ACTH和吗啡对创伤痛大鼠海马锥体神经元NMDA受体通道的抑制

目的 探讨创伤痛大鼠海马锥体神经元NMDA受体通道动力学特性的变化ACTH和吗啡的作用。方法 实验以双侧踝关节离断大鼠为创伤痛模型，应用细胞贴附式膜片钳技术。结果 在正常7－10d大鼠急性分离的海马CA1区锥体神经元上，记录到多数膜下的NMDA受体通道有两个电导水平，分别为50pS及38pS,以50pS占多数，且以短开放为主，但也有长开放通道。38pS电导仅有短开放通道。大鼠双侧踝关节完全离断后2h,50pS有38pS短开放通道，50pS长开放通道的开放概率和开放时间均比正常对照组显著增加还出现了38pS长开放通道。在50pS短开放通道的记录中，ACTH^1-24和吗啡可显著抑制创伤大鼠海马CA1区锥体神经元NMDA受体通道的开放概率和开放时间；预中入阿片受体拮抗剂纳络酮能阻断上述的抑制效应。结论 ACTH和吗啡对伤害性信息传递的调制作用可能与其通过阿片受体抑制创伤大鼠海马NMDA受体通道动力学特性的变化有关。

The inhibitory effects of ACTH and morphine on NMDA receptor channel of hippocampal pyramidal neurons in rats suffering from traumatic pain

Objective To observe the changes of kinetic properties of N methyl D asparate (NMDA) receptor channel in acutely dissociated hippocampal pyramidal neurons in rats suffering from traumatic pain and the effects of ACTH 1 24 and morphine. Methods Model of trauma resulting from amputation in bilateral ankles was established in rats. Cell attached patch clamp technique was used. Results In acutely dissociated normal rat hippocampal CA1 pyramidal neurons, two conductance levels which were 50 pS and 38pS were found in NMDA receptor channel with 50pS prevailing. The forms of 50 pS channel included short opening and burst opening, but the 38 pS channel included only short opening. At 2 h after amputation in bilateral ankles, the open times and open probabilities of 50 pS and 38 ps short opening channel and 50 ps burst opening channel increased significantly as compared with those of the control. Furthermore, the 38 pS burst opening channel emerged. In the recording of 50 pS short opening channel, ACTH 1 24 as well as morphine markedly reduced the open time and open probabilities of NMDA receptor channel after amputation, which could be blocked by naloxone, the opiate receptor antagonist. Conclusion The modulation of ACTH and morphine on transmission of nociceptive information may be related to their inhibitory effects mediated by opiate receptor on the changes of kinetic properties of NMDA receptor channel of hippocampus in traumatic rats.