Siegfried B, Frischknecht H R, Riggio G, Waser P G
Institute of Pharmacology, University of Zurich, Switzerland.
Behav Neurosci. 1987 Dec;101(6):797-805. doi: 10.1037//0735-7044.101.6.797.
Four experiments were designed to characterize long-term analgesic (LTA) reaction in attacked mice. In Experiment 1 we showed that analgesic reaction in DBA mice, induced by the stress of being attacked (30 or 50 bites), is reinstated upon reexposure to seven bites 24 hr later. The magnitude of the LTA response depended on the level of analgesia on Day 1 and was smaller than the original response. In Experiment 2 we showed that LTA was prevented by naloxone or beta-chlornaltrexamine given before exposure (50 bites) on Day 1. Results of Experiment 3 revealed that naloxone or beta-chlornaltrexamine injected before reexposure to seven bites on Day 2 antagonized LTA measured 10 min, but not 1 min, after reexposure. In Experiment 4 we showed that morphine substituted for being attacked on Day 1 failed to produce LTA. We concluded that pain inhibitory mechanisms remain in a state of increased readiness for at least 24 hr after attack stress and that activation of opioid systems is necessary but not sufficient to produce LTA, a response that is only partly sensitive to opioid antagonists.
设计了四项实验来表征受攻击小鼠的长期镇痛(LTA)反应。在实验1中,我们表明,DBA小鼠因遭受攻击(30次或50次咬伤)的应激而产生的镇痛反应,在24小时后再次暴露于7次咬伤时会恢复。LTA反应的强度取决于第1天的镇痛水平,且小于原始反应。在实验2中,我们表明,在第1天暴露(50次咬伤)前给予纳洛酮或β-氯诺他明可预防LTA。实验3的结果显示,在第2天再次暴露于7次咬伤前注射纳洛酮或β-氯诺他明,可拮抗再次暴露10分钟后而非1分钟后测得的LTA。在实验4中,我们表明,第1天用吗啡替代遭受攻击未能产生LTA。我们得出结论,攻击应激后疼痛抑制机制至少在24小时内保持增强的准备状态,阿片系统的激活对于产生LTA是必要的,但并不充分,LTA反应仅部分对阿片拮抗剂敏感。