Ontogeny of the area centralis in the cat

Previous studies have shown that after embryonic day 50 (E50) the kitten retina undergoes a relatively rapid period of maturation that begins at the area centralis and spreads toward the retinal periphery. The mechanism controlling this pattern is unknown. One possibility is that the area centralis is the most developmentally advanced region of retina from the earliest stages of eyecup formation. The present study tests this hypothesis. Retinae from ten kittens aged between E21 and E54 were sectioned horizontally at 10 micron and stained with haematoxylin and eosin. During the earliest stages of development in other vertebrate species, the oldest part of the retina is at the posterior pole of the eyecup, just dorsal to the optic fissure. At E21 in the kitten retina, this site appeared to be developmentally advanced by several criteria. A developmentally advanced region (DAR) was recognized at each subsequent age. It gradually became displaced temporally toward the site of the area centralis in the adult. Developmental events beginning here include the formation of cell-free channels at the vitreal margin; the appearance of the first ganglion cells and their axons; the formation of continuous inner and outer plexiform layers; the differentiation of cells in the ganglion cell, inner, and outer nuclear layers; and the cessation of cytogenesis at the outer limiting membrane. By E54 the DAR could be recognized as the area centralis by the criteria used in the adult. Between E25 and E37 cell density in the ganglion cell layer is higher in the DAR than at other retinal eccentricities. During the E40s cell density becomes uniform across the retina because more cells migrate into the ganglion cell layer in peripheral retina than in the DAR. Several observations suggest that cells added to the ganglion cell layer from E37 onward are not ganglion cells. The proportion of retinal area occupied by the DAR decreases geometrically between E21 and E54, indicating that this region grows at a slower rate than the rest of the retina. It is suggested that this differential growth combined with differential cell addition may be the principal mechanism responsible for generating centroperipheral cell gradients in the retina.