Wong C L
Department of Pharmacology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, N.T.
Arch Int Pharmacodyn Ther. 1989 Jul-Aug;300:22-8.
A 30 sec swim in water at 30 degrees C reduced the writhing response produced in the female mice by i.p. acetic acid. Peripherally administered, naloxone and beta-endorphin1-27 antagonized this swim-induced antinociception. However, i.c.v. administration of these compounds had minimal effects on this phenomenon. beta-Endorphin1-27 was effective in antagonizing the antinociceptive effect of beta-endorphin, but not that of morphine. Furthermore, the doses of naloxone required to antagonize the swim-induced antinociception were similar to those required to antagonize beta-endorphin which produced the same degree of antinociceptive response, but were much higher than those required to block the effect of morphine. These results suggest the involvement of beta-endorphin in swim-induced antinociception in female mice and its interaction with some peripheral opioid receptor(s) other than the mu-receptor.
在30摄氏度的水中游泳30秒可减少腹腔注射醋酸所致雌性小鼠的扭体反应。外周给予纳洛酮和β-内啡肽1-27可拮抗这种游泳诱导的抗伤害感受作用。然而，脑室内注射这些化合物对此现象影响极小。β-内啡肽1-27可有效拮抗β-内啡肽的抗伤害感受作用，但对吗啡的抗伤害感受作用无效。此外，拮抗游泳诱导的抗伤害感受作用所需的纳洛酮剂量与拮抗产生相同程度抗伤害感受反应的β-内啡肽所需剂量相似，但远高于阻断吗啡作用所需剂量。这些结果提示β-内啡肽参与雌性小鼠游泳诱导的抗伤害感受作用，且其与除μ受体以外的某些外周阿片受体相互作用。
