Peripheral activation of nociceptors or pruriceptors elicits pain and itch signals, respectively, being conveyed to the spinal dorsal horn. Recent researches have demonstrated that there are some common neural pathways shared by pain and itch signals in the central nervous system, and thus pharmacological reduction of neuronal excitability may result in analgesia and also antipruritic effects. In the present study, we investigated whether retigabine, an opener of the KCNQ (Kv7) K⁺channels which mediate low threshold and non-inactivating neuronal M-currents, produce analgesic effects in mice after peripheral injury (Seltzer model) and antipruritic effects in acute itch models in mice. Retigabine (10 and 30 mg/kg, i.p. or 10 and 30 μg, i.t.) inhibited thermal and mechanical hypersensitivity in a dose-dependent manner, which disappeared in the presence of the KCNQ channel blocker XE-991 dihydrochloride (5 and 10 mg/kg, i.p. or 5 and 10 μg, i.t.). Retigabine (30 mg/kg, i.p.) also attenuated scratching behavior induced by both histamine-independent chloroquine (1 mmol/50 μL, i.d.) and histamine-dependent compound 48/80 (100 μg/50 μL, i.d.). Therefore, the opening of KCNQ channels is effective to produce both analgesic and antipruritic effects.