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ＣＣＫ－８在脊髓水平可对抗μ－阿片受体介导的抗伤害性作用，但其作用位，点及机制尚不清楚。本实验以急性分离的大鼠背根节（ＤＲＧ）神经元为标本，用全细胞膜片钳（ｗｈｏｌｅ－ｃｅｌｌｐａｔｃｈ－ｃｌａｍｐ）方法记录钙通道电流，观察分析特异性μ－受体激动剂羟甲芬太尼（ＯＭＦ）对电压依赖性钙通道电流的作用，以及在同一细胞上ＣＣＫ－８对此作用的影响。结果显示ＯＭＦ可明显抑制钙通道电流，其抑制作用可被μ－受体拮抗剂纳络酮或ＣＣＫ－８所翻转，而ＣＣＫ－８的作用又可被ＣＣＫ－Ｂ受体拮抗剂Ｌ３６５，２６０所对抗。结果提示：ＣＣＫ－８可在同一细胞上经ＣＣＫ－Ｂ受体对抗阿片效应。ＣＣＫ－８本身对钙通道电流并无增强效应，相反它可引起抑制作用。关于ＣＣＫ－８如何对抗μ－受体介导的机制有待进一步研究。
CCK-8 can antagonize μ-opioid receptor-mediated antinociception at the spinal cord level, but its location, location and mechanism are still unclear. In this study, an acutely isolated rat dorsal root ganglion (DRG) neurons were used as a sample. The whole-cell patch-clamp method was used to record the calcium channel currents. The effects of the specific μ-receptor agonist, The effect of telamin (OMF) on voltage-dependent calcium channel currents and the effect of CCK-8 on this effect on this same cell. The results showed that OMF can significantly inhibit the calcium channel current, its inhibitory effect can be reversed by the μ-receptor antagonist naloxone or CCK-8, and the role of CCK-8 can be CCK-B receptor antagonist L365,260 Confrontation. The results suggest that CCK-8 can antagonize the opioid effect on the same cell via CCK-B receptor. CCK-8 itself has no potentiating effect on calcium channel current, on the contrary it can cause an inhibitory effect. The mechanism of how CCK-8 antagonizes μ-receptor remains to be further studied.