The basic mechanism of anesthetic action by volatile anesthetics is not completely understood. The early hypothesis that the anesthetic state was dependent on nonspecific interactions of anesthetics with the membrane bilayer has largely given way to the current idea that membrane-associated proteins, particulady ion channels, are specifically modulated by volatile anesthetics. Depression of glutamate-mediated excitatory transmission and potentiation of gamma-aminobutyric acid (GABA)-mediated inhibitiry transmission appear to be primary mechanisms by which general anesthetics produce anesthesia. More recent studies, however, have revealed that volatile anesthetics both enhance and inhibit ligand-gated ion channels by means of actions at distinct sites. The author proposes that volatile general anesthetics may act as partial agonists or partial inverse agonists of ligand-gated ion channels of central neurons, therefore the overall effect of an anaesthetic agent depends on summation of events occurring at the many individual ion channels of different neurones that make up the network with specific interactions between anesthetics and the receptor or binding sites of some subunits.