of label for IRBP was observed also in the Golgi of a small population of photoreceptor cells at P18, P19 and P21 in rds retinas. These cells were found to represent approximately 3-5% of the photoreceptor population. The density of label for IRBP at the apical RPE region was obviously low in the rds retinas by P18, P19 and P21. However, this same region in controls of the same ages was densely labeled for IRBP. The low density of labeling at the apical RPE region in the rds retinas may indicate a change in the rate of synthesis, secretion, distribution and/or degradation in the IPM. The high density of intracellular labeling in a small population of cells may be indicative of impaired secretion, an increase in IRBP synthesis or the initiation of photoreceptor deterioration. Whether the differences observed in the distribution of IRBP in the rds mutant are primary or secondary effects of the genetic lesion remains undetermined.
