Sodium leak channel non-selective protein (NALCN) was first described as a voltage-independent, cation-nonselective channel which is permeable to sodium, potassium and calcium ions [], however, it was recently reported to be selective only for monovalent cations and to be blocked by extracellular divalent cations []. Coexpression of NALCN, UNC79, UNC80, and NALF1 results in voltage-dependent NALCN currents [, ]. It is responsible for the background sodium ion leak current in neurons and controls neuronal excitability. It is activated either by neuropeptides substance P or neurotensin []. NALCN is required for normal respiratory rhythm and neonatal survival [].
