| First Author | Lu B | Year | 2007 |
| Journal | Cell | Volume | 129 |
| Issue | 2 | Pages | 371-83 |
| PubMed ID | 17448995 | Mgi Jnum | J:141581 |
| Mgi Id | MGI:3818816 | Doi | 10.1016/j.cell.2007.02.041 |
| Citation | Lu B, et al. (2007) The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm. Cell 129(2):371-83 |
| abstractText | 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. |
