Pelletier M R, Corcoran M E
University of Victoria, Department of Psychology, BC, Canada.
Brain Res. 1993 Dec 31;632(1-2):29-35. doi: 10.1016/0006-8993(93)91134-e.
We reported previously that activation of alpha-2 adrenoceptors with infusions of clonidine into the amygdala/pyriform region is sufficient to retard kindling. To characterize further the involvement in kindling of alpha-2 receptors in the amygdala/pyriform, we exposed rats to unilateral intraamygdaloid infusions of a variety of noradrenergic drugs followed by either low-frequency stimulation of the amygdala, to induce rapid kindling, or conventional high-frequency stimulation. Infusions and electrical stimulation were administered once every 48 h. The prophylactic effects of clonidine were blocked by simultaneous infusion of idazoxan, an alpha-2 adrenergic antagonist, which suggests strongly that these effects were produced at an alpha-2 receptor. Intraamygdaloid infusions of xylazine, another alpha-2 agonist, also significantly retarded low-frequency kindling. Unexpectedly, intraamygdaloid infusions of the alpha-2 antagonists idazoxan, yohimbine, and SK&F 104856 failed to accelerate kindling. Infusion of the alpha-1 antagonist corynanthine also failed to affect kindling. We propose that the alpha-2 adrenoceptors in the amygdala/pyriform region contribute to the prophylactic effects of systemically administered clonidine and that the facilitation of kindling observed after systemic administration of alpha-2 antagonists may be due to blockade of alpha-2 adrenoceptors outside of the amygdala/pyriform region.
我们之前报道过，向杏仁核/梨状区注入可乐定激活α-2肾上腺素能受体足以延缓点燃效应。为了进一步明确杏仁核/梨状区α-2受体在点燃效应中的作用，我们给大鼠单侧杏仁核内注入多种去甲肾上腺素能药物，随后进行低频杏仁核刺激以诱导快速点燃效应，或进行传统的高频刺激。注入和电刺激每48小时进行一次。同时注入α-2肾上腺素能拮抗剂咪唑克生可阻断可乐定的预防作用，这强烈表明这些作用是通过α-2受体产生的。向杏仁核内注入另一种α-2激动剂赛拉嗪也显著延缓了低频点燃效应。出乎意料的是，向杏仁核内注入α-2拮抗剂咪唑克生、育亨宾和SK&F 104856未能加速点燃效应。注入α-1拮抗剂育亨宾也未能影响点燃效应。我们认为，杏仁核/梨状区的α-2肾上腺素能受体有助于全身给药可乐定的预防作用，并且全身给药α-2拮抗剂后观察到的点燃效应增强可能是由于杏仁核/梨状区以外的α-2肾上腺素能受体被阻断所致。
