Temporal changes in the expression of some neurotrophins in spinal cord transected adult rats

被引:65
作者
Li, Xiao-Li
Zhang, Wei
Zhou, Xue
Wang, Xu-Yang
Zhang, Hong-Tian
Qin, Dan-Xia
Zhang, Han
Li, Qun
Li, Min
Wang, Ting-Hua [1 ]
机构
[1] Kunming Med Coll, Inst Neurosci, Kunming 650031, Peoples R China
[2] Sichuan Univ, Coll Preclin Forens Med, Dept Histol Embryol & Neurobiol, Chengdu 610065, Peoples R China
基金
美国国家科学基金会;
关键词
NGF; BDNF; NT-3; expression; transection; immunohistochemistry; rat;
D O I
10.1016/j.npep.2007.02.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Functional recovery of neurons in the spinal cord after physical injury is essentially abortive in clinical cases. As neurotrophins had been reported to be responsible, at least partially, for the lesion-induced recovery of spinal cord, it is not surprising that they have become the focus of numerous studies. Studies on endogenous neurotrophins, especially the three more important ones, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) in injured spinal cord might provide some important clues in clinical treatment. Here we investigate the immunohistological expression of the above three factors at lower thoracic levels of the spinal cord as well as changes in the motor functions of the adult rat hindlimbs after cord transection. The injured rats were allowed to survive 3, 7, 14 and 21 days post operation (dpo). Flaccid paralysis was seen at 3 dpo following cord transection, however, hindlimb function showed partial recovery from 7 dpo to 21 dpo. The numbers of NGF, BDNF and NT-3 immunopositive neurons and their optical densities all increased in the lesion-induced cord. The immuno-expression of NGF and BDNF peaked at 7 dpo, while that of NT-3 peaked at 7 dpo and remained so at least up to 14 dpo. These results suggested that neurotrophins might play essential roles in functional recovery of after spinal cord injury, but the time points for the expression of the three factors differed somewhat. (C) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:135 / 143
页数:9
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