Effects of brain epinephrine depletion on thermoregulation, reflex bradycardia, and motor activity in rats.

Two hours after i.p. administration of 2-cyclooctyl-2-hydroxyethylamine (CONH), 1-aminomethylcycloundecanol (CUNH), 2,3-dichloro-alpha-methylbenzylamine (DCMB), or 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline (SKF64139), the hypothalamic and brain stem epinephrine (EPI) contents of rat brain were decreased. Depletions of brain EPI with these phenylethanolamine N-methyltransferase (PNMT) inhibitors reduced the rectal temperatures of rats at ambient temperatures of 8 and 22 degrees C. The hypothermia in response to these PNMT inhibitors was due to decreased metabolism and cutaneous vasodilatation. The locomotor stimulant responses induced by thyrotropin-releasing hormone were also reduced by administration of any one of these PNMT inhibitors. On the other hand, acute administration of any of these PNMT inhibitors enhanced the reflex bradycardia induced by i.v. infusion of EPI. The data suggest that brain (particularly the hypothalamus and brain stem) EPI-containing neurons are involved in the regulation of body temperature, reflex bradycardia, and motor performance in the rat.