3-iodothyroacetic acid, a metabolite of thyroid hormone, induces itch and reduces threshold to noxious and to painful heat stimuli in mice

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Abstract

Background and purpose Itch is associated with increased sensitization to nociceptive stimuli. We investigated whether 3-iodothyroacetic acid (TA1), by releasing histamine, induces itch and increases sensitization to noxious and painful heat stimuli. Experimental Approach Itch was evaluated after s.c. administration of TA1 (0.4, 1.32 and 4 μg·kg-1). Mice threshold to noxious (NHT) and to painful heat stimuli were evaluated by the increasing-temperature hot plate (from 45.5 to 49.5°C) or by the hot plate (51.5°C) test, respectively, 15 min after i.p. injection of TA1 (0.4, 1.32 and 4 μg·kg-1). Itch, NHT and pain threshold evaluation were repeated in mice pretreated with pyrilamine. Itch and NHT were also measured in HDC+/+ and HDC-/- following injection of saline or TA1 (1.32, 4 and 11 μg·kg-1; s.c. and i.p.). pERK1/2 levels were determined by Western blot in dorsal root ganglia (DRG) isolated from CD1 mice 15 min after they received (i.p.): saline, saline and noxious heat stimulus (46.5°C), TA1 (0.1, 0.4, 1.32, 4 μg·kg-1) or TA1 1.32 μg·kg-1 and noxious heat stimulus. Key Results TA1 0.4 and 1.32 μg·kg-1 induced itch and reduced NHT; pyrilamine pretreatment prevented both of these effects. TA1 4 μg·kg-1 (i.p.) reduced pain threshold without inducing itch or modifying NHT. In HDC-/- mice, TA1 failed to induce itch and to reduce NHT. In DRG, pERK1/2 levels were significantly increased by noxious heat stimuli and by TA1 0.1, 0.4 and 1.32 μg·kg-1; i.p. Conclusions and Implications Increased TA1 levels induce itch and an enhanced sensitivity to noxious heat stimuli suggesting that TA1 might represent a potential cause of itch in thyroid diseases.

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Laurino, A., De Siena, G., Resta, F., Masi, A., Musilli, C., Zucchi, R., & Raimondi, L. (2015). 3-iodothyroacetic acid, a metabolite of thyroid hormone, induces itch and reduces threshold to noxious and to painful heat stimuli in mice. British Journal of Pharmacology, 172(7), 1859–1868. https://doi.org/10.1111/bph.13032

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