Decerebration activates thermogenesis in the rat.

Area of Science:

• Neuroscience
• Physiology
• Endocrinology

Background:

• Brainstem pathways regulate thermogenesis.
• Descending pathways normally inhibit thermogenic drives.
• Sympathetic activation of brown adipose tissue is crucial for thermoregulation.

Purpose of the Study:

• To investigate the role of brainstem pathways in thermoregulation.
• To examine the effect of decerebration on body temperature and metabolic rate.
• To explore the involvement of beta-adrenergic pathways and brown adipose tissue in the thermogenic response.

Main Methods:

• Decerebration at the pre-pontine level in Sprague-Dawley and Zucker rats.
• Measurement of rectal, interscapular brown adipose tissue (i.b.a.t.), and tail skin temperatures.
• Assessment of oxygen consumption.
• Pharmacological inhibition using propranolol (a beta-adrenergic antagonist).

Main Results:

• Decerebration caused a significant increase in rectal temperature and oxygen consumption in Sprague-Dawley rats.
• Propranolol inhibited the rise in temperature and oxygen consumption.
• The thermogenic response was blunted in genetically obese Zucker rats.
• Interscapular brown adipose tissue temperature increased significantly after decerebration.

Conclusions:

• Descending pathways normally inhibit a sustained thermogenic drive from the lower brain stem.
• Decerebration releases this inhibition, leading to increased body temperature and metabolic rate via sympathetic activation of i.b.a.t.
• Genetically obese Zucker rats exhibit an impaired thermogenic response to decerebration, suggesting a role for genetic factors in thermoregulation.