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XB-ART-40008
EMBO Rep 2009 Aug 01;108:873-80. doi: 10.1038/embor.2009.125.
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The NALCN ion channel is activated by M3 muscarinic receptors in a pancreatic beta-cell line.

Swayne LA , Mezghrani A , Varrault A , Chemin J , Bertrand G , Dalle S , Bourinet E , Lory P , Miller RJ , Nargeot J , Monteil A .


Abstract
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.

PubMed ID: 19575010
PMC ID: PMC2710536
Article link: EMBO Rep


Species referenced: Xenopus
Genes referenced: dtl nalcn npy4r


Article Images: [+] show captions
References [+] :
Altier, Multiple structural elements contribute to voltage-dependent facilitation of neuronal alpha 1C (CaV1.2) L-type calcium channels. 2001, Pubmed, Xenbase