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The Journal of Neuroscience, February 11, 2004, 24(6):1312-1318; doi:10.1523/JNEUROSCI.3145-03.2004

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Behavioral/Systems/Cognitive
A Novel Antipyretic Action of 15-Deoxy-^12,14-Prostaglandin J₂ in the Rat Brain

Abdeslam Mouihate, Lysa Boissé, and Quentin J. Pittman

Neuroscience Research Group, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Alberta, T2N 4N1 Canada

Fever is an important part of the host defense response, yet fever can be detrimental if it is uncontrolled. We provide the first evidence that 15-deoxy-^12,14-prostaglandin J₂ (15d-PGJ₂), an endogenous ligand for peroxisome proliferator-activated receptor (PPAR), can attenuate the febrile response to lipopolysaccharide (LPS) in rats via an action on the brain. Furthermore, we show that PPAR is expressed in the hypothalamus, an important locus in the brain for fever generation. In addition, 15d-PGJ₂ and its synthesizing enzyme (PGD₂ synthase) were present in rat cerebrospinal fluid, and their levels were enhanced in response to systemic injection of LPS. The antipyretic effect of 15d-PGJ₂ was associated with reduction in LPS-stimulated cyclooxygenase-2 expression in the hypothalamus but not in p44/p42 mitogen-activated protein kinase phosphorylation or in the expression of the PPAR.

Thus it is likely that there is a parallel induction of an endogenous prostanoid pathway in the brain capable of limiting deleterious actions of the proinflammatory prostaglandin E₂-dependent pathway.

Key words: stress; central autonomic pathways; hypothalamus; fever; lipopolysaccharide; PPAR

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Received July 1, 2003; revised November 4, 2003; accepted December 18, 2003.

This article has been cited by other articles:

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