Chance W T, Rosecrans J A
Pharmacol Biochem Behav. 1979 Dec;11(6):643-6. doi: 10.1016/0091-3057(79)90256-9.
Autoanalgesia (behaviorally-induced antinociception) may be elicited by acute stress or clasically conditioned fear. Antinociception within both of these paradigms is reportedly associated with increased CNS opioid peptide activity. Large doses of naloxone (20 mg/kg) failed to modify antinociception elicited by acute footshock or conditioned fear in rats. Naloxone (4 mg/kg) was also ineffective against antinociception following footshock in mice. These data suggest that if an endorphin does mediate autoanalgesia, the affinity of its receptor for naloxone is very low. Alternatively, parallel opioid and non-opioid systems may be activated by autoanalgesic procedures, with antagonism of the opioid component being insufficient to reduce the antinociception.
自身镇痛(行为诱导的抗伤害感受)可由急性应激或经典条件恐惧引发。据报道,在这两种范式中,抗伤害感受都与中枢神经系统阿片肽活性增加有关。大剂量纳洛酮(20毫克/千克)未能改变急性足部电击或条件恐惧在大鼠中引发的抗伤害感受。纳洛酮(4毫克/千克)对小鼠足部电击后的抗伤害感受也无效。这些数据表明,如果内啡肽确实介导自身镇痛,其受体对纳洛酮的亲和力非常低。或者,自身镇痛程序可能会激活平行的阿片类和非阿片类系统,阿片类成分的拮抗作用不足以降低抗伤害感受。