The effect of treadmill training on the expression of BDNF, TrkB and Synaptophysin around motor neurons of the lumbar spinal cord in spinally transected rats

Previous studies showed that treadmill training improved stepping ability in spinally transected (ST) rats. Biochemical analyses indicated that the cellular expression of brain-derived neurotrophic factors (BDNF) was up-regulated in the lumbar spinal cord by treadmill training. Identifying the BDNF-expressing cells is important for understanding potential plasticity mechanisms; however, the amount of activity required to influence the cellular expression of these proteins has not been determined. In this study, we examined the effects of treadmill training on the expression of BDNF, TrkB receptor and synaptophysin around motor neurons of the lumbar spinal card in female neonatal ST rats. Thirty days after transection, 24 rats were randomly assigned to four groups, control and three experimental groups, based on the number of steps imposed during daily treadmill training: 0 steps, 100 steps, 1000 steps. After 4 weeks, the rats were sacrificed and the spinal cords were processed for immunohistochemistry. BDNF and TrkB receptors were identified using BDNF and TrkB antibodies, respectively. Motor neurons were identified using HSP-27 antibodies. Pre-synaptic terminals of the motor neurons were identified using the Synaptophysin antibodies. Quantitative analyses were performed using fluorescence and confocal microscopy to examine the expression of BDNF, TrkB and Synaptophysin around motor neurons. Our results showed that BDNF expression in the lumbar spinal cord was activity-dependent. There was increase in BDNF expression in 100 and 1000 steps group when compared to 0 steps group. Unlike BDNF, TrkB expression was unaffected by activity levels. Finally, Synaptophysin expression increased in 1000 steps group when compared to 0 steps group. Differences in expressions between BDNF, TrkB and Synaptophysin around motor neurons in lumbar spinal cord amongst different stepping groups indicated a possible mechanism for BDNF-mediated plasticity following spinal cord injury.