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Hydrogen sulfide (H₂S) has been shown in previous studies to cause hypothermia and hypometabolism in mice, and its thermoregulatory effects were subsequently investigated. However, the molecular target through which H₂S triggers its effects on deep body temperature has remained unknown. We investigated the thermoregulatory response to fast-(Na₂S) and slow-releasing (GYY4137) H₂S donors in C57BL/6 mice, and then tested whether their effects depend on the transient receptor potential ankyrin-1 (TRPA1) channel in <i>Trpa1</i> knockout (<i>Trpa1^−/−</i>) and wild-type (<i>Trpa1^+/+</i>) mice. Intracerebroventricular administration of Na₂S (0.5–1 mg/kg) caused hypothermia in C57BL/6 mice, which was mediated by cutaneous vasodilation and decreased thermogenesis. In contrast, intraperitoneal administration of Na₂S (5 mg/kg) did not cause any thermoregulatory effect. Central administration of GYY4137 (3 mg/kg) also caused hypothermia and hypometabolism. The hypothermic response to both H₂S donors was significantly (<i>p</i> < 0.001) attenuated in <i>Trpa1^−/−</i> mice compared to their <i>Trpa1^+/+</i> littermates. <i>Trpa1</i> mRNA transcripts could be detected with RNAscope in hypothalamic and other brain neurons within the autonomic thermoeffector pathways. In conclusion, slow- and fast-releasing H₂S donors induce hypothermia through hypometabolism and cutaneous vasodilation in mice that is mediated by TRPA1 channels located in the brain, presumably in hypothalamic neurons within the autonomic thermoeffector pathways.