摘要
目的:研究地昔帕明(desipramine,DMI)对大鼠背根神经节神经元电压依赖性钠电流的影响。方法:分离单个大鼠背根神经节,应用全细胞膜片钳技术观察地昔帕明对内向钠电流(INa)的影响。结果:地昔帕明浓度依赖性地抑制INa,即分别加入10,50,100μmol/L的DMI可使钠电流的抑制率达(5.56±0.62)%,(54.67±13.39)%和(86.63±16.08)%,并且,50μmol/L的DMI可使INa稳态失活曲线左移,V1/2分别由对照组的-(43.71±0.79)mV降低至-(47.91±1.14)mV,k值无明显变化。结论:DMI浓度依赖性地抑制背根神经节神经元Na+通道,并改变通道的失活,这可能是其影响痛觉传导通路,产生镇痛作用的机制之一。
Aim： To study the effects of desipramine, a tricyclic antidepressant, on the sodium currents in the isolated rat dorsal root ganglion neurons. Methods： Isolate rat dorsal mot ganglion and observe the effects of desipramine on sodium current by whole cell patch clamp recordings. Results： Desipramine blocked the whole cell sodium currents evoked by a voltage step from - 60 mV to ＋ 20 mV from a holding potential of - 70 mV. This block has concentration dependente property with the percentage of inhibition of （5.56 ± 0.62）%, （54.67 ± 13.39）% and （86.63 ± 16.08）% in the presence of 10,50 and 100 μmol/L desipramline, respectively. In addition, desipramine of 50 μmol/L shifted the state inactivation of sodium current to left with V1/2 be changed from - （43.71 ± 0.79）mV to - （47.91 ± 1.14）mV. However, no significant change occurred to k. Conclusion： Desipramine blocked the whole cell sodium currents in the dose dependent manner, and elicited the inactivation of this channel; This suggests that desipramine may affect neuropathy of pain and induce analgesic effect by inhibiting sodilum currents of dorsal mot ganglion neurons.
出处
《中国药科大学学报》
CAS
CSCD
北大核心
2006年第3期259-262,共4页
Journal of China Pharmaceutical University
基金
国家自然科学基金资助项目(No.30271137)~~
