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

摘要

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