| pubmed-article:583333 | pubmed:abstractText | Microinjected directly into the preoptic anterior hypothalamus (POAH), beta-endorphin (0.74--7.4 nmol) induced an increase in rectal temperature (RT) in the free-moving rat. Whereas the initial phase of the endorphin-induced rise in RT was partially attenuated by naloxone (5 or 20 mg/kg i.p.) or naltrexone (3 mg/kg i.p.), the late phase was completely blocked by the prostaglandin synthetase inhibitor, indomethacin (15 mg/kg i.p.). Pretreatment with a combination of indomethacin and naloxone resulted in an almost total block of the endorphin-induced increase in RT. Furthermore, the central serotonin antagonist, methergoline (1 mg/kg i.p.) antagonized the endorphin-evoked fever indicating serotonin may mediate the rise in RT. In contrast to the fever evoked in the POAH, beta-endorphin (7.4 nmol), given into the lateral cerebral ventricle (LCV), elicited a marked drop in RT, catalepsy, and analgesia which were completely blocked by naloxone (5 mg/kg). Similar to morphine, beta-endorphin elicited a naloxone-reversible hyperthermia when administered into the subarachnoid space surrounding the spinal cord. The similarities between beta-endorphin and morphine in their actions on RT as well as the possible role of serotonin or prostaglandins in beta-endorphin's thermogenic action are discussed. | lld:pubmed |
