Humans detect skin temperature changes that are perceived as warm or cool. Like humans, mice report forepaw skin warming with perceptual thresholds of less than 1°C and do not confuse warm with cool. We identify two populations of polymodal C-fibers that signal warm. Warm excites one population, whereas it suppresses the ongoing cool-driven firing of the other. In the absence of the thermosensitive TRPM2 or TRPV1 ion channels, warm perception was blunted, but not abolished. In addition, trpv1:trpa1:trpm3^−/− triple-mutant mice that cannot sense noxious heat detected skin warming, albeit with reduced sensitivity. In contrast, loss or local pharmacological silencing of the cool-driven TRPM8 channel abolished the ability to detect warm. Our data are not reconcilable with a labeled line model for warm perception, with receptors firing only in response to warm stimuli, but instead support a conserved dual sensory model to unambiguously detect skin warming in vertebrates.

人类检测到被感知为温暖或凉爽的皮肤温度变化。像人类一样，老鼠报告前爪皮肤变暖的感知阈值低于1°C，并且不会将温暖与凉快混淆。我们确定两个群体的多峰C纤维信号温暖。温暖激发了一个群体，而它却抑制了持续的以凉爽为动力的另一群体的射击。在没有热敏TRPM2或TRPV1离子通道的情况下，温暖的感觉减弱了，但没有消除。另外，trpv1：trpa1：trpm3 ^-/-尽管敏感性降低，但不能感应到有害热量的三突变小鼠检测到皮肤变暖。相反，冷驱动的TRPM8通道的丢失或局部药理学沉默消除了检测热的能力。我们的数据与温暖感知的标记线模型不一致，受体仅响应温暖刺激而激发，而是支持保守的双重感觉模型来明确检测脊椎动物的皮肤变暖。