PubMed 17448995
Referenced in: none
Automatically associated channels: Kir6.2
Title: The neuronal channel NALCN contributes resting sodium permeability and is required for normal respiratory rhythm.
Authors: Boxun Lu, Yanhua Su, Sudipto Das, Jin Liu, Jingsheng Xia, Dejian Ren
Journal, date & volume: Cell, 2007 Apr 20 , 129, 371-83
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/17448995
Abstract
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.