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目的研究辣椒素(CAP)在急性分离的大鼠骶髓后连合核(SDCN)神经元的药理学特性。方法采用制霉菌素穿孔膜片钳全细胞记录方法。结果当钳制电压为-40 mV时,在所有被检测的SDCN神经元上给予CAP不引起任何电流;CAP(10～3 000μmol/L)可以呈浓度依赖方式可逆性的抑制海人藻酸(KA)所激活的AMPA受体介导的电流,IC_(50)为(60.7±19.2)μmol/L;该抑制作用呈电压非依赖性。结论CAP在大鼠SDCN神经元可对AMPA受体激活的电流产生抑制作用,此作用可能和内脏痛的调节有关。
Objective To study the pharmacology of capsaicin (CAP) in acutely isolated rat sacral commissural commissural nucleus (SDCN) neurons. Methods The nystatin perforated patch clamp whole cell recording method was used. Results When the clamping voltage was -40 mV, CAP did not induce any current in all tested SDCN neurons; CAP (10-3 000 μmol/L) could reversibly inhibit kainic acid in a concentration-dependent manner (KA The activated AMPA receptor-mediated current IC50 was (60.7±19.2) μmol/L; the inhibition was voltage-independent. Conclusion CAP can inhibit AMPA receptor-activated currents in rat SDCN neurons, which may be related to the regulation of visceral pain.