Microperfusion of etomidate into the ventrobasal complex of wild-type mice increases α-β electrocortical activity, sleep spindles, and non–rapid-eye-movement (NREM) sleep through T-type Ca²⁺ channel–independent alterations in thalamocortical activity in vivo. (A) Exemplar electromyogram (EMG) and electroencephalogram (EEG) recordings from a wild-type mouse during bilateral microperfusion of the ventrobasal complex with artificial cerebrospinal fluid (aCSF; left) and etomidate (right). The vertical scale bar corresponds to the EMG trace and equals 1 mV. Hypnograms are superimposed as white traces on the EEG spectrograms. Note the decrease in slow electrocortical activity with etomidate. (B) Microperfusion of etomidate into the thalamus elicits a non-REM sleep–specific reduction in 1 to 4-Hz EEG power and increased 8 to 12-Hz and 12 to 30-Hz powers. These effects persist during coadministration of 3,5-dichloro-N-[1-(2,2-dimethyl-tetrahydro-pyran-4-ylmethyl)-4-fluoro-piperidin-4-ylmethyl]-benzamide (TTA-P2) (two-way repeated measures [RM] ANOVA). (C) Both NREM 10 to 15-Hz (sigma) power and the incidence of spindle-like oscillations increase with etomidate at the thalamus. Note that coapplication of TTA-P2 with etomidate does not alter these effects and that neither treatment significantly alters the duration of spindle-like oscillations (one-way RM ANOVA). (D) Etomidate at the thalamus also elicits a reduction in wakefulness that persists with coapplication of TTA-P2. NREM sleep is increased with etomidate plus TTA-P2 at the thalamus (two-way RM ANOVA). All data represent mean ± SD. n = 9; *P < 0.05, **P < 0.01, and ***P < 0.001.