Abstract

Experiments were conducted to determine if the hyperthermia after acute morphine sulfate (MS) administration was due to selective activation of brown adipose tissue (BAT) thermogenesis. Interscapular BAT temperature (TIBAT) and core (rectal) temperature (TR) were measured concurrently in groups of unrestrained, male Sprague-Dawley rats kept at 21.0 degrees C before and after i.p. (0.75, 2.0 or 10.0 mg/kg) or intracerebroventricular injections (200 ng- greater than 5 ul) of MS or sterile saline. TRS and TIBATS increased 0.6-1.0 degree C after i.p. intracerebroventricular injections of MS but the time course and magnitude of the changes in TIBATS from mean preinjections readings were not different from the increases in TRS. By contrast, isoproterenol HCl (0.5 mg/kg i.p.), known to activate BAT heat production, given to rats kept at 4 or 21 degrees C raised the TIBATS significantly above changes seen in TRS. Rats given MS in which the capacity for brown fat heat production had been increased previously (cold adaptation) or decreased (fasting or bilateral denervation) again evoked increases in TIBAT and TRS that were not significantly different from one another or from the response of warm-adapted, normophagic controls. Furthermore, oxygen uptakes were reduced after MS compared to oxygen uptakes after saline injections. [3H]Guanosine diphosphate binding to interscapular BAT mitochondria isolated from rats sacrificed at peak morphine hyperthermia (greater than 1.0 degree C) was not different from that of saline control animals. The results indicate clearly that the hyperthermia occurring in unrestrained rats after acute central or peripheral opiate administration is not due to selective activation of BAT thermogenesis.