Nonshivering thermogenesis without interscapular brown adipose tissue involvement during conditioned fear in the rat.

As with other forms of psychological stress, conditioned fear causes an increase in body temperature. The mechanisms underlying this stress-induced hyperthermia are not well understood, but previous research suggests that nonshivering thermogenesis might contribute, as it does during cold exposure. The major source of nonshivering thermogenesis in the rat is brown adipose tissue (BAT), and the largest BAT deposit in that species is in the interscapular area just below the skin. BAT is also under sympathetic control via beta-adrenoceptors. If BAT contributes to fear-induced hyperthermia, then the interscapular skin should warm up faster than other skin areas, and this response should be suppressed by the beta-adrenoceptor antagonist, propranolol. We tested this noninvasively by infrared thermography. In conscious rats, 30 min of contextual fear caused hyperthermia (as indicated by a +1.5 degrees C increase in lumbar back skin temperature) and increased the difference in temperature between interscapular and lumbar back skin (TiScap - TBack) by +1 degrees C. Propranolol (10 mg/kg ip) completely abolished this hyperthermia; however, the TiScap-TBack increase was not reduced. In contrast, exposure to cold air (4 degrees C) induced a +2.7 degrees C increase in TiScap-TBack, which was reduced to +1 degrees C after propranolol. The results show that conditioned fear-induced hyperthermia is of nonshivering origin and mediated by beta-adrenoceptors, but interscapular BAT does not contribute to it and does not appear to be activated, either.