Bogdanov A I, Yarushkina N I
Department of Endocrine System Physiology, I.P. Pavlov Institute of Physiology, Russian Academy of Sciences, 6 Makarov Bank, 199034 St. Petersburg, Russia.
Neurosci Behav Physiol. 2004 Jul;34(6):575-8. doi: 10.1023/b:neab.0000028287.61380.05.
Experiments on conscious male Sprague-Dawley rats were performed to study the effects of adrenocorticotropic hormone (ACTH) on pain reactions. Pain sensitivity was assessed in terms of the latent period of tail withdrawal in response to heat. Systemic administration of ACTH and glucocorticoids to animals with normal levels of hormone production led to increases in the latent period of the tailflick reaction. The roles of glucocorticoids and opioid peptides in ACTH-induced analgesia were addressed in experiment on animals with deficient glucocorticoid production and animals in which opiate receptors were blocked with naltrexone. Deficiency in glucocorticoid production had no effect on ACTH-induced increases in the latent period of the tailflick reaction, while blockade of opiate receptors completely eliminated this effect of ACTH. ACTH-induced analgesia in conscious rats is mediated by opiate receptors and not by glucocorticoids.
对清醒的雄性斯普拉格-道利大鼠进行实验,以研究促肾上腺皮质激素(ACTH)对疼痛反应的影响。根据对热刺激的甩尾潜伏期来评估疼痛敏感性。对激素产生水平正常的动物全身给予促肾上腺皮质激素和糖皮质激素,导致甩尾反应潜伏期延长。在糖皮质激素产生不足的动物以及用纳曲酮阻断阿片受体的动物身上进行实验,探讨了糖皮质激素和阿片肽在促肾上腺皮质激素诱导的镇痛中的作用。糖皮质激素产生不足对促肾上腺皮质激素诱导的甩尾反应潜伏期延长没有影响,而阿片受体的阻断则完全消除了促肾上腺皮质激素的这种作用。促肾上腺皮质激素在清醒大鼠中诱导的镇痛是由阿片受体介导的,而非糖皮质激素。