Sustained increase in α5GABAA receptor function impairs memory after anesthesia.

Using a murine model, a single in vivo treatment with the injectable anesthetic etomidate increased a tonic inhibitory current generated by α5 subunit-containing GABA(A)Rs (γ-aminobutyric acid type A receptors) and cell-surface expression of α5GABA( a)Rs for at least 1 week, suggesting a mechanism to account for persistent memory deficits after general anesthesia.