Cold-sensitive channels in thermoregulation: TRPA1 and TRPM8

  • A. Garami
    Affiliations
    Department of Pathophysiology and Gerontology, Medical School, University of Pecs, Hungary

    Systemic Inflammation Laboratory (FeverLab), Trauma Research, St. Joseph’s Hospital and Medical Center, USA
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  • M.C. Almeida
    Affiliations
    Systemic Inflammation Laboratory (FeverLab), Trauma Research, St. Joseph’s Hospital and Medical Center, USA

    Natural and Humanities Sciences Center, Federal University of ABC, Brazil
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  • A.A. Romanovsky
    Affiliations
    Systemic Inflammation Laboratory (FeverLab), Trauma Research, St. Joseph’s Hospital and Medical Center, USA
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      The molecular nature of sensors responsible for the detection of cold for thermoregulation is largely unknown. Two members of the transient receptor potential (TRP) channels can be activated by low temperature in vitro: the melastatin-8 (M8) channel by moderate and the ankyrin-1 (A1) channel by noxious cold. These channels have been hypothesized to serve as cold sensors for thermoregulation. At this symposium, we discuss literature data and our own published studies [1, 2] aimed at testing the proposed involvement of the two channels in thermoregulation by using pharmacological blockade of TRPA1 and TRPM8 in rats and deletion of the Trpa1 gene in mice. We studied how the blockade of TRPA1 or TRPM8 affected the autonomic (brown fat thermogenesis, tail-skin vasoconstriction) and behavioral (thermopreferendum) thermoeffectors under different thermal conditions. The results of these studies suggest that TRPM8 is a universal cold receptor in the thermoregulation system, because its pharmacological blockade inhibits both autonomic and behavioral cold-defense responses. In contrast with TRPM8, neither the genetic nor the pharmacological blockade of TRPA1 influenced autonomic thermoregulatory responses, even during severe cold exposure, thus suggesting that TRPA1 channels in rodents are not thermosensors used by the thermoregulation system. Our presentation at this symposium was supported in part by the Hungarian Scientific Research Fund Grant PD105532 to A.G. and the Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences to A.G.
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