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

• Published in: 中国神经再生研究（英文版） Vol. 6; no. 13; pp. 1017 - 1022
• Main Author: Ruxin Xing Jia Liu Hua Jin Ping Dai Tinghua Wang
• Format: Journal Article
• Language: English
• Published: Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China%Institute of Neuroscience, Kunming Medical College, Kunming 650031, Yunnan Province, China%Laboratory of Neurological Disease, West China Hospital of Sichuan University, Chengdu 610041, Sichuan Province, China 05.05.2011
• Subjects: BDNF; 信号调节; 免疫印迹分析; 单纯疱疹病毒载体; 大鼠模型; 神经可塑性; 脊髓; 脑源性神经营养因子; extracellular-signal regulated kinase1/2; brain-derived neurotrophic factor; replication-defective herpes simplex virus vector; replication-incompetent herpes simplex virus vector; spinal cord transection; neuroplasticity
• ISSN: 1673-5374
• DOI: 10.3969/j.issn.1673-5374.2011.13.010

The present study employed a rat model of T10 spinal cord transection. Western blot analyses revealed increased brain-dedved 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 kinasel/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 kinasel/2 signaling pathway in a rat model of adult spina cord transection.