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1 Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: r.mcallen{at}hfi.unimelb.edu.au.
In fever, as in normal thermoregulation, signals from the preoptic area drive both cutaneous vasoconstriction and thermogenesis by brown adipose tissue (BAT). Both these responses are mediated by sympathetic nerves whose premotor neurons are located in the medullary raphe. EP3 receptors, key prostaglandin E2 (PGE2) receptors responsible for fever induction, are expressed in this same medullary raphe region. To investigate whether PGE2 in the medullary raphe might contribute to the febrile response, we tested whether direct injections of PGE2 into the medullary raphe could drive sympathetic nerve activity (SNA) to BAT and cutaneous (tail) vessels in anesthetized rats. Microinjections of glutamate (50 mM, 60-180 nl) into the medullary raphe activated both tail and BAT SNA, as did cooling the trunk skin. PGE2 injections (150-500 ng in 300-1000 nl) into the medullary raphe had no effect on tail SNA, BAT SNA, body temperature or heart rate. By contrast, 150 ng PGE2 injected into the preoptic area caused large increases in both tail and BAT SNA (+60±17 spikes/15s and 1591±150% of control, respectively), increased body temperature (+1.8±0.2°C), blood pressure (+17±2 mmHg) and heart rate (+124±19 bpm). These results suggest that despite expressing of EP3 receptors, neurons in the medullary raphe are unable to drive febrile responses of tail and BAT SNA independently of the preoptic area. Rather, they appear merely to transmit signals for heat production and heat conservation originating from the preoptic area.
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