Noradrenaline modulates transmission at a central synapse by a presynaptic mechanism
Noradrenaline modulates transmission at a central synapse by a presynaptic mechanism
复制标题
DOI：
10.1016/j.neuron.2007.10.022
复制
发表时间：
2007-12-06
期刊：
影响因子：
16.2
通讯作者：
Sah, Pankaj
中科院分区：
文献类型：
--
作者：
Delaney, Andrew J.;Crane, James W.;Sah, Pankaj
中央杏仁核 (CeAL) 的外侧部分是脑干中疼痛反应和压力反应核的上行纤维的目标。我们表明，从伤害性脑桥臂旁核到 CeAL 神经元的单纤维输入形成具有多个释放位点的阈上谷氨酸突触。去甲肾上腺素作用于突触前 α2 受体，有效抑制该突触。这种抑制是由于活性释放位点数量减少而释放概率没有变化。引入 G β γ 亚基突触前清道夫可阻断去甲肾上腺素的作用，而肉毒杆菌毒素 A 则降低其作用，表明 β γ 亚基对释放机制有直接作用。这些数据说明了突触前调节机制，其中大的多释放位点突触的输出受到内源性释放的去甲肾上腺素的有效调节，并表明 CeA 可能是去甲肾上腺素中枢伤害性作用的目标。
The lateral division of the central amygdala (CeAL) is the target of ascending fibers from the pain-responsive and stress-responsive nuclei in the brainstem. We show that single fiber inputs from the nociceptive pontine parabrachial nucleus onto CeAL neurons form suprathreshold glutamatergic synapses with multiple release sites. Noradrenaline, acting at presynaptic alpha 2 receptors, potently inhibits this synapse. This inhibition results from a decrease in the number of active release sites with no change in release probability. Introduction of a presynaptic scavenger of G beta gamma subunits blocked the effects of noradrenaline, and botulinum toxin A reduced its effects, showing a direct action of beta gamma subunits on the release machinery. These data illustrate a mechanism of presynaptic modulation where the output of a large multiple-release-site synapse is potently regulated by endogenously released noradrenaline and suggests that the CeA may be a target for the central nociceptive actions of noradrenaline.