Elsevier

Neuroscience Letters

Volume 378, Issue 1, 11 April 2005, Pages 28-33
Neuroscience Letters

Attenuated fever response in mice lacking TRPV1

https://doi.org/10.1016/j.neulet.2004.12.007Get rights and content

Abstract

TRPV1, the capsaicin receptor, is expressed not only in nociceptive neurons, but also in other locations, including the hypothalamus. Studies involving systemic or intrahypothalamic capsaicin administration have suggested a role for TRPV1 in body temperature control. To explore this possibility, we examined thermoregulatory responses in TRPV1−/− mice. These mutant animals exhibited no obvious changes in circadian body temperature fluctuation, tolerance to increased (35 °C) or decreased (4 °C) ambient temperature or ethanol-induced hypothermia. In contrast, fever production in response to the bacterial pyrogen, lipopolysaccharide (LPS) was significantly attenuated in TRPV1−/− mice. Despite this finding, we detected no significant differences between TRPV1−/− and control mice in the extent of LPS-induced c-Fos expression in numerous fever-related brain subregions. These results suggest that TRPV1 participates in the generation of polyphasic fever, perhaps at sites outside the brain.

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Acknowledgements

The authors thank J. Wang for expert technical assistance and members of the Caterina lab for valuable discussion. Supported by grants from The W.M. Keck Foundation, The Searle Scholars Program, The Arnold and Mabel Beckman Foundation and Dainippon Pharmaceuticals to M.J.C.

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      The latter has been evidenced from studies in which the deletion of TRPV1 in mice alters noxious and mild temperature sensation (6,7), whereas knockout of other thermo-TRPs such as TRPV2, TRPV3, and TRPV4 shows little effect in sensory transduction in rodents (6,8,9). Moreover, whereas deletion of TRPV1 in rodents does not affect corporal temperature, blockage of TRPV1 in vivo triggers hyperthermia (10). The rat TRPV1 structure is a tetramer (Fig. 1 a), with every monomer consisting of 838 amino acids (Fig. 1 c).

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      The amplitude of core temperature of TrpV1 KO mice is higher in comparison to WT animals [25,79,83]. On the other hand, Iida et al. [39] did not find a relationship between the lack of TRPV1 and the amplitude of core temperature. These controversial data have been found in studies with genetically modified animals; in contrast, unequivocal results have been obtained with a pharmacological approach, demonstrating a clear involvement of TRPV1 channel in the core body temperature: TRPV1 agonist causes hypothermia while an antagonist causes hyperthermia [26,63], corroborating what we and others have found in TrpV1 KO mice.

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    These authors contributed equally to this study.

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