Fig. 2. Behavioral experiments implicate γ-aminobutyric acid receptor type A (GABAA) receptors in dexmedetomidine's sedative mechanism. (A ) Illustration of systemically administered GABAAreceptor antagonist gabazine (5 mg/kg, subcutaneous) rightward shifts the dexmedetomidine dose–loss of righting reflex (LORR) response curve to centrally administered α2-adrenoceptor agonist dexmedetomidine (2–6 μg/10 μl, intracerebroventricular; n = 6 per cohort). In addition, systemically administered gabazine (5 mg/kg, subcutaneous; n = 6) attenuates the sedation (B ) induced by and increases the latency (C ) of response to systemically administered dexmedetomidine (150 μg/kg, subcutaneous; n = 6). Data are presented as mean ± SEM, and asterisk denotes P < 0.05 versus  NS. DEX = dexmedetomidine; GBZ = gabazine; NS = normal saline.

Fig. 2. Behavioral experiments implicate γ-aminobutyric acid receptor type A (GABAA) receptors in dexmedetomidine's sedative mechanism. (A ) Illustration of systemically administered GABAAreceptor antagonist gabazine (5 mg/kg, subcutaneous) rightward shifts the dexmedetomidine dose–loss of righting reflex (LORR) response curve to centrally administered α2-adrenoceptor agonist dexmedetomidine (2–6 μg/10 μl, intracerebroventricular; n = 6 per cohort). In addition, systemically administered gabazine (5 mg/kg, subcutaneous; n = 6) attenuates the sedation (B ) induced by and increases the latency (C ) of response to systemically administered dexmedetomidine (150 μg/kg, subcutaneous; n = 6). Data are presented as mean ± SEM, and asterisk denotes P < 0.05 versus  NS. DEX = dexmedetomidine; GBZ = gabazine; NS = normal saline.

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