title: Na+ currents that fail to inactivate.
abstract: Textbook accounts give the impression that Na+ channels are short-acting binary switches: depolarization opens them, but only for about one millisecond. In contrast to this simplified view, a small but significant fraction of the total Na+ current in neurons occurs because channels open after long delays or in long-duration bursts of openings. Such non-inactivating Na+ current acts physiologically in neurons to amplify synaptic potentials and enhance endogenous rhythmicity, and also to aid repetitive firing of action potentials. In glial cells it also may regulate Na(+)-K+ ATPase activity. The evidence for non-inactivating Na+ current in a variety of neurons and glia is reviewed, along with a brief discussion of its ion channel substrate and its relevance for neurological diseases and drug therapy.
authors.affiliation: Dept of Neuroscience Pharmacology, Parke-Davis Pharmaceutical Research, Division of Warner-Lambert Co., Ann Arbor, MI 48105.
authors.forename: C P
authors.initials: CP
authors.lastname: Taylor
mesh_terms: D000818:Animals; D006801:Humans; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*
chemical_list: D015222:Sodium Channels