Abstract
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 non-shivering thermogenesis
might contribute, as it does during cold exposure. The major source of non-shivering
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 β-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 β-adrenoceptor antagonist, propranolol.
We tested this non-invasively by infrared thermography. In conscious rats, 30 min of
contextual fear caused hyperthermia (as indicated by a +1.5°C increase in lumbar
back skin temperature) and increased the difference in temperature between
interscapular and lumbar back skin (TiScap-TBack) by +1°C. Propranolol (10 mg/kg,
i.p.) completely abolished this hyperthermia, however, the TiScap-TBack increase
was not reduced. In contrast, exposure to cold air (4°C) induced a +2.7°C increase in
TiScap-TBack which was reduced to +1°C after propranolol. The results show that
conditioned fear-induced hyperthermia is of non-shivering origin and mediated by β-
adrenoceptors, but interscapular BAT does not contribute to it and does not appear to
be activated, either.