中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (6): 972-975.doi: 10.4103/1673-5374.158364

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

损伤坐骨神经的病理性疼痛:或是是唾液酸加快脊髓背根神经节神经元电泳速率所致吗?

  

  • 收稿日期:2015-04-22 出版日期:2015-06-18 发布日期:2015-06-18
  • 基金资助:

    山西省自然科学基金项目(2012011042-3)

Sialic acid accelerates the electrophoretic velocity of injured dorsal root ganglion neurons

Chen-xu Li, Guo-ying Ma, Min-fang Guo, Ying Liu   

  1. Institute of Brain Sciences; Department of Physiology, Medical College, Shanxi Datong University, Datong, Shanxi Province, China
  • Received:2015-04-22 Online:2015-06-18 Published:2015-06-18
  • Contact: Chen-xu Li, M.D., lichenxv20021208@aliyun.com
  • Supported by:

    This study was supported by the Natural Science Foundation of Shanxi Province in China, No. 2012011042-3.

摘要:

外周神经损伤可导致初级感觉神经元胞体和轴突损伤位点产生异位自发电活动,引起神经病理性疼痛。由此,我们假设损伤性神经元上增加的唾液酸使其所带负电荷增加,在细胞电泳中其向阳极的电泳速率应快于正常神经元。实验建立大鼠坐骨神经慢性压迫性损伤模型,细胞电泳实验结果显示:与正常神经元相比,大鼠损伤性背根神经节神经元向正极的电泳速率明显加快;利用Ca2+及带正电的聚赖氨酸去中和损伤神经元胞膜外侧的唾液酸所带负电,或用唾液酸酶特异性地降解唾液酸,这些因素都能减慢损伤神经元泳动速率。结果证实,坐骨神经慢性压迫性损伤背根神经元膜上唾液酸增加,从而使其泳动速率加快,引起了神经病理性疼痛。

关键词: 神经再生, 周围神经损伤, 痛觉模型, 背根神经节, 初级感觉神经元, 膜表面糖蛋白, 唾液酸, 细胞电泳, 电泳速率, 热痛敏行为, 痛觉过敏, 唾液酸酶

Abstract:

Peripheral nerve injury has been shown to result in ectopic spontaneous discharges on soma and injured sites of sensory neurons, thereby inducing neuropathic pain. With the increase of membrane proteins on soma and injured site neurons, the negatively charged sialic acids bind to the external domains of membrane proteins, resulting in an increase of this charge. We therefore speculate that the electrophoretic velocity of injured neurons may be faster than non-injured neurons. The present study established rat models of neuropathic pain via chronic constriction injury. Results of the cell electrophoresis test revealed that the electrophoretic velocity of injured neuronal cells was faster than that of non-injured (control) cells. We then treated cells with divalent cations of Ca2+ and organic compounds with positive charges, polylysine to counteract the negatively charged sialic acids, or neuraminidase to specifically remove sialic acids from the membrane surface of injured neurons. All three treatments significantly reduced the electrophoretic velocity of injured neuronal cells. These findings suggest that enhanced sialic acids on injured neurons may accelerate the electrophoretic velocity of injured neurons.

Key words: nerve regeneration, peripheral nerve injury, pain sense model, dorsal root ganglion, primary sensory neuron, glycosylated membrane protein, sialic acid, cell electrophoresis, electrophoresis velocity, heat-hyperalgesia behavior, hyperalgesia, neuraminidase, neural regeneration