Weiss J, Thompson M L, Shuster L
Neuropharmacology. 1984 May;23(5):483-9. doi: 10.1016/0028-3908(84)90019-4.
The hypothermia produced by injecting apomorphine into mice was potentiated by morphine; it was antagonized by haloperidol, by naloxone and by naltrexone. The hypothermic responses to morphine, chlorpromazine and ethanol were also blocked by naltrexone. However, naltrexone potentiated the hypothermic response to pentobarbital. Tolerance to morphine, produced by subcutaneous implantation of a morphine pellet, was accompanied by cross-tolerance to apomorphine-induced hypothermia. Animals made tolerant to apomorphine were not tolerant to morphine-induced hypothermia. The dopamine supersensitivity resulting from chronic treatment with haloperidol potentiated the hypothermic response to apomorphine but not to morphine. These results suggest that endogenous opioids may serve as mediators in the control of thermoregulation by dopamine.
给小鼠注射阿扑吗啡所产生的体温过低现象会被吗啡增强;它会被氟哌啶醇、纳洛酮和纳曲酮拮抗。纳曲酮也会阻断对吗啡、氯丙嗪和乙醇的体温过低反应。然而,纳曲酮会增强对戊巴比妥的体温过低反应。通过皮下植入吗啡丸产生的对吗啡的耐受性伴随着对阿扑吗啡诱导的体温过低的交叉耐受性。对阿扑吗啡产生耐受性的动物对吗啡诱导的体温过低并不耐受。长期用氟哌啶醇治疗导致的多巴胺超敏反应增强了对阿扑吗啡的体温过低反应,但对吗啡没有增强作用。这些结果表明内源性阿片类物质可能作为多巴胺调节体温过程中的介质。