Abstract: A method is disclosed of treating pain with senicapoc, a potent Ca2+-activated K+ channel, KCa3.1 antagonist in CNS-resident microglia. Senicapoc is shown to cause in a decrease of IL-1? and NO release from microglia cells vivo and in vitro. Because of contribution of KCa3.1 to neuropathological processes, senicapoc is useful in the treatment of chronic, neuropathic, visceral, and inflammatory pain and the reversal of tactile allodynia.