Neonatal brain injury triggers compensatory processes that can be adaptive or detrimental, but little is known about the mechanisms of compensation or how they might affect the response properties of neurons within the injured region. We have studied this issue in a rodent model. Partial ablation of the hamster superior colliculus (SC) at birth results in a compressed, but complete visual field map in the remaining SC, and a compensatory conservation of receptive field (RF) size and stimulus velocity and size tuning. The circuit underlying stimulus tuning in this system or its preservation after brain lesions is not known. Our previous work has shown that NMDA receptors are necessary for the development and conservation of RF size after partial SC ablation. In this study, we examined whether NMDA receptor function is also necessary for the development and conservation of stimulus velocity and size tuning. We found that velocity and size tuning were unaffected by chronic postnatal blockade of NMDA receptors and the resulting increases in RF size. Thus, NMDA receptors in the SC are not necessary for the development of stimulus velocity and size tuning or in the compensatory maintenance of these properties following brain damage. These results suggest that stimulus velocity and size tuning may arise in the retina or from NMDA receptor-independent circuitry intrinsic to SC. The lack of conflict between NMDA receptor activity-dependent and -independent processes may allow conservation of some RF properties while others change during injury-induced or evolutionary changes in afferent/target convergence.