In normal hamsters the visual cortex sends a retinotopically organized projection to the ipsilateral superior colliculus. 2. Acute or chronic unilateral ablations of visual cortex in adult animals decrease the incidence of directionally selective cells encountered in the superficial laminae of the ipsilateral colliculus, but not in the deeper layers (those ventral to the stratum opticum). 3. Unilateral ablations of visual cortex in infant hamsters induce an aberrant crossed projection to the contralateral superior colliculus, confirming the finding of Mustari and Lund (58) in the rat. Horseradish peroxidase (HRP) experiments demonstrated that the cells whose axons comprise the normal as well as the anomalous projection are pyramidal neurons in layer V of cortex. 4. In adult hamsters that underwent early brain damage, about 13% of the cells in the colliculus could be activated by stimulation of the contralateral visual cortex. Only 1 unit (of the 159 cells tested) could be driven by similar stimulation in normal adult hamsters. This indicates that the anomalous crossed projection forms functional synapses in the contralateral tectum. 5. No cells (of the 113 tested) could be activated from the contralateral cortex in hamsters that sustained chronic ablations of visual cortex in adulthood; thus indicating that there is some limited time period during development when unilateral ablations of visual cortex induce an anomalous corticotectal pathway. 6. The visual response properties of superior collicular neurons in the neonatally brain-damaged animals were compared to those of normal hamsters, as well as to those with acute or chronic ablations of visual cortex sustained in adulthood. 7. There was no indication that the anomalous projection contributes to the organization of normal visual response properties in the superior colliculus of the neonatally brain-damaged animals. In fact, the incidence of directionally selective cells in these hamsters was found to be significantly lower than that of normals in both the superficial and deep laminae of the colliculus. 8. We conclude that while unilateral damage of visual cortex in the hamster induces an anomalous corticotectal projection that makes functional synapses, this aberrant input does not compensate for missing, normal corticotectal pathway in the organization of superior collicular response properties.
