Ultrasonic vocalization production of preweanling rats: Effects of central and peripheral administration of α2-adrenoceptor agonists

Stimulation of α2-adrenoceptors increases the ultrasonic vocalization production of preweanling rats, however it is not known whether these critical α2-adrenoceptors are located peripherally or centrally. In a series of three experiments, ultrasonic vocalizations were measured after 11-day-old rats had been administered clonidine or 2-[2,6-diethylphenylamino]-2-imidazole (ST-91) either systemically (i.p.) or into the third ventricle (i.c.v.). These particular α2-adrenoceptor agonists were chosen because clonidine is lipophilic and enters the central nervous system, while ST-91 is hydrophilic and does not readily cross the blood-brain barrier. In the third experiment, clonidine- (1 μg, i.c.v.) and ST-91-induced (15 μg, i.c.v.) ultrasonic vocalizations were measured after systemic injection of the α2-adrenoceptor antagonist yohimbine (0.5 or 1 mg/kg, i.p.). Results showed that central administration of both clonidine and ST-91 increased the ultrasonic vocalization production of 11-day-old rats, whereas peripheral administration of only clonidine, and not ST-91, increased ultrasonic vocalizations. These results indicate that the α2-adrenoceptors mediating ultrasonic vocalization production are located in the central nervous system. Yohimbine fully attenuated clonidine-induced ultrasonic vocalizations but only partially attenuated ST-91-induced vocalizations. This pattern of results may have been due to the differential selectivity of clonidine and ST-91 for α2-adrenoceptor subtypes (α2A, α2B, and α2C) or imidazoline receptors. When combined with past research, the present results are consistent with the hypothesis that centrally located α2-adrenoceptors are a component of a neural system that mediates ultrasonic vocalization production.