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[目的] 探讨在吗啡引起的痛觉超敏状态下,SD大鼠延髓头端腹内侧区电压门控钙通道(voltage-gated calcium channels, VGCCs)蛋白的表达变化和功能变化.[方法] 采用western blot方法检测α1C和α1H亚基蛋白在大鼠延髓头端腹内侧区(the rostral ventromedial medulla,RVM)的表达,采用脑片全细胞膜片钳技术记录大鼠RVM神经元的VGCCs电流.[结果] 在吗啡诱导的痛觉超敏状态下,SD大鼠RVM的α1C亚单位蛋白表达显著增加,同时神经元的VGCCs总电流和L-型VGCCs电流也显著增加.[结论] 延髓RVM的L-型电压门控钙通道的可塑性变化,可能是导致吗啡痛觉超敏的重要原因.“,”[Objective]To investigate the changes of voltage-gated calcium channels (VGCCs) in the rostral ventromedial medulla of SD rats under morphine-induced hyperalgesia.[Methods]The expression of a1C and a1H subunit proteins in the rostral ventromedial medulla (RVM) was detected by western blot.The VGCCs current of RVM neurons was recorded by the whole-cell patch-clamp technique.[Results]Our results indicated that the expression of α1C subunit in the RVM significantly increased under morphine-induced hyperalgesia, which was followed by the significant increase in total VGCCs currents and L-type VGCCs currents.[Conclusion]This data implicates that α1C-subunit-containing L-type VGCCs in RVM may play an essential role as a cellular mechanism leading to hyperalgesia.