The effects of early prenatal monocular enucleation on the routing of uncrossed retinofugal axons and the cellular environment at the chiasm of mouse embryos.

Whereas it has been shown that early monocular enucleations produce a reduction in the uncrossed pathway from the surviving eye in rats and ferrets, similar evidence for binocular interactions in the development of the uncrossed component in mice is currently open to question. Using retrograde tracing, we have investigated the time course of changes in the uncrossed retinofugal pathway immediately after the early prenatal monocular enucleation in mouse embryos. Removal of one eye from C57 pigmented mice at embryonic day (E) 13 does not cause a reduction of the earliest uncrossed component from the central retina examined 1 day later at E14. However, a substantial reduction of the uncrossed pathway is seen at E15, the time when the major uncrossed projection first arises from the ventral temporal retina. This reduction is greater in E16 one-eyed embryos, indicating that most retinal axons from the ventral temporal retina rely on a binocular interaction for their turning at the chiasm. Further, early removal of one eye at E13 does not produce any obvious changes in the cytoarchitecture of RC-2-immunopositive radial glia at the chiasm, nor of the stage-specific antigen-1 (SSEA-1) -expressing neurons. This lack of changes in the cellular organization at the chiasm indicates that the reduction of the uncrossed pathway is probably produced by an elimination of binocular fibre interactions at the chiasm, rather than through a degenerative change of cellular elements at the chiasm as a consequence of the eye removal procedure.