Recovery of function after spinal cord injury: mechanisms underlying transplant-mediated recovery of function differ after spinal cord injury in newborn and adult rats.

Fetal spinal cord transplants placed into the site of spinal cord injury support axonal growth of host systems in both newborn and adult animals. The amount of axonal growth, however, is much more robust in the newborn animals. The current studies were designed to determine if the differences in the magnitude of the anatomical plasticity of host pathways in the presence of transplants is reflected in differences in recovery of function between the neonatal and adult operates. Newborn and adult rats received a midthoracic "overhemisection." Immediately following the hemisection embryonic (E14) spinal cord transplants were placed into the lesion site. All animals were trained and tested as adults, on a battery of qualitative and quantitative tests of motor function. Immunocytochemical methods were used to compare the extent of growth of descending (serotonergic and noradrenergic) and segmental (calcitonin gene-related peptide containing dorsal root axons) pathways in both groups. The growth of descending pathways into the transplants was substantially greater in density and spatial extent after lesions at birth than at maturity. The distribution of segmental dorsal root axons, in contrast, was similar in both groups. Fetal spinal cord transplants promoted recovery of motor function in both newborn and adult operates. The particular aspects of locomotor function which recover differ between the neonatal and adult operates, suggesting that the mechanisms underlying recovery of function must differ between the two groups.