中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (2): 368-374.doi: 10.4103/1673-5374.346548

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

重复经颅磁刺激上调突触可塑性相关蛋白促进创伤性脑损伤后的神经功能恢复

  

  • 出版日期:2023-02-15 发布日期:2022-08-08
  • 基金资助:
    南方医科大学南方医院院长基金(2016Z003 (50107021))

Repetitive transcranial magnetic stimulation promotes neurological functional recovery in rats with traumatic brain injury by upregulating synaptic plasticity-related proteins

Fang-Fang Qian1, #, You-Hua He2, #, Xiao-Hui Du1, Hua-Xiang Lu1, Ren-Hong He1, *, Jian-Zhong Fan1, *   

  1. 1Department of Rehabilitation Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China; 2Department of Comprehensive Ward, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China
  • Online:2023-02-15 Published:2022-08-08
  • Contact: Jian-Zhong Fan, MD, fjz@smu.edu.cn; Ren-Hong He, MD, he462766164@163.com.
  • Supported by:
    This study was supported by the President Foundation of Nanfang Hospital, Southern Medical University, No. 2016Z003 (50107021) (to JZF).

摘要:

多项研究表明重复经颅磁刺激可增强突触可塑性,改善神经功能障碍,但其对中度创伤性脑损伤大鼠的治疗机制尚需明确。实验采用Feeney法建立中度创伤性脑损伤大鼠模型,给予重复经颅磁刺激。见其增加了损伤侧脑组织中与长时程增强的发生密切相关的脑源性神经营养因子、TrkB、N-甲基-D-天冬氨酸受体1以及磷酸化环磷酸腺苷反应成分结合蛋白的蛋白和mRNA的表达水平,治疗还部分逆转了损伤后突触素的缺失,促进了突触超微结构的重塑。表明重复经颅磁刺激通过上调突触可塑性相关蛋白表达是促进中度创伤性脑损伤神经功能恢复得到一种机制。

https://orcid.org/0000-0001-7516-4497 (Jian-Zhong Fan)

关键词: 创伤性脑损伤, 中度创伤性脑损伤, 重复经颅磁刺激, 神经功能障碍, 功能改善, 脑源性神经营养因子, TrkB, N-甲基-D-天冬氨酸受体, 突触素, 突触可塑性

Abstract: Studies have shown that repetitive transcranial magnetic stimulation (rTMS) can enhance synaptic plasticity and improve neurological dysfunction. However, the mechanism through which rTMS can improve moderate traumatic brain injury remains poorly understood. In this study, we established rat models of moderate traumatic brain injury using Feeney’s weight-dropping method and treated them using rTMS. To help determine the mechanism of action, we measured levels of several important brain activity-related proteins and their mRNA. On the injured side of the brain, we found that rTMS increased the protein levels and mRNA expression of brain-derived neurotrophic factor, tropomyosin receptor kinase B, N-methyl-D-aspartic acid receptor 1, and phosphorylated cAMP response element binding protein, which are closely associated with the occurrence of long-term potentiation. rTMS also partially reversed the loss of synaptophysin after injury and promoted the remodeling of synaptic ultrastructure. These findings suggest that upregulation of synaptic plasticity-related protein expression is the mechanism through which rTMS promotes neurological function recovery after moderate traumatic brain injury. 

Key words: brain-derived neurotrophic factor, moderate traumatic brain injury, neurological dysfunction, neurological improvement, N-methyl-D-aspartic acid receptor, repetitive transcranial magnetic stimulation, synaptic plasticity, synaptophysin, traumatic brain injury, TrkB