Early monocular enucleations in fetal ferrets produce a decrease of uncrossed and an increase of crossed retinofugal components: a possible model for the albino abnormality.

Abstract

The terminal distributions of retinofugal axons to geniculate laminae or cell groups have been studied in monocular ferrets that had had one eye removed on the 28th or 29th day of intrauterine life and survived until the end of the fourth postnatal week. Normally pigmented and albino animals were studied and the patterns of retinogeniculate terminations in these were compared with earlier accounts of the patterns that develop normally or after a monocular enucleation on the day of birth. Birth normally occurs after 41 days of gestation. In albino animals the neonatal and prenatal enucleations produce essentially the same result. The abnormally large crossed retinogeniculate component, which is also characteristic of normal adult albinos, innervates the major (A) laminae and these fuse medially and caudally as in normal albinos. These represent geniculate Layers A and A1. The abnormally small uncrossed component resembles the abnormally small uncrossed component of normal albinos in innervating several separate terminal islands within the geniculate region. These are larger than in a normal albino animal and are surrounded by a zone of sparser termination not seen in a normal albino. In normally pigmented animals the prenatal enucleation produces a result essentially like that produced by the enucleation in albinos, whereas the postnatal enucleation produces a relatively more symmetrical retinogeniculate pathway in which the crossed component innervates an abnormally enlarged Lamina A and the uncrossed component innervates an enlarged Lamina A1. These results can be most readily explained by assuming that between embryonic Day 28 and the day of birth there is an interaction between the two retinofugal pathways that produces an increase in the uncrossed component from the levels characteristic of albinos and early monocular enucleates to normal levels. This interaction must then be absent in albinos.