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.
journal_name
EMBO Repjournal_title
EMBO reportsauthors
Swayne LA,Mezghrani A,Varrault A,Chemin J,Bertrand G,Dalle S,Bourinet E,Lory P,Miller RJ,Nargeot J,Monteil Adoi
10.1038/embor.2009.125subject
Has Abstractpub_date
2009-08-01 00:00:00pages
873-80issue
8eissn
1469-221Xissn
1469-3178pii
embor2009125journal_volume
10pub_type
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