Linalool, an essential oil component of lavender is commonly used in fragrances. It is known that linalool has anxiolytic, sedative, and analgesic actions. However, the mechanism of its analgesic action is not fully clear. Pain signals elicited by the activation of nociceptors on peripheral neurons are transmitted to the central nervous system. In this study, we focused the effects of linalool on TRP channels and voltage-gated channels, both of which are important for pain signaling via nociceptors in somatosensory neurons. For detection of channel activity, the intracellular Ca²⁺ concentration ([Ca²⁺]_i) was measured using a Ca²⁺ imaging system and membrane currents were recorded by a whole-cell patch-clamp technique. In mouse dorsal root ganglion neurons linalool did not affect [Ca²⁺]_i responses to capsaicin and acids, TRP vanilloid 1 (V1) agonists. On the other hand, linalool suppressed the increases of [Ca²⁺]_i induced by allylisothiocyanate and carvacrol, TRPA1 agonists. In heterologously expressed channels, linalool suppressed [Ca²⁺]_i responses to TRPA1 agonists but not those to TRPV1 agonists. Linalool attenuated the [Ca²⁺]_i responses to high concentrations of KCl and voltage-gated Ca²⁺ currents but only slightly suppressed voltage-gated Na⁺ currents. These results suggest that linalool exerts an analgesic action via the suppression of the nociceptive TRPA1 channel and voltage-gated Ca²⁺ channels.