Enhanced axonal transport: A novel form of "plasticity" after primate and rodent spinal cord injury

Deficient axonal transport after injury is believed to contribute to the failure of CNS regeneration. To better elucidate neural mechanisms associated with CNS responses to injury, we transected the dominant voluntary motor system, the corticospinal tract (CST), in the dorsolateral T10 spinal cord of rhesus monkeys. Three months later, a 4.5-fold increase in the number of CST axons located in the spared ventral corticospinal tract at both the lesion site and, surprisingly, remotely in the cervical spinal cord was observed. Additional studies of increases in corticospinal axon numbers in rat and primate models demonstrated that increases were transient and attributable to enhanced axonal transport rather than axonal sprouting. Accordingly, increases in axonal transport occur after CNS injury even in the longest projecting pathways of the non-human primate, likely representing an attempted adaptive response to injury as observed in the PNS.