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目的:观察电压门控性氯通道(voltage-gated chloride channel,ClC)3型在腓总神经结扎神经病理性痛模型大鼠脊髓背角(spinal dorsal horn,SDH)和背根神经节(dorsal root ganglion,DRG)内的表达变化及阻断氯离子通道后痛行为的改变。方法:应用免疫组织化学染色法、蛋白印迹法以及痛行为检测观察ClC-3在神经病理性痛大鼠SDH和DRG的变化和作用。结果:在正常大鼠,ClC-3主要位于DRG神经元胞膜;在SDH,ClC-3阳性纤维主要位于Ⅰ层。在腓总神经结扎大鼠,1周内结扎侧背角Ⅰ层及DRG的ClC-3表达增加,2～4周表达逐渐减少,在DRG也观察到相同的现象。给予氯离子通道阻断剂后,腓总神经结扎大鼠的痛阈下降。结论:ClC-3在神经病理性痛早期表达上调,随病程发展逐渐下降;阻断ClC-3可使大鼠痛阈下降。
Objective: To observe the effect of voltage-gated chloride channel (ClC) 3 on spinal dorsal horn (SDH) and dorsal root ganglion , DRG) and the change of pain behavior after blocking the chloride channel. Methods: The changes and roles of ClC-3 in SDH and DRG of neuropathic pain rats were observed by immunohistochemical staining, Western blot and pain behavior test. Results: In normal rats, ClC-3 mainly located in the membrane of DRG neurons; in SDH, ClC-3 positive fibers mainly located in layer Ⅰ. In the common peroneal nerve ligation, the expression of ClC-3 was increased in the ligation of dorsal horn Ⅰ layer and DRG in 1 week, and gradually decreased in 2 ~ 4 weeks. The same phenomenon was also observed in DRG. After giving chloride ion channel blocker, the pain threshold of rats with common peroneal ligation decreased. Conclusion: The expression of ClC-3 is up-regulated in the early stage of neuropathic pain and gradually decreases with the progression of the disease. Blocking ClC-3 can decrease the pain threshold in rats.