摘要
目的观察吗啡急性中枢应用,对外周电刺激坐骨神经诱导的海马CA1区LTP及海马痛觉调制作用的影响,并探讨其可能的机制。方法25只雄性SD大鼠200~260g,随机分为5组。单刺激坐骨神经,各组侧脑室给药后给予强直刺激,观察场电位的变化。结果单刺激坐骨神经可在海马CA1区诱导出场电位(21.43±4.54)μV,其潜伏期较长(169.94±14.65)ms及阈值较高(平均15V),据此,推断是C类纤维诱发的;强直刺激后海马CA1区可出现持续时间在2h以上LTP现象;中、大剂量吗啡侧脑室注射可抑制海马CA1区LTP,纳洛酮可阻断这种作用。结论LTP是海马痛觉调制的生物学机制之一,阿片受体在其中起重要作用。吗啡对C-类纤维诱导的海马CA1区LTP的抑制作用可能通过阿片受体实现。
Objective To observe the effects of morphine on long-term potency (LTP) in hippocampal CA1 area which was induced by peripheral stimulation, and the action of hippocampus in pain modulation was also observed. Methods This experiment was performed on 25 male SD rats randomized into 5 groups. Single stimulation pulses were delivered to the sciatic nerve to evoke the hippocampal field potentials. Tetanic stimulation was used to induce hippocampal LTP. Before the titanic delivery, different doses were injected into intracerebroventricular( i. c. v) in each group. Results The electric stimulus to the sciatic nerve evoked LTP in rat hippocampal CA1 area. Intracerebroventricular injection of morphine[ ( 100 ng/5 μl), (1 μg/5 p2) ] inhibited C-fiber-evoked LTP in the hippocampal CA1 area, and this effect of morphine was blocked by the pretreatment with opioid receptor antagonist, Naloxone. Conclusion LTP is one of the mechanisms of the action of hippocampus in pain modulation, opioid receptor plays a significant role. Morphine can inhibit C-fiber-evoked LTP in the hippocampal CA1 area, and this effect is dependent on opioid receptor.
出处
《公共卫生与预防医学》
2007年第4期17-20,共4页
Journal of Public Health and Preventive Medicine