Brain-derived neurotrophic factor and neuralplasticity in a rat model of spinal cord transection

The present study employed a rat model of T10 spinal cord transection. Western blot analysesrevealed increased brain-derived neurotrophic factor (BDNF) expression in spinal cord segmentscaudal to the transection site following injection of replication incompetent herpes simplex virusvector (HSV-BDNF) into the subarachnoid space. In addition, hindlimb locomotor functions wereimproved. In contrast, BDNF levels decreased following treatment with replication defective herpessimplex virus vector construct small interference BDNF (HSV-siBDNF). Moreover, hindlimblocomotor functions gradually worsened. Compared with the replication incompetent herpessimplex virus vector control group, extracellular signal regulated kinase1/2 expression increased inthe HSV-BDNF group on days 14 and 28 after spinal cord transection, but expression was reducedin the HSV-siBDNF group. These results suggested that BDNF plays an important role in neuralplasticity via extracellular signal regulated kinase1/2 signaling pathway in a rat model of adult spinalcord transection.