中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (10): 1753-1758.doi: 10.4103/1673-5374.238618

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

创伤性脑损伤后认知障碍与大鼠海马齿状回兴奋性突触后电位长时程抑制减弱有关

  

  • 收稿日期:2018-07-06 出版日期:2018-10-15 发布日期:2018-10-15
  • 基金资助:

    天津市自然科学基金(17JCQNJC 12000)；国家自然科学基金(81330029，81501057)；天津医科大学总医院基金(ZYYFY 2016014)

Cognitive impairment after traumatic brain injury is associated with reduced long-term depression of excitatory postsynaptic potential in the rat hippocampal dentate gyrus

Bao-Liang Zhang, Yue-Shan Fan, Ji-Wei Wang, Zi-Wei Zhou, Yin-Gang Wu, Meng-Chen Yang, Dong-Dong Sun, Jian-Ning Zhang   

  1. Department of Neurosurgery, Tianjin Medical University General Hospital; Tianjin Neurological Institute; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education; Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Tianjin, China
  • Received:2018-07-06 Online:2018-10-15 Published:2018-10-15
  • Contact: Jian-Ning Zhang, PhD, MD,jianningzhang@hotmail.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81330029, 81501057; the Natural Science Foundation of Tianjin of China, No. 17JCQNJC12000; the Tianjin Medical University General Hospital Funding in China, No. ZYYFY2016014.

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摘要：

创伤性脑损伤可引起脑组织神经元损伤缺失，患者可能会出现远期症状性癫痫和认知障碍，发生的机制尚不清楚。有研究表明，海马不同区域兴奋性的改变与认知功能障碍及远期症状性癫痫的发作密切相关。实验设计观察创伤性脑损伤导致的中间神经元缺失与海马区域兴奋性变化之间的关系，以明确该机制。以液压打击法建立创伤性脑损伤大鼠模型，建模后7 d神经损伤严重程度评分平均分为9.5分，表明大鼠神经功能有明显的损害。神经电生理及免疫细胞化学染色显示，模型大鼠海马齿状回兴奋性突触后电位斜率及长时程抑制值均增高（说明长时程抑制减弱），中间神经元标记物缩胆囊素和小清蛋白免疫反应活性细胞显著减少，说明海马齿状回中间神经元出现缺失，兴奋性发生改变。上述数据说明，创伤性脑损伤导致的海马齿状回中间神经元缺失与海马齿状回区域的长时程抑制减弱有关。

orcid:0000-0002-7290-0994(Jian-Ning Zhang)

 

关键词: 长时程抑制, 创伤性脑损伤, 海马, 中间神经元, 兴奋性, 齿状回, 小清蛋白, 缩胆囊素, 电生理, 定量, 神经再生

Abstract:

Traumatic brain injury can cause loss of neuronal tissue, remote symptomatic epilepsy, and cognitive deficits. However, the mechanisms underlying the effects of traumatic brain injury are not yet clear. Hippocampal excitability is strongly correlated with cognitive dysfunction and remote symptomatic epilepsy. In this study, we examined the relationship between traumatic brain injury-induced neuronal loss and subsequent hippocampal regional excitability. We used hydraulic percussion to generate a rat model of traumatic brain injury. At 7 days after injury, the mean modified neurological severity score was 9.5, suggesting that the neurological function of the rats was remarkably impaired. Electrophysiology and immunocytochemical staining revealed increases in the slope of excitatory postsynaptic potentials and long-term depression (indicating weakened long-term inhibition), and the numbers of cholecystokinin and parvalbumin immunoreactive cells were clearly reduced in the rat hippocampal dentate gyrus. These results indicate that interneuronal loss and changes in excitability occurred in the hippocampal dentate gyrus. Thus, traumatic brain injury-induced loss of interneurons appears to be associated with reduced long-term depression in the hippocampal dentate gyrus.

Key words: nerve regeneration, long-term depression, traumatic brain injury, hippocampus, interneurons, excitability, dentate gyrus, parvalbumin, cholecystokinin, electrophysiology, quantification, neural regeneration