Krall Catherine M, Andicochea Chad T, McDougall Sanders A
Department of Psychology, California State University, San Bernardino, CA 92407, USA.
Eur J Pharmacol. 2005 Jul 11;517(3):200-7. doi: 10.1016/j.ejphar.2005.05.021.
Stimulation of alpha2-adrenoceptors increases the ultrasonic vocalization production of preweanling rats, however it is not known whether these critical alpha2-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 alpha2-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 microg, i.c.v.) and ST-91-induced (15 microg, i.c.v.) ultrasonic vocalizations were measured after systemic injection of the alpha2-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 alpha2-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 alpha2-adrenoceptor subtypes (alpha2A, alpha2B, and alpha2C) or imidazoline receptors. When combined with past research, the present results are consistent with the hypothesis that centrally located alpha2-adrenoceptors are a component of a neural system that mediates ultrasonic vocalization production.
刺激α2-肾上腺素能受体会增加断奶前大鼠的超声发声，但尚不清楚这些关键的α2-肾上腺素能受体是位于外周还是中枢。在一系列三个实验中，在给11日龄大鼠全身（腹腔注射）或第三脑室（脑室内注射）给予可乐定或2-[2,6-二乙基苯基氨基]-2-咪唑（ST-91）后，测量超声发声。选择这些特定的α2-肾上腺素能受体激动剂是因为可乐定具有亲脂性，可进入中枢神经系统，而ST-91具有亲水性，不易穿过血脑屏障。在第三个实验中，在全身注射α2-肾上腺素能受体拮抗剂育亨宾（0.5或1mg/kg，腹腔注射）后，测量可乐定（1μg，脑室内注射）和ST-91诱导（15μg，脑室内注射）的超声发声。结果表明，可乐定和ST-91的中枢给药均增加了11日龄大鼠的超声发声，而仅可乐定的外周给药而非ST-91增加了超声发声。这些结果表明，介导超声发声的α2-肾上腺素能受体位于中枢神经系统。育亨宾完全减弱了可乐定诱导的超声发声，但仅部分减弱了ST-91诱导的发声。这种结果模式可能是由于可乐定和ST-91对α2-肾上腺素能受体亚型（α2A、α2B和α2C）或咪唑啉受体的选择性差异所致。结合以往的研究，目前的结果与以下假设一致，即位于中枢的α2-肾上腺素能受体是介导超声发声的神经系统的一个组成部分。
