Plasticity in the developing visual system: the effects of retinal lesions made in young rats.

ABSTRACT

The central visual pathways of the rat have been used as a model for investigating the significance of axonal interactions in mammalian neural development. Attention is restricted largely to the aberrant distribution of optic axons to the ipsilateral side of the brain and their distribution in the superior colliculus after early unilateral eye damage. The normal ipsilateral retinotectal pathway in pigmented rats appears as a series of patches located anteriorly and laterally in the stratum opticum, whereas in albino animals it is a small area lying anteromedially. In both, a few axons are often found at the extreme posterior border of the superior colliculus. After unilateral eye enucleation at birth, an aberrant ipsilateral pathway from the remaining eye arises at the optic chiasm. It originates from all parts of the retina and terminates in the ipsilateral superior colliculus in a topographic fashion such that the upper retina projects laterally and the lower retina, medially. The pathway is heaviest anteromedially (from lower temporal retina) and lightest posterolaterally (from upper nasal retina). There is always a heavy projection to the extreme posterior border of the superior colliculus. In only two animals of a large series was direct intertectal sprouting found. After partial retinal lesions, there is again an ipsilateral pathway from the unlesioned eye which fills the projection area of the lesion. As after total enucleation, the pathway arises from most of the ipsilateral retina, not just that region homotypic to the lesion site, being heaviest from the lower temporal and lightest (or deficient) from the upper retina. There is suggestion of ordering of the projection into the deafferented region in that the ipsilateral degeneration after lesions in the intact eye is compact but does not fill the gap in the crossed projection completely. There is also indication that some intact parts of the retina lesioned at birth may also project in an inappropriate retinotopic fashion to the deafferented region. The corticotectal pathway shows a normal map. Study of the ipsilateral retinotectal pathway indicates that the axons terminating at the extreme posterior border of the superior colliculus arise from the lower temporal retina. The results are interpreted as indicating that the aberrant uncrossed pathways after complete or local retinal lesions, compare very closely in most features. Both distribute to the deafferented area of the superior colliculus -- in one, this is the whole surface, while in the other it is a small area. The fact that in the latter case axons are ending in quite inappropriate parts of the tectal map, may be explained more simply in terms of interactions between adjacent axons in the optic pathway rather than by an hypothesis involving a change in the cell labels across the tectal map.