Search

Female mice showing albino mosaicism due to an X-autosome translocation [Is(In7;X)Ct] have been studied in order to investigate the relationship between the distribution of melanin and the formation, early in development, of the abnormally small uncrossed retinofugal pathway characteristically found in all albino mammals. Earlier evidence indicates that cells normally bearing melanin play a role in producing the abnormality. In the mosaic mice, the albino gene is expressed in only about half of the cells due to random X-inactivation and the patches of normal and albino cells are extremely small relative to total retinal size (less than 1/50). We argued that if all the cells that would normally bear melanin play a role in producing the albino abnormality then the mosaic mice would have a pathway abnormality, about half the size of that in the albino mice. If, however, only a small patch of these cells plays a role, as has been proposed in earlier studies, then one would expect the size of the uncrossed pathway to be highly variable in the mosaic mice. The size of the uncrossed pathway was assessed by placing horseradish peroxidase in the region of the optic tract and lateral geniculate nucleus unilaterally and then counting the number of retrogradely labelled retinal ganglion cells on the same side. The mosaic mice showed a highly variable uncrossed pathway. In some of the mosaic mice, it was the same size as in the albinos and, in others, it was the same size as in normally pigmented mice. Surprisingly, in a small number of mosaic mice, the uncrossed pathway was larger than normal. Whether this relatively rare occurrence of a supernormal uncrossed pathway is due to the higher gene dosage or to the translocation itself remains an open question.

The development of the cells in the ganglion cell layer in the rat retina has been studied from 3 to 30 days of age postnatal by means of Golgi-stained whole-mounted retinae. The retina grows rapidly from birth to ten days of age and then more slowly from 10 to 30 days of age. The different classes of ganglion cell can be clearly recognized by 10 days of age, but type I ganglion cells with a size comparable to those found in the adult rat retina are not seen until thirty days of age. Type II cells may attain their adult size before type I cells do. The growth of the retina and the resulting decrease in cell density in the ganglion cell layer occur with the same time course as the increase in the size of the cell soma and their dendritic fields.

The total number of optic nerve fibers of the chicken was determined at twenty sequential developmental stages from incubation day 5 to 104 days after hatching. It was found that the total number of optic nerve fibers increases from 4400 on incubation day 5 to about 4.0 million on incubation days 10 and 11. Thereafter, it decreases to a final value of about 2.4 million by incubation day 18 and remains constant from that time on until adulthood. Thus, 40% of optic fibers degenerate. Degenerating ganglion cells in the retina are first detectable by incubation day 9. Initially degenerating cells are located mainly in the central retina, but on subsequent days they can be found predominantly in peripheral zones. It is postulated that cell death occurs because of competition for adequate arborization space. If more retinal afferent fibers arrive than tectal termination sites are available, supernumerary fibers may degenerate. By degeneration the two systems retina and optic tectum, are matched in size.

Quantitative data on generation and degeneration of retinal ganglion cells during development (Rager and Rager, 1978) are interpreted in terms of a mathematical model which consists of a system of differential equations. By these equations we attempt to describe the formation of retinal ganglion cells and their termination domains in the tectum. Since ganglion cells seem not to degenerate before their axons have arrived at their termination site and start branching, from the arrival time on they may become competent either to continue to mature or to die. Therefore, to find the actual number of competent cells the extension of the fiber pathway between the retina and the optic tectum had also to be measured and computed. The differential equations are united by the principle that at any given time cells in excess of the number of termination domains have to die. By this model the mathematical function was determined. Several parameter values of this function were optimized with the Gauss-Newton method by which the curve was fitted to the measured values. The high correlation obtained by this method allows to conclude that, to a first approximation, the model may be satisfactory. The evidence of competition for termination sites and of systems-matching by cell death is discussed.

In the retina of the mouth-brooding teleost Tilapia leucosticta, light causes and accelerated development of ganglion cells. This effect is presumably not mediated by receptor and interneuronal cells.