The right superior colliculus and right eye were ablated in hamsters within 12 h of birth and the visual and somatosensory representations in the remaining (left) superior colliculus were evaluated using standard single unit recording and receptive field mapping techniques when the animals reached adulthood (at least 3 months of age). In a number of the hamsters used for recording, injections of [3H]leucine were made into the left eye 6-10 days prior to the terminal experiment. This was done to insure that the neonatal lesions did, in fact, produce the extensive recrossing of retinal fibers demonstrated by others who have employed this preparation. All of the hamsters which received [3H]leucine injections prior to the recording experiment exhibited a markedly expanded ipsilateral retinocollicular projection and retinal axons which recrossed the midline at the level of the tectum. The recording experiments showed further that this projection resulted in a visual map which was generally mirror symmetric to that in normal hamsters. There were, however, numerous irregularities and discontinuities in this representation and, in a few hamsters, it appeared almost completely disorganized. There were also a number of abnormalities in the somatosensory representation in the deep tectal laminae of the neonatally brain damaged hamsters. There was a substantial increase in the number of cells with receptive fields that extended onto the ipsilateral side of the body, neurons with split receptive fields were recorded and there were changes in the magnification of different portions of the body surface. These alterations did not, however, change the organization of the somatosensory map in a manner which brought it into alignment with the visual representation in the superficial laminae. Nevertheless, additional recording experiments in animals subjected to enucleation of both eyes and ablation of the superficial laminae of one superior colliculus did indicate that the existence of the aberrant retinal projection was a necessary condition for the somatosensory abnormalities which we observed. Additional anterograde and retrograde tracing experiments demonstrated only one abnormality in the organization of the somatosensory afferent input to the remaining colliculus. In 75% of the brain damaged hamsters, there was a weak crossed projection from the sensorimotor cortex that was never observed in normal animals. Ablation of this cortex at the time of the recording experiment did not, however, reduce the incidence of abnormal somatosensory receptive fields in these hamsters.