中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (21): 1897-1901.doi: 10.4103/1673-5374.145357

• 原著:脑损伤修复保护与再生 • 上一篇    下一篇

地西泮对创伤性脑损伤大鼠海马CA1区谷氨酸能突触传递的影响

  

  • 收稿日期:2014-10-01 出版日期:2014-11-15 发布日期:2014-11-15
  • 基金资助:

     中国国家自然科学基金项目（81201984），陕西省卫生厅科研项目（2010E03），榆林市科技研究开发项目（Sf12-06）

Effects of diazepam on glutamatergic synaptic transmission in the hippocampal CA1 area of rats with traumatic brain injury

Lei Cao 1, 2, Xiaohua Bie 1, Su Huo 2, Jubao Du 2, Lin Liu 2, Weiqun Song 2   

  1. 1 Department of Functional Neurosurgery, Xi’an Red Cross Hospital, Xi’an, Shaanxi Province, China
    2 Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing, China
  • Received:2014-10-01 Online:2014-11-15 Published:2014-11-15
  • Contact: Weiqun Song, Ph.D., Department of Rehabilitation Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, China, songwq66@vip.163.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81201984; the Scientific Research Project of Shaanxi Provincial Health Department in China, No. 2010E03; and the Yulin Municipal Science and Technology Research and Development Project, No. Sf12-06.

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摘要：

已有研究显示脑液压冲击伤后海马CA3区神经元Schaffer侧枝的活性高和海马CA1区神经元活性升高，而地西泮能抑制大鼠海马神经元损伤后过度兴奋，但其影响兴奋性突触传递的机制并不明确。实验中以膜片钳技术记录显示，经地西泮治疗可显著增加液压脑颅损伤大鼠神经元输入-输出曲线斜率；在γ-氨基丁酸A型受体拮抗剂牡丹荷包碱15 µmol/L存在条件下，地西泮能减少损伤引起的海马放电次数，提示损伤大鼠海马中存在抑制通路。实验还发现地西泮能有效增加液压脑颅损伤诱导海马CA1区Schaffer侧枝配对脉冲易化比值，减少微小兴奋性突触后电位数量，减少动作电位依赖性谷氨酸的释放，逆转自发性谷氨酸释放。表明地西泮可以抑制大鼠海马CA1区中液压脑颅损伤诱导的兴奋性突触传递的增强。

关键词: 神经再生, 创伤性脑损伤, 液压脑颅损伤, 兴奋性突出传递, 海马CA1区锥体神经元, 配对脉冲易化, 微小兴奋性突触后电位, γ-氨基丁酸, 创伤性兴奋, 细胞内记录, NSFC grant

Abstract:

The activity of the Schaffer collaterals of hippocampal CA3 neurons and hippocampal CA1 neurons has been shown to increase after fluid percussion injury. Diazepam can inhibit the hyperexcitability of rat hippocampal neurons after injury, but the mechanism by which it affects excitatory synaptic transmission remains poorly understood. Our results showed that diazepam treatment significantly increased the slope of input-output curves in rat neurons after fluid percussion injury. Diazepam significantly decreased the numbers of spikes evoked by super stimuli in the presence of 15 µmol/L bicuculline, indicating the existence of inhibitory pathways in the injured rat hippocampus. Diazepam effectively increased the paired-pulse facilitation ratio in the hippocampal CA1 region following fluid percussion injury, reduced miniature excitatory postsynaptic potentials, decreased action-potential-dependent glutamine release, and reversed spontaneous glutamine release. These data suggest that diazepam could decrease the fluid percussion injury-induced enhancement of excitatory synaptic transmission in the rat hippocampal CA1 area.

Key words: nerve regeneration, traumatic brain injury, fluid percussion injury, excitatory synaptic transmission, hippocampal CA1 pyramidal neurons, paired-pulse facilitation, miniature excitatory postsynaptic potential, gamma-aminobutyric acid, post-traumatic hyperactivity, intracellular recording, NSFC grant, neural regeneration