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Decerebration activates thermogenesis in the rat.

Under fluothane anaesthesia, 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 degrees C (decerebrate) following recovery from anaesthesia. Propranolol inhibited this rise. In a separate group of continuously (urethane) anaesthetized rats, brain transection at the immediate pre‐pontine level produced marked increases in rectal temperature and oxygen 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 degrees C) after transection was preceded by a greater increase (3.6 +/‐ 0.3 degrees C) in the temperature of the interscapular brown adipose tissue (i.b.a.t.). Skin temperature on the tail showed no immediate response. In anaesthetized lean (+/?) male Zucker rats, rectal and i.b.a.t. temperatures showed similar responses to Sprague‐Dawley rats after decerebration, but in the genetically obese (fa/fa) Zucker rat, temperatures were not significantly altered by decerebration. The above 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.