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A photoactivable diazirine derivative of etomidate, azietomidate, shares many actions of etomidate, including a capacity to abolish the righting reflexes in tadpoles and enhance gamma-aminobutyric acid (GABA)-induced currents. Azietomidate’s usefulness in studies of mechanisms of anesthesia depends on the assumption that it shares a site of action with etomidate. Mice bearing an N265M β3 subunit point mutation in GABAA receptors have a markedly decreased sensitivity to loss of righting reflexes induced by etomidate over a range of doses. Accordingly, in the present study we measured the time to recovery of righting reflexes of wild type and mutant mice as a function of dose given as an IV bolus. Analysis of the data for azietomidate yielded mean times to recovery of righting reflexes at a dose of 7.5 mg/kg of 10.0 ± 0.9 min and 3.0 ± 1.6 min for wild type and mutant mice, respectively (mean ± sd). A similar analysis for etomidate yielded mean times to recovery of righting reflexes at a dose of 7.5 mg/kg of 12.0 ± 1.3 min and 4.0 ± 0.7 min for wild type and mutant mice respectively. Thus, at this dose a single mutation, N265M on the β3 subunit of the GABAA receptor, approximately halved the time to recovery of righting reflexes for both etomidate and azietomidate (by 7.6 ± 1.5 min and 7.2 ± 1.8 min, respectively), emphasizing the contribution of this residue as a determinant of a behavioral response of azietomidate in mice.