The goal of this study was to determine the molecular identity of a small-conductance (~5-pS) background K⁺ channel expressed in trigeminal ganglion (TG) neurons. We tested the hypothesis that the 5-pS channel is a K_2P channel by comparing the pharmacological and single-channel properties of THIK-1 expressed in HEK293 cells. As reported earlier, whole-cell THIK-1 current was inhibited by halothane and activated by arachidonic acid. Among 25 additional modulators tested, bupivacaine (100 μM), quinidine (50 μM) and Ba²⁺ (3 mM) and cold (10 °C) were most effective inhibitors of THIK-1 current (>50 % inhibition). In cell-attached patches with high KCl in the pipette and bath solutions, THIK-1 produced a small-conductance (~5 pS) channel with a weak inwardly rectifying current–voltage relationship. Halothane, bupivacaine and cold inhibited the single-channel activities of both THIK-1 and the 5-pS channel in TG neurons, whereas arachidonic acid augmented them. THIK-1 expressed in HEK293 cells and the 5-pS channels in TG neurons were insensitive to hypoxia. Reverse transcriptase-PCR, Western blot and immunocytochemical analyses suggested that THIK-1 mRNA and protein were expressed in TG neurons. These results show that THIK-1 is functionally expressed in TG neurons and contributes to the background K⁺ conductance.