ClC-3在神经病理性痛大鼠脊髓背角及背根神经节的表达及其参与痛行为调控的研究

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。

Studies on the expression of ClC-3 in spinal dorsal horn and dorsal root ganglion in neuropathic pain modal and involvement in pain behavior regulation

Objective: To observe the expression of voltage-gated chloride channel type Ⅲ(ClC-3) in the spinal dorsal horn(SDH) and dorsal root ganglion(DRG) in the common peroneal nerve ligation neuropathic pain modal of the rat,and involvement in pain behavior regulation induced by ClC-3 blockage.Methods: Immunohistochemistry,Western Blot and pain-behavior tests were employed to detect the expression changes of ClC-3 in neuropathic pain rats and the effect of ClC-3 on the nocieptive regulation.Results: In the intact normal rats,ClC-3 was principally located in neurons in the DRG;in the SDH,only ClC-3-immunorecative(ClC-3-ir) fibers were observed in lamina Ⅰ and Ⅱ,especially in lamina Ⅰ.In the common peroneal nerve ligated rats,ClC-3 immunoreactivities were increased in ipsilateral SDH and DRG before postoperative 7 days.Then ClC-3 was decreased gradually.After intrathecal injected chloride channel blocker,threshold of pain in the common peroneal nerve ligated rats was decreased.Conclusion: ClC-3 is increased in early stage of neuropathic pain,then decreased along with the deterioration of neuropathic pain gradually.Blocking-up ClC-3 could lessen the pain threshold.