Rotiroti D, Silvestri R, de Sarro G B, Bagetta G, Nisticò G
J Psychiatr Res. 1982;17(3):231-9. doi: 10.1016/0022-3956(82)90001-2.
The effects of guanfacine and other drugs acting at alpha 1- and alpha 2-adrenoceptors on behaviour, electrocortical activity and ECoG spectrum power were studied in chicks and rats. Guanfacine, given systematically in chicks, produced behavioural and electrocortical slow-wave sleep lasting 100-200 min, depending on the dose; these effects were prevented by yohimbine, a selective antagonist, at alpha 2-adrenoceptors and potentiated by prazosin, a selective antagonist, at alpha 1-adrenoceptors. Similar behavioural and electrocortical effects were obtained after systemic or intraventricular infusion of guanfacine in rats. In addition, a significant increase in total and in lower frequency band (0-4; 4-8 Hz) voltage power was observed. Behavioural and ECoG effects of guanfacine were prevented by phentolamine or yohimbine, whereas prazosin and propranolol were ineffective. Yohimbine itself, given systemically in chicks, produced behavioural stimulation, vocalization, increase in locomotor activity and ECoG desynchronization, with a significant fall in total and 0-3, 3-6, 6-9 and 9-12 Hz voltage power lasting approx. 3 h. Desipramine, an inhibitor of noradrenaline reuptake, produced in chicks behavioural and ECoG arousal, vocalization, pecking, escape responses and aggressive behaviour. In conclusion, the present experiments show that guanfacine sedative effects seem to be mediated predominantly via an activation of presynaptic alpha 2-adrenoceptors and suggest that arousal is due to stimulation of post-synaptic alpha 1-adrenoceptors.
研究了胍法辛及其他作用于α1和α2肾上腺素能受体的药物对雏鸡和大鼠行为、皮层电活动及脑电（ECoG）频谱功率的影响。给雏鸡系统性给予胍法辛后，根据剂量不同可产生持续100 - 200分钟的行为和皮层电慢波睡眠；这些效应可被α2肾上腺素能受体选择性拮抗剂育亨宾阻断，而被α1肾上腺素能受体选择性拮抗剂哌唑嗪增强。给大鼠系统性或脑室内注入胍法辛后也获得了类似的行为和皮层电效应。此外，还观察到总电压功率以及低频段（0 - 4；4 - 8赫兹）电压功率显著增加。胍法辛的行为和脑电效应可被酚妥拉明或育亨宾阻断，而哌唑嗪和普萘洛尔则无效。给雏鸡系统性给予育亨宾本身可产生行为兴奋、鸣叫、运动活动增加及脑电去同步化，总电压功率以及0 - 3、3 - 6、6 - 9和9 - 12赫兹电压功率显著下降，持续约3小时。去甲肾上腺素再摄取抑制剂地昔帕明可使雏鸡产生行为和脑电觉醒、鸣叫、啄食、逃避反应及攻击行为。总之，本实验表明胍法辛的镇静作用似乎主要通过激活突触前α2肾上腺素能受体介导，提示觉醒是由于刺激突触后α1肾上腺素能受体所致。
