Administration of capsaicin (CAP) and its related pungent, nonanoyl vanillylamide (NVA) produced significant dose-dependent hypothermic response in mice at an ambient temperature of 24 degrees C. CAP was approximately equieffective to NVA in producing hypothermia. After large doses, desensitization occurred to the hypothermic effects of both CAP and NVA. The hypothermia produced by CAP and NVA was prevented by a small dose of thyrotropin-releasing hormone (TRH) (0.25 nmol/animal) which by itself had little effect on body temperature. Histidyl-proline diketopiperazine, a metabolite of TRH, was without effect on the hypothermic response of CAP and NVA. The result suggests that a TRH neuronal system in the brain may explain a part of the mechanism of CAP- and NVA-induced hypothermia in mice.
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