Amygdala inputs drive feedforward inhibition in the medial prefrontal cortex
Amygdala inputs drive feedforward inhibition in the medial prefrontal cortex
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DOI：
10.1152/jn.00531.2012
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发表时间：
2013-07-01
影响因子：
2.5
通讯作者：
O'Donnell, Patricio
中科院分区：
文献类型：
--
作者：
Dilgen, Jonathan;Tejeda, Hugo A.;O'Donnell, Patricio
虽然杏仁核和前额叶皮质(PFC)之间的相互作用对行为的情绪指导至关重要，但杏仁核影响PFC功能的方式尚不清楚。尽管基底外侧杏仁核(BLA)的输出神经元表现出许多与兴奋性神经传递相关的特征，但刺激BLA通常会抑制PFC细胞的放电。这种明显的差异可以解释如果局部的PFC抑制中间神经元被BLA输入激活。在这里，我们使用麻醉大鼠的活体细胞旁和细胞内记录来研究BLA输入是否在PFC中引起前馈抑制。细胞外记录显示，刺激BLA可诱发PFC中间神经元的动作电位，并使大部分锥体神经元沉默。来自PFC锥体神经元的细胞内记录显示出去极化的突触后电位，刺激BLA可诱发多个成分。这些反应表现出相对负的反转电位(EREV)，表明氯化物成分的贡献。细胞内给药或压力喷射GABA-A拮抗剂印防己毒素导致动作电位在BLA诱发的反应中被激发，这具有更去极化的EREV。这些结果表明，刺激BLA在局部环路中间神经元介导的PFC内参与了一种强大的抑制机制。
Although interactions between the amygdala and prefrontal cortex (PFC) are critical for emotional guidance of behavior, the manner in which amygdala affects PFC function is not clear. Whereas basolateral amygdala (BLA) output neurons exhibit many characteristics associated with excitatory neurotransmission, BLA stimulation typically inhibits PFC cell firing. This apparent discrepancy could be explained if local PFC inhibitory interneurons were activated by BLA inputs. Here, we used in vivo juxtacellular and intracellular recordings in anesthetized rats to investigate whether BLA inputs evoke feedforward inhibition in the PFC. Juxtacellular recordings revealed that BLA stimulation evoked action potentials in PFC interneurons and silenced most pyramidal neurons. Intracellular recordings from PFC pyramidal neurons showed depolarizing postsynaptic potentials, with multiple components evoked by BLA stimulation. These responses exhibited a relatively negative reversal potential (Erev), suggesting the contribution of a chloride component. Intracellular administration or pressure ejection of the GABA-A antagonist picrotoxin resulted in action-potential firing during the BLA-evoked response, which had a more depolarized Erev. These results suggest that BLA stimulation engages a powerful inhibitory mechanism within the PFC mediated by local circuit interneurons.