Decerebration activates thermogenesis in the rat.

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Abstract
Under fluothane anesthesia, suction decerebration was performed at the immediate pre-pontine level in adult, male, Sprague-Dawley rats. This resulted in a large and sustained rise in rectal temperature from 35.6 .+-. 0.2 (control) to 38.8 .+-. 0.5.degree. C (decerebrate) following recovery from anesthesia. Propranolol inhibited this rise. In a separate group of continuously (urethane) anesthetized rats, brain transection at the immediate pre-pontine level produced marked increases in rectal temperature and O2 consumption, both of which were inhibited by injection of the .beta.-adrenergic antagonist propranolol (10 mg/kg). The rise in rectal temperature (2.8 .+-. 0.4.degree. C) after transection was preceded by a greater increase (3.6 .+-. 0.3.degree. C) in the temperature of the interscapular brown adipose tissue (i.b.a.t.). Skin temperature on the tail showed no immediate response. In anesthetized lean (+/?) male Zucker rats, rectal and i.b.a.t. temperatures showed similar responses to Sprague-Dawley rats after decerebration. In the genetically obese (fa/fa) Zucker rat, temperatures were not significantly altered by decerebration. The results, together with macroscopic examination of the transected brains, suggest that descending pathways (possibly arising in the mid-brain tegmentum) normally inhibit a sustained thermogenic drive from areas in the lower brain stem. Decerebration can release this inhibition and cause a large rise in body temperature and in metabolic rate, which apparently result from sympathetic activation of i.b.a.t. The genetically obese Zucker rat exhibits an impaired thermogenic response to decerebration.