Male New Zealand White rabbits, Oryctolagus cuniculus, were stereotaxically implanted with a guide tube above the preoptic/anterior hypothalamus area (PO/AH) for the injection of the opioid peptide, beta-endorphin (beta-E), naloxone, sodium salicylate, or physiological saline. PO/AH and ear temperature, oxygen consumption, and evaporative heat loss (EHL) were recorded in free-moving rabbits before and after injection of saline followed with beta-E, naloxone, or sodium salicylate at ambient temperatures (Ta) of 2-31 degrees C. A 5-micrograms injection of beta-E promoted a rapid reduction in ear temperature followed by a prolonged rise in PO/AH (body) temperature. Preinjection with an isovolumetric amount of the opiate antagonist, naloxone, inhibited the thermoregulatory effects of beta-E. The beta-E-induced rise in body temperature was directly correlated with Ta. beta-E had no effect on oxygen consumption at Ta's of 5 and 27 degrees C. When measured 30 min after injection, beta-E demonstrated a significant inhibition of EHL at Ta's of 27 and 31 but not 5 degrees C. The beta-E-induced rise in body temperature was not antagonized with preinjections of sodium salicylate in the PO/AH. These data indicate that beta-E promotes a regulated increase in body temperature. The mechanism of activation appears to be distinct from that of an infectious fever.
Alterations in nociception and body temperature after intracisternal administration of neurotensin, beta-endorphin, other endogenous peptides, and morphine.
