Synaptic plasticity modulates the spontaneous recovery of locomotion after spinal cord hemisection.

Several evidences have demonstrated that adult mammals could achieve a wide range of spontaneous sensory-motor recovery after spinal cord injury by means of various forms of neuroplasticity. In this study we evaluated the possibility that after low-thoracic spinal cord hemisection in the adult rat, significant hindlimb locomotor recovery could occur, and that this recovery may be driven, at least in part, by mechanisms of synaptic plasticity. In order to address these issues, we measured the expression levels of synapsin-I and brain-derived neurotrophic factor by Western blotting, at various time points after hemisection and correlated them with the motor performance on a grid walk test. Regression analysis showed that the expression of synapsin-I was strongly correlated with the spontaneous recovery of hindlimb locomotion (R=0.78). Conversely, neither the expression levels of synapsin-I nor the locomotor recovery were associated with the expression of brain-derived neurotrophic factor. Overall results indicate that after spinal cord hemisection, substantial recovery of hindlimb locomotion could occur spontaneously, and that synaptic plasticity within spinal circuitries below the level of the lesion, could be an important mechanism involved in these processes.

Kinematic features of passive forelimb movements and rat cuneate neuron discharges.

We examined the role of main and external cuneate nuclei neurons in processing sensory information during forelimb passive movement. We recorded activity of neurons using circular and figure-eight trajectories, at different speeds, in anaesthetized rats. A multivariate regression analysis was performed to correlate neural discharge to movement direction and speed, the two components of the velocity vector. We found that the activity of the majority of cuneate neurons related to passive movement velocity and that the directional component of the velocity vector accounted for a larger fraction of the variability in the firing rate than the scalar component (speed). These results indicate that cuneate cells can process whole limb afferent information to elaborate a representation of the movement velocity vector.

Levels of brain-derived neurotrophic factor and neurotrophin-4 in lumbar motoneurons after low-thoracic spinal cord hemisection.

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.