Fig. 3. Dexmedetomidine sedation induces c-Fos expression pattern of nonrapid eye movement (NREM) sleep. (A ) Sedation induced by systemically administered α2-adrenoceptor agonist dexmedetomidine (500 μg/kg, intraperitoneal) at night (rodent waking period) results in a pattern of c-Fos expression (a surrogate marker of neuronal activation) in the locus coeruleus (LC), ventrolateral preoptic nucleus (VLPO), and tuberomammillary nucleus (TMN) similar to that seen previously during NREM sleep, i.e. , a decrease in c-Fos expression in the LC and TMN and an increase in the VLPO. α2-Adrenoceptor antagonist atipamezole (ATI; 2 mg/kg, intraperitoneal) reverses these changes in all three areas, and the γ-aminobutyric acid receptor type A (GABAA) receptor antagonist gabazine (5 mg/kg, intraperitoneal) reverses them in the VLPO and TMN but further increases c-Fos expression in the LC relative to wakefulness. Asterisks denote P < 0.05 versus NS, crosses denote P < 0.05 versus dexmedetomidine, and data are shown as mean ± SEM. (B ) The changes in c-Fos expression during sedation induced by α2-adrenoceptor agonist dexmedetomidine (400 μg/kg, intraperitoneal) were not observed in transgenic D79N mice lacking a functional α2A-adrenoceptor subtype, indicating that these changes are causally linked to the induction of sedation. DEX = dexmedetomidine; GBZ = gabazine; LORR = loss of righting reflex; NS = normal saline.