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目的:探讨大鼠CCD模型模拟的腰背痛诱致的DRG大神经元兴奋性改变及其离子通道机制。方法:建立大鼠慢性压迫腰膨大L4/L5 DRG的CCD模型,模拟临床常见的腰背痛的触诱发痛表现。制备整节L4/L5 DRG标本,应用全细胞膜片钳技术记录去极化电流刺激诱致的DRG大型神经元的兴奋性改变及其离子通道机制。结果:对直径>50μm的健康的DRG大神经元进行全细胞膜片钳记录。结果显示:给予去极化方波电流刺激可以诱致CCD模型大鼠DRG大神经元呈现兴奋性增强的表现,具体表现为相同刺激强度的电流注射在CCD模型DRG大神经元上诱致的动作电位的频率显著高于对照组神经元。同样的细胞放电增强也见于给予细胞斜波电流刺激。进一步的机制研究分析显示CCD模型大鼠上DRG大神经元的I_h电流明显高于对照组大鼠。结论:CCD模型可以诱致DRG大神经元呈现超兴奋状态,该兴奋性增强的状态主要由I_h电流增强来介导,为认识神经损伤诱致的病理性痛觉敏化尤其是触诱发痛的神经机制提供了实验证据。
OBJECTIVE: To investigate the excitatory changes of DRG neurons induced by low back pain in rat model of CCD and its ion channel mechanism. Methods: The CCD model of chronic lumbar lumbosacral L4 / L5 DRG was established in rats to simulate the painful tactile allodynia of common lower back pain. Whole L4 / L5 DRG specimens were prepared and the whole cell patch clamp technique was used to record excitatory changes of DRG large neurons induced by depolarization current and its ion channel mechanism. Results: Whole-cell patch-clamp recording of healthy DRG neurons> 50 μm in diameter. The results showed that the depolarization square wave current stimulation can induce the excitement enhancement of the DRG neurons in the CCD model rats, and the current injection with the same stimulation intensity can induce the action potentials induced by the DRG neurons in the CCD model The frequency was significantly higher than that of the control group neurons. The same increase in cell discharge is also seen in cells given stimulation of the ramp current. Further mechanism studies showed that I_h currents of DRG neurons in CCD model rats were significantly higher than those in control rats. CONCLUSION: The CCD model can induce hyperontimulation of DRG neurons. The enhanced excitability is mainly mediated by the enhancement of I_h current, which provides a basis for understanding the neural mechanism of pathological pain sensitization induced by nerve injury, especially tactile allodynia The experimental evidence.