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The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm.

Sodium plays a key role in determining the basal excitability of the nervous systems through the resting "leak" Na(+) permeabilities, but the molecular identities of the TTX- and Cs(+)-resistant Na(+) leak conductance are totally unknown. Here we show that this conductance is formed by the protein NALCN, a substantially uncharacterized member of the sodium/calcium channel family. Unlike any of the other 20 family members, NALCN forms a voltage-independent, nonselective cation channel. NALCN mutant mice have a severely disrupted respiratory rhythm and die within 24 hours of birth. Brain stem-spinal cord recordings reveal reduced neuronal firing. The TTX- and Cs(+)-resistant background Na(+) leak current is absent in the mutant hippocampal neurons. The resting membrane potentials of the mutant neurons are relatively insensitive to changes in extracellular Na(+) concentration. Thus, NALCN, a nonselective cation channel, forms the background Na(+) leak conductance and controls neuronal excitability.

Pubmed ID: 17448995

Authors

  • Lu B
  • Su Y
  • Das S
  • Liu J
  • Xia J
  • Ren D

Journal

Cell

Publication Data

April 20, 2007

Associated Grants

None

Mesh Terms

  • Amino Acid Sequence
  • Animals
  • Animals, Newborn
  • Calcium
  • Cell Line
  • Central Nervous System
  • Cesium
  • DNA, Complementary
  • Embryo, Mammalian
  • Embryo, Nonmammalian
  • Genes, Lethal
  • Hippocampus
  • Humans
  • Ion Channels
  • Membrane Potentials
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Nerve Tissue Proteins
  • Neurons
  • Potassium
  • Rats
  • Respiration
  • Sequence Alignment
  • Sodium
  • Tetrodotoxin
  • Transfection
  • Xenopus