Neuroplasticity represents a common phenomenon after spinal cord (SC) injury or deafferentation that compensates for the loss of modulatory inputs to the cord. Neurotrophins play a crucial role in cell survival and anatomical reorganization of damaged spinal cord, and are known to exert an activity-dependent modulation of neuroplasticity. Little is known about their role in the earliest plastic events, probably involving synaptic plasticity, which are responsible for the rapid recovery of hindlimb motility after hemisection, in the rat. In order to gain further insight, we evaluated the changes in BDNF and NT-4 expression by lumbar motoneurons after low-thoracic spinal cord hemisection. Early after lesion (30 min), the immunostaining density within lumbar motoneurons decreased markedly on both ipsilateral and contralateral sides of the spinal cord. This reduction was statistically significant and was then followed by a significant recovery along the experimental period (14 days), during which a substantial recovery of hindlimb motility was observed. Our data indicate that BDNF and NT-4 expression could be modulated by activity of spinal circuitry and further support putative involvement of the endogenous neurotrophins in mechanisms of spinal neuroplasticity.