title: Sodium leak channels in neuronal excitability and rhythmic behaviors.
abstract: Extracellular K⁺, Na⁺, and Ca²⁺ ions all influence the resting membrane potential of the neuron. However, the mechanisms by which extracellular Na⁺ and Ca²⁺ regulate basal neuronal excitability are not well understood. Recent findings suggest that NALCN, in association with UNC79 and UNC80, contributes a basal Na⁺ leak conductance in neurons. Mutations in Nalcn, Unc79, or Unc80 lead to severe phenotypes that include neonatal lethality and disruption in rhythmic behaviors. This review discusses the properties of the NALCN complex, its regulation, and its contribution to neuronal function and animal behavior.
authors.affiliation: Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA. dren@sas.upenn.edu
authors.forename: Dejian
authors.initials: D
authors.lastname: Ren
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D006801:Humans; D007473:Ion Channels; D008565:Membrane Proteins; D008969:Molecular Sequence Data; D009474:Neurons / Q000502:physiology*; D010507:Periodicity; D024683:Potassium Channels, Tandem Pore Domain / Q000737:chemistry / Q000502:physiology*; D015222:Sodium Channels / Q000737:chemistry / Q000502:physiology*
chemical_list: D007473:Ion Channels; D008565:Membrane Proteins; C544681:NALCN protein, human; D024683:Potassium Channels, Tandem Pore Domain; D015222:Sodium Channels