The corticospinal tract (CST) of the rat undergoes a prolonged period of postnatal development. Lesions of the presumptive CST pathway at birth are followed by the aberrant rerouting of the developing corticospinal axons around the lesion site through adjacent undamaged CNS tissue. This developmental plasticity becomes severely restricted by 5-6 days of age, so the axons are no longer capable of growth around the site of injury. The aim of the current study was to determine whether altering the environment at the site of injury by filling the lesion with transplanted fetal spinal cord tissue could prolong the critical period for developmental plasticity of the corticospinal pathway. The spinal cord was damaged (overhemisection) at three stages in the development of the corticospinal (CS) pathway: 1) prior to the arrival of CS axons, 2) after the axons elongated through the cord but prior to synaptogenesis, and 3) after both axonal elongation and synaptogenesis were completed. One to 9 months later, anterograde neuronal tracing with horseradish peroxidase was used to assess the growth of the corticospinal pathway with or without a fetal transplant at the site of injury, and the pattern of labeling was compared with that observed in adult nonlesioned control animals. Our results indicate that the presence of a transplant prolongs the critical period for developmental plasticity of the CST. Transplants elicited growth of CST axons throughout the postnatal period examined. CST axons damaged prior to synaptogenesis exhibited more robust growth than those lesioned after synaptogenesis had been completed. These results suggest that both environmental and neuronal factors interact to regulate the response of immature CS neurons to injury.