The precise mechanism is not well understood, but it appears to be the direct effect of gas dissolving into nerve membranes and causing temporary disruption in nerve transmissions. While the effect was first observed with air, other gases including argon, krypton and hydrogen cause very similar effects at higher than atmospheric pressure.[26] Some of these effects may be due to antagonism at NMDA receptors and potentiation of GABAA receptors,[27] similar to the mechanism of nonpolar anesthetics such diethyl ether or ethylene.[28] However, their reproduction by the very chemically inactive gas argon makes them unlikely to be a strictly chemical bonding to receptors in the usual sense of a chemical bond. An indirect physical effect—such as a change in membrane volume—would therefore be needed to affect the ligand-gated ion channels of nerve cells.[29] Trudell et al. have suggested non-chemical binding due to the attractive van der Waals force between proteins and inert gases.[30]
Similar to the mechanism of ethanol's effect, the increase of gas dissolved in nerve cell membranes may cause altered ion permeability properties of the neural cells' lipid bilayers. The partial pressure of a gas required to cause a measured degree of impairment correlates well with the lipid solubility of the gas: the greater the solubility, the less partial pressure is needed.[29]
An early theory, the Meyer-Overton hypothesis suggested that narcosis happens when the gas penetrates the lipids of the brain's nerve cells, causing direct mechanical interference with the transmission of signals from one nerve cell to another.[12][13][17] More recently, specific types of chemically-gated receptors in nerve cells have been identified as being involved with anesthesia and narcosis. However, the basic and most general underlying idea, that nerve transmission is altered in many diffuse areas of the brain as a result of gas molecules dissolved in the nerve cells' fatty membranes, remains largely unchallenged.[14][31]
