Light microscopic autoradiography, following injection of tritiated thymidine, was used to study the postnatal development of cells in the inner nuclear layer (INL) of the normal and rd (C57BL/6J-rd le) mouse retina. Specific attempts were made to determine whether some bipolar cell degeneration occurs in conjunction with previously noted photoreceptor cell degeneration in the retina of the mutant (rd) mouse. A differential count of cell types in the INL of both the central and peripheral retina indicates that the same ratio of bipolar cells to Müller cells (3:1) exists in the normal and the rd retina during postnatal development. The density of cells in the INL was similar in both groups during development and similar decreases in width of the INL occurred in the normal and rd mouse during maturation. In addition, autoradiographic analysis of the proliferation of postnatally forming bipolar cells suggested that the rd gene is not lethal to the bipolar cell population which forms after birth. The labeling index (percent labeled cells) in the INL, determined as a function of the date of 3H-thymidine injection and assessed in the mature retina (day 41), was similar in both mice. Analysis of the number of silver grains/nucleus presented a more complete picture of how the progenitor pool of cells contributes to the cell types formed postnatally in the retinas of both mice.
The conclusion that bipolar cell death does not occur to any significant degree in the retina of the rd also suggests that transneuronal degeneration does not occur in the retina of the mutant mouse during the period (up to day 41) when most of the photoreceptor cells die. The observation in both groups of mice that cell density remains constant between postnatal day 14 and day 41, while the width of the INL changes tremendously, suggests that there is a significant redistribution of cells during growth of the eyeball and/or cell death which occurs in all cell types found in the INL in both the normal and mutant mouse.