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

被引：2
|
作者：
Xing, Ruxin [2 ]
Liu, Jia [3 ]
Jin, Hua [3 ]
Dai, Ping [3 ]
Wang, Tinghua [1 ]
机构：
[1] Sichuan Univ, W China Hosp, Lab Neurol Dis, Chengdu 610041, Sichuan Prov, Peoples R China
[2] Sichuan Univ, W China Hosp, Dept Neurosurg, Chengdu 610041, Sichuan Prov, Peoples R China
[3] Kunming Med Coll, Inst Neurosci, Kunming 650031, Yunnan Prov, Peoples R China
来源：
NEURAL REGENERATION RESEARCH | 2011年 / 6卷 / 13期
关键词：
spinal cord transection; brain-derived neurotrophic factor; neuroplasticity; extracellular-signal regulated kinase1/2; replication-incompetent herpes simplex virus vector; replication-defective herpes simplex virus vector; FUNCTIONAL RECOVERY; CORTICOSPINAL NEURONS; AXONAL REGENERATION; GROWTH-FACTOR; CELL-DEATH; BDNF; EXPRESSION; INJURY; PROTEIN; NEUROPROTECTION;
D O I：
10.3969/j.issn.1673-5374.2011.13.010
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The present study employed a rat model of T-10 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.
引用
收藏
页码：1017 / 1022
页数：6
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