title: Blocking sodium channels to treat neuropathic pain.
abstract: Neuropathic pain remains a large unmet medical need. A number of therapeutic options exist, but efficacy and tolerability are less than satisfactory. Based on animal models and limited data from human patients, the pain and hypersensitivity that characterize neuropathic pain are associated with spontaneous discharges of normally quiescent nociceptors. Sodium channel blockers inhibit this spontaneous activity, reverse nerve injury-induced pain behavior in animals and alleviate neuropathic pain in humans. Several sodium channel subtypes are expressed primarily in sensory neurons and may contribute to the efficacy of sodium channel blockers. In this report, the authors review the current understanding of the role of sodium channels and of specific sodium channel subtypes in neuropathic pain signaling.
authors.affiliation: Merck Research Laboratories, Department of Ion Channels, Rahway, NJ 07065, USA. birgit_priest@merck.com
authors.forename: Birgit T
authors.initials: BT
authors.lastname: Priest
authors.forename: Gregory J
authors.initials: GJ
authors.lastname: Kaczorowski
mesh_terms: D000818:Animals; D006801:Humans; D015640:Ion Channel Gating; D009437:Neuralgia / Q000188:drug therapy* / Q000503:physiopathology; D026941:Sodium Channel Blockers / Q000627:therapeutic use*; D015222:Sodium Channels / Q000737:chemistry / Q000502:physiology
chemical_list: D026941:Sodium Channel Blockers; D015222:Sodium Channels