激活脊髓小电导钙离子激活钾通道可抑制小鼠吗啡痛觉过敏

Activation of small conductance Ca^(2+) activated K^+ channel in spinal cord could inhibit morphine-induced hyperalgesia in mice

目的探究脊髓小电导钙离子激活钾通道(small conductance Ca^(2+)-activated K^+channels,SK通道)激活后对小鼠吗啡所致痛觉过敏的影响。方法选用♂C57BL6/N小鼠,建立吗啡痛觉过敏模型,鞘内注射SK通道激活剂1-EBIO后,测量小鼠热甩尾潜伏期(tail withdrawal latency,TWL),机械缩足阈值(mechanical withdrawal threshold,MWT)和内脏痛阈的变化。结果吗啡痛觉过敏模型小鼠与生理盐水对照组小鼠相比,热甩尾潜伏期、机械缩足阈值和内脏痛阈均降低;而鞘内注射SK通道激活剂1-EBIO后,与给药前相比,小鼠的痛阈热甩尾潜伏期,机械缩足阈值和内脏痛阈均升高;吗啡模型组小鼠的脊髓SK2膜蛋白表达量较对照组明显降低,而给予1-EBIO后,脊髓SK2膜蛋白表达量较模型组明显升高。结论脊髓SK通道参与小鼠吗啡引起的痛觉过敏。

Aim To explore the effect of activated SK channels（ small conductance Ca2＋-activated K＋ channels） on morphine-induced hyperalgesia in the spinal cord in mice.Methods Adult C57BL6/N male mice were chosen to establish the model of morphine-hyperalgesia.The changes of tail withdrawal latency（ TWL）,mechanical withdrawal threshold（ MWT） and the threshold of visceral pain were observed after intrathecal 1-EBIO,the agonist of SK channels.Results Compared with the control group,TWL,MWT and the threshold of visceral pain were decreased after morphine injection.After intrathecal 1-EBIO,the TWL,MWT and visceral pain threshold were increased.The level of spinal membrane SK2 expression in morphinetreated mice was decreased compared with that of control group.After intrathecal 1-EBIO,the level of spinal membrane SK2 expression was increased.Conclusion SK channels in the spinal cord are involved in morphine-induced hyperalgesia in mice.