中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2013, Vol. 8 ›› Issue (32): 3013-3019.doi: 10.3969/j.issn.1673-5374.2013.32.004

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

瞬时受体电位通道A1参与神经元降钙素基因相关肽的释放

  

  • 收稿日期:2013-07-23 修回日期:2013-09-12 出版日期:2013-11-15 发布日期:2013-11-15
  • 基金资助:

    日本私立大学基础研究支撑项目

Transient receptor potential channel A1 involved in calcitonin gene-related peptide release in neurons

Nobumasa Ushio1, Yi Dai1, 2, 3, Shenglan Wang1, 2, 3, Tetsuo Fukuoka1, Koichi Noguchi1   

  1. 1 Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan
    2 Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo 650-8530, Japan
    3 Traditional Medicine Research Center, Chinese Medicine Confucius Institute at Hyogo College of Medicine, Kobe, Hyogo 650-8530, Japan
  • Received:2013-07-23 Revised:2013-09-12 Online:2013-11-15 Published:2013-11-15
  • Contact: Yi Dai, Ph.D., Associate professor, Department of Pharmacy, School of Pharmacy, Hyogo University of Health Sciences, Kobe, Hyogo 650-8530, Japan, ydai@huhs.ac.jp.
  • About author:This work was supported by the Research Basis Formation Supporting Project for Private University.
  • Supported by:

    This work was supported by the Research Basis Formation Supporting Project for Private University.

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摘要：

瞬时受体电位通道A1是初级传入神经末梢中可以被伤害性刺激激活的离子通道，参与机械性感觉、痛觉的传导以及炎性反应的产生。实验目的在于观察激活的瞬时受体电位通道A1是否能诱导初级传入神经元释放降钙素基因相关肽。我们发现瞬时受体电位通道A1激活剂异硫氰酸丙烯酯可促进大鼠背根神经节神经元释放降钙素基因相关肽。而用反义寡聚脱氧核苷酸敲低瞬时受体电位通道A1是能阻止AITC对背根神经节神经元降钙素基因相关肽的促释放作用。由此我们提出，激活瞬时受体电位通道A1可引发感觉神经元释放降钙素基因相关肽的观点。

关键词: 瞬时受体电位通道A1, 降钙素基因相关肽, 背根神经节, 疼痛, 痛觉增敏, 伤害性刺激, 感觉神经元, 基金资助文章

Abstract:

Transient receptor potential channel A1 is one of the important transducers of noxious stimuli in the primary afferents, which may contribute to generation of neurogenic inflammation and hyperalgesia. The present study was designed to investigate if activation of transient receptor potential channel A1 may induce calcitonin gene-related peptide release from the primary afferent neurons. We found that application of allyl isothiocyanate, a transient receptor potential channel A1 activator, caused calcitonin gene-related peptide release from the cultured rat dorsal root ganglion neurons. Knock-down of transient receptor potential channel A1 with an antisense oligodeoxynucleotide prevented calcitonin gene-related peptide release by allyl isothiocyanate application in cultured dorsal root ganglion neurons. Thus, we concluded that transient receptor potential channel A1 activation caused calcitonin gene-related peptide release in sensory neurons.

Key words: neural regeneration, transient receptor potential channel A1, calcitonin gene-related peptide, dorsal root ganglion neurons, pain, hyperalgesia, noxious stimuli, sensory neuron, grants-supported paper, neuroregeneration