Stress-induced hyperthermia is not mediated by brown adipose tissue in mice

Abstract

Psychological stress leads to sympathetically mediated increases in body temperature. Brown adipose tissue (BAT) is often thought to be the main organ to produce heat in response to sympathetic activation. However, we have previously shown that the hyperthermia evoked by conditioned fear in rats is not the result of thermogenesis in the interscapular area of the back, where the largest deposit of BAT is found. Stress-induced hyperthermia is widely used as an anxiety indicator in mice. We thus sought to verify if this response can be attributed to BAT thermogenesis. Eight C57BL/6 mice were shaved in the interscapular and lumbar back areas prior to testing. Animals received injections of 20mg/kg dl-propranolol or saline and were placed in either an open field or 4°C enclosure for 30min. Infrared thermographic images were taken each minute to record interscapular, lumbar and tail skin temperatures. Propranolol reduced the stress-induced hyperthermia observed during open field exposure (p<0.01), as indicated by the lumbar back skin temperature. Nevertheless, the difference between interscapular and lumbar skin temperatures remained constant, suggesting that this hyperthermia was not caused by BAT thermogenesis. There was no observable effect of propranolol on behavior, as animals remained active throughout the test. In contrast, the difference between interscapular and lumbar back skin temperature was increased by 2°C during cold exposure. This increase was abolished after propranolol (p<0.001), indicating BAT thermogenesis during this challenge. Hence, just as rats exposed to conditioned fear, mice exposed to an open field display a stress-induced hyperthermia that is not caused by BAT thermogenesis.