Menthol, a topical analgesic substance, as well as low temperatures evoke cold sensation by activating transient receptor potential channels (TRPM8, TRPA1) in peripheral cold receptor neurons. However, block of potassium channels by menthol and cold might be an additional mechanism of cold sensation which was investigated in the current study. Using two-electrode voltage-clamp (TEVC) of Xenopus oocytes, we screened for potassium channels that are menthol sensitive. Interestingly, we found that human KCNQ1 channels which play a crucial role in the repolarisation of human cardiac myocytes, are blocked by menthol in a similar concentration range as previously shown to activate TRPM8 channels. Using TEVC and patch clamp experiments, we found that menthol is an open channel blocker of KCNQ1 channels. Recordings of S6 segment and pore loop mutants, together with molecular modelling experiments, predict that menthol binds within the central pore cavity by interacting with the residues T312, I337 and F339. We confirm previous data on the temperature sensitivity of the channel and elaborated that KCNQ1 is most temperature sensitive in a mild cold range between 25 and 35°C. RT-PCR experiments revealed that KCNQ1 is expressed in the human skin. Combining whole-cell electrophysiology and immunocytochemistry in cultured dorsal root ganglia (DRG) neurons, we show that KCNQ1 channels are functionally expressed in small and medium sized DRGs. Due to the previously unknown expression of KCNQ1 in the peripheral nervous system, together with its menthol- and temperature-sensitivity, we propose that the KCNQ1 channel might act as a modulator of cold sensation.