Siegfried B, Frischknecht H R, Riggio G, Waser P G
Behav Neurosci. 1987 Jun;101(3):423-6. doi: 10.1037//0735-7044.101.3.423.
In a first experiment, exposure of DBA/2 mice to a small number of attack bites by a C57BL/6 mouse resulted in low-intensity analgesia as assessed by the tail-flick test. The analgesia dissipated within 10 min and was insensitive to naloxone (10 mg/kg, sc) but was antagonized by the irreversible opioid antagonist beta-chlornaltrexamine (5 mg/kg, sc). In a second experiment, preexposure to a nonaggressive C57BL/6 opponent prevented low-intensity analgesia induced by a small number of attack bites 24 hr later. The preexposure effect was abolished by naloxone (10 mg/kg, sc) given before the nonaggressive confrontation. This suggests that the release of endogenous opioids during preexposure interferes with the subsequent activation of endogenous opioid-mediated pain control mechanisms.
在第一个实验中,将DBA/2小鼠暴露于C57BL/6小鼠的少量攻击咬伤之下,通过甩尾试验评估,结果显示为低强度镇痛。这种镇痛作用在10分钟内消散,对纳洛酮(10毫克/千克,皮下注射)不敏感,但可被不可逆的阿片类拮抗剂β-氯代三嗪(5毫克/千克,皮下注射)拮抗。在第二个实验中,预先暴露于无攻击性的C57BL/6对手,可防止24小时后少量攻击咬伤诱导的低强度镇痛。在无攻击性对峙之前给予纳洛酮(10毫克/千克,皮下注射)可消除预先暴露的效果。这表明预先暴露期间内源性阿片类物质的释放会干扰内源性阿片类物质介导的疼痛控制机制的后续激活。