神经病理性痛大鼠背根神经节神经元高电压激活钙电流的变化

Changes of High-Voltage-Activated Calcium Current in Dorsal Root Ganglion Neurons Isolated From Neuropathic Pain Rats

目的：观察神经病理性痛模型大鼠损伤侧损伤和邻近未损伤背根神经节神经元高电压激活钙电流的变化．以探讨两组神经元钙电流在大鼠神经病理性痛发病过程中的潜在作用。方法：采用SD雄性大鼠，以左侧L5脊神经结扎离断术建立神经病理性痛模型。酶消化法急性分离模型组损伤侧L5（SNL-L5组）、L4（SNL-L4组）以及正常对照组L5，L4背根神经节神经元（C组），采用全细胞膜片钳技术记录神经元高电压激活钙电流。结果：SNL—L5组与SNL-L4组峰值钙流密度均较C组降低（P〈0．05）。且SNL-L5组的峰值钙电流密度亦低于SNL-L4组（P〈0．05）。与C组和SNL-L4组相比．SNL-L5组钙电流半数激活电压向超级化方向移动（P〈0．05）．其N型钙电流比例上升（P〈0．05）。三组钙电流稳态失活曲线均无显著性差异（P〉0．05）。结论：神经病理性痛模型大鼠损伤背根神经节神经元高电压激活钙电流密度降低．电流激活曲线向超级化方向移动。N型Ca^2＋电流比例升高．提示损伤背根神经节神经元高电压激活钙电流可能在诱发神经病理性痛的过程中起主导作用。

Objective： We investigate the changes of high-voltage-actived （HVA） current in axotomized and neighboring intact dorsal root ganglion （DRG） neurons in a rat model of spinal nerve ligation （SNL） and the underlying contribution. Methods： Pathogen-free male SD rats （weight ,180-220mg） aged 4-6 weeks were used in this study. The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg. L5 spinal nerve was ligated between DRG and sciatic nerve and cut distal to the ligature. The animals were decapitated on the 14th postoperative day. L5 and L4 DRGs were respectively isolated and the neurons in the ganglion were enzymatically dissociated. The control group of rats were not accepted the surgery. The lumbar DRG neurons of this group were gained with the same method.The HVA-Ca2. current was recorded using whole cell patch clamp technique. Results： Peak calcium current density was significantly diminished in the SNL-L5 and SNL-L4groups compared with that in the control group （ P〈0.05 ） . Compared with the SNL-L4group, the SNL-L5 group also markedly reduced peak current density （P〈0.05）. Half＊activation value （Vail2） was also significantly lower Jn the SNL-L5 group versus in the control and SNL-L4 groups （P〈0.05） . The N-type relative contribution to the total HVA-Ca2. current markedly elevated in the SNL-L5 group compared with that in the control and SNL-L4 groups （P〈0,05） . There was no significant difference in steady-state inactivation curves among the three groups（P〉0.05）. Conclusion： In neuropathic pain rats, the HVA-Ca^2＋ cuurent of the injured DRG neurons may play a key role in inducing neuropathic pain.