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Am J Physiol Regul Integr Comp Physiol 279: R960-R965, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 3, R960-R965, September 2000

Vagal CCK and 5-HT3 receptors are unlikely to mediate LPS or IL-1beta -induced fever

S. M. Martin1, B. C. Wilson2, X. Chen2, Y. Takahashi2, P. Poulin2, and Q. J. Pittman2

1 Mt. Saint Vincent University, Halifax, Nova Scotia B3M 2J6, 2 Neuroscience Research Group, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada T2N 4N1

Previous studies suggested that peripheral immune mediators may involve intermediates acting on the vagus nerve, such as CCK or serotonin (5-HT). We have therefore investigated a possible role for vagal CCK-A and 5-HT3 receptors in the febrile response after intraperitoneal human recombinant interleukin-1beta (IL-1beta ) or lipopolysaccharide (LPS). Unanesthetized, adult male rats instrumented with abdominal thermistors were given intraperitoneal CCK-8 sulfate (100 or 150 µg/kg) or 2-methyl-5-hydroxytryptamine maleate (4 mg/kg). In other experiments, rats were treated with either antagonists to the 5-HT3 receptor (ondansetron HCl; 100 µg/kg) or the CCK-A receptor (L-364,718, 100 or 200 µg/kg) in combination with LPS or IL-1beta . CCK administration caused a short-lived hypothermia, but interference with the action of endogenous CCK at CCK-A receptors was without effect on IL-1beta - or LPS-induced fever. Neither activation of 5-HT3 receptors nor blockade of 5-HT3 receptors affected body temperature or LPS fever. Taken together, our data support the idea that vagal afferents responsive to pyrogenic cytokines may be different from those responsive to CCK or 5-HT.

lipopolysaccharide; interleukin; cholecystokinin; serotonin; 5-hydroxytryptamine


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