title: Voltage-Gated Ion Channels in the PNS: Novel Therapies for Neuropathic Pain?
abstract: Neuropathic pain arises from injury to the nervous system. Conditions associated with neuropathic pain are diverse, and lesions and/or pathological changes in the central nervous system (CNS) or peripheral nervous system (PNS) can frequently, but not always, be identified. It is difficult to treat, with patients often on multiple, different classes of medications, all with appreciable adverse side effect profiles. Consequently, there is a pressing need for the development of new medications. The development of such therapeutics is predicated on a clear understanding of the relevant molecular and cellular processes that contribute to the development, and maintenance, of the neuropathic pain state. One proposed mechanism thought to contribute to the ontogeny of neuropathic pain is altered expression, trafficking, and functioning of ion channels expressed by primary sensory neurons. Here, we will focus on three voltage-gated ion channel families, CaV, HCN, and NaV, first reviewing the preclinical data and then the human data where it exists.
authors.affiliation: Department of Anesthesiology, Weill Cornell Medical College, New York, NY, USA.
authors.forename: Gareth R
authors.initials: GR
authors.lastname: Tibbs
authors.affiliation: Department of Anesthesiology, Weill Cornell Medical College, New York, NY, USA.
authors.forename: David J
authors.initials: DJ
authors.lastname: Posson
authors.affiliation: Department of Anesthesiology, Weill Cornell Medical College, New York, NY, USA; Department of Medicine, Weill Cornell Medical College, New York, NY, USA. Electronic address: pag2014@med.cornell.edu.
authors.forename: Peter A
authors.initials: PA
authors.lastname: Goldstein
mesh_terms: D000818:Animals; D020864:Calcium Channels, N-Type / Q000502:physiology; D020747:Calcium Channels, T-Type / Q000502:physiology; D006574:Heterocyclic Compounds, 2-Ring / Q000627:therapeutic use; D006801:Humans; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels / Q000037:antagonists & inhibitors; D007473:Ion Channels / Q000037:antagonists & inhibitors* / Q000502:physiology; D062559:NAV1.8 Voltage-Gated Sodium Channel / Q000502:physiology; D062558:NAV1.9 Voltage-Gated Sodium Channel / Q000502:physiology; D009437:Neuralgia / Q000188:drug therapy* / Q000503:physiopathology; D017933:Peripheral Nervous System / Q000502:physiology*; D013449:Sulfonamides / Q000627:therapeutic use; D000096926:Benzenesulfonamides
chemical_list: D020864:Calcium Channels, N-Type; D020747:Calcium Channels, T-Type; D006574:Heterocyclic Compounds, 2-Ring; D064428:Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; D007473:Ion Channels; D062559:NAV1.8 Voltage-Gated Sodium Channel; D062558:NAV1.9 Voltage-Gated Sodium Channel; D013449:Sulfonamides; C000589982:4-chloro-2-fluoro-N-(2-fluorophenyl)-5-(hexahydropyrrolo(1,2-a)pyrazin-2(1H)-ylcarbonyl)benzenesulfonamide; D000096926:Benzenesulfonamides; C500545:CACNA1B protein, human; C479952:CACNA1H protein, human; C568317:SCN10A protein, human; C491886:SCN11A protein, human
keywords: Ca(V) channel; HCN channel; Na(V) channel; chemotherapy; diabetes; nerve injury