| First Author | Swayne LA | Year | 2009 |
| Journal | EMBO Rep | Volume | 10 |
| Issue | 8 | Pages | 873-80 |
| PubMed ID | 19575010 | Mgi Jnum | J:233576 |
| Mgi Id | MGI:5784983 | Doi | 10.1038/embor.2009.125 |
| Citation | Swayne LA, et al. (2009) The NALCN ion channel is activated by M3 muscarinic receptors in a pancreatic beta-cell line. EMBO Rep 10(8):873-80 |
| abstractText | A previously uncharacterized putative ion channel, NALCN (sodium leak channel, non-selective), has been recently shown to be responsible for the tetrodotoxin (TTX)-resistant sodium leak current implicated in the regulation of neuronal excitability. Here, we show that NALCN encodes a current that is activated by M3 muscarinic receptors (M3R) in a pancreatic beta-cell line. This current is primarily permeant to sodium ions, independent of intracellular calcium stores and G proteins but dependent on Src activation, and resistant to TTX. The current is recapitulated by co-expression of NALCN and M3R in human embryonic kidney-293 cells and in Xenopus oocytes. We also show that NALCN and M3R belong to the same protein complex, involving the intracellular I-II loop of NALCN and the intracellular i3 loop of M3R. Taken together, our data show the molecular basis of a muscarinic-activated inward sodium current that is independent of G-protein activation, and provide new insights into the properties of NALCN channels. |
