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This Article Full Text Full Text (PDF) All Versions of this Article: 294/4/R1294    most recent 00709.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Ootsuka, Y. Articles by Romanovsky, A. A. PubMed PubMed Citation Articles by Ootsuka, Y. Articles by Romanovsky, A. A.

NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

Fever response to intravenous prostaglandin E₂ is mediated by the brain but does not require afferent vagal signaling

¹Department of Human Physiology, Centre for Neuroscience, Flinders University, Adelaide, Australia; and ²Systemic Inflammation Laboratory, Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, Arizona

Submitted 2 October 2007 ; accepted in final form 22 January 2008

PGE₂ produced in the periphery triggers the early phase of the febrile response to infection and may contribute to later phases. It can be hypothesized that peripherally synthesized PGE₂ transmits febrigenic signals to the brain via vagal afferent nerves. Before testing this hypothesis, we investigated whether the febrigenic effect of intravenously administered PGE₂ is mediated by the brain and is not the result of a direct action of PGE₂ on thermoeffectors. In anesthetized rats, intravenously injected PGE₂ (100 µg/kg) caused an increase in sympathetic discharge to interscapular brown adipose tissue (iBAT), as well as increases in iBAT thermogenesis, end-expired CO₂, and colonic temperature (T_c). All these effects were prevented by inhibition of neuronal function in the raphe region of the medulla oblongata using an intra-raphe microinjection of muscimol. We then asked whether the brain-mediated PGE₂ fever requires vagal signaling and answered this question by conducting two independent studies in rats. In a study in anesthetized rats, acute bilateral cervical vagotomy did not affect the effects of intravenously injected PGE₂ (100 µg/kg) on iBAT sympathetic discharge and T_c. In a study in conscious rats, administration of PGE₂ (280 µg/kg) via an indwelling jugular catheter caused tail skin vasoconstriction, tended to increase oxygen consumption, and increased T_c; none of these responses was affected by total truncal subdiaphragmatic vagotomy performed 2 wk before the experiment. We conclude that the febrile response to circulating PGE₂ is mediated by the brain, but that it does not require vagal afferent signaling.

temperature; thermoregulation; febrile; vagotomy; raphe; brown adipose tissue

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