Cationic channel with similar permeabilities for Na(+) and K(+), that is activated by an increase of the proton concentration on the extracellular side. Displays no permeability for chloride ions. Shows slow kinetics of activation, no desensitization and a single channel conductance of 8 pS. Might contribute to adaptation to external pH change. Tetraethylammonium (TEA) and tetrabutylammonium (TBA) inhibit the proton-activated currents in a dose- and voltage-dependent manner in vitro, whereas the blocker of acid sensing ion channels, amiloride, has no effect. Channel current of GLIC can be inhibited by inhaled and intravenous general anesthetics at and below concentrations used clinically. Ion conduction is also inhibited by lidocaine and by divalent transition metal ions such as cadmium ions. Homopentamer. Consists of an N-terminal ligand-binding domain that encloses a wide aqueous vestibule and a transmembrane domain that forms a narrow channel. The homologous nature of GLIC to eukaryotic nicotinic acetylcholine receptors and other eukaryotic pentameric ligand-gated ion channels, and its sensitivity to general anesthetics, define GLIC as a structural and functional model of signal transduction in the nervous system, also relevant for exploring the molecular basis of anesthetic action. Belongs to the ligand-gated ion channel (TC 1.A.9) family.