Central amygdala activity during fear conditioning.

Central amygdala activity during fear conditioning.
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DOI:
10.1523/jneurosci.4985-10.2011
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发表时间:
2011-01-05
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
通讯作者:
Paré D
Paré D
中科院分区:
其他
文献类型:
--
作者:
Duvarci S;Popa D;Paré D

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杏仁核中央区(Central amygdala,Ce),尤其是内侧区(medial sector,CeM)是杏仁核条件性恐惧反应的主要输出站。然而,有不确定性的性质CeM控制条件恐惧。本研究的目的是澄清这个问题,使用单位记录大鼠。恐惧条件反射导致大多数脑前膜神经元的CS反应性增加。第二天,CeM细胞在回忆测试中做出了类似的反应,但随着条件恐惧的消退,这些反应消失了。相比之下,CS引起没有显着的平均变化,中央外侧(CeL)的放电率在恐惧条件反射和一个小的,但显着的减少在回忆测试。然而,细胞的细胞分析揭示了大,但异质CS诱发的反应在细胞。在恐惧条件反射结束时,大致相同比例的CeL细胞表现出兴奋性(CeL+)或抑制性(CeL−)CS诱发反应(约10%)。第二天,CeL−细胞的比例增加了两倍,而CeL+细胞的发生率没有变化,这表明条件反射导致了对CeL−细胞的抑制性输入的过夜突触可塑性。与CeM一样,消退训练导致CeL中CS诱发的活动消失。总的来说,这些研究结果表明,条件冻结取决于增加脑电反应的CS。从条件反射到回忆,CeL−而不是CeL+细胞的发生率大幅增加,这使我们提出了一个恐惧条件反射模型,该模型涉及对CeL的外部抑制输入(来自杏仁核或其他地方)的增强,最终导致CeM神经元的去抑制。
The central amygdala (Ce), particularly its medial sector (CeM), is the main output station of the amygdala for conditioned fear responses. However, there is uncertainty regarding the nature of CeM control over conditioned fear. The present study aimed to clarify this question using unit recordings in rats. Fear conditioning caused most CeM neurons to increase their CS responsiveness. The next day, CeM cells responded similarly during the recall test, but these responses disappeared as extinction of conditioned fear progressed. In contrast, the CS elicited no significant average change in central lateral (CeL) firing rates during fear conditioning and a small but significant reduction during the recall test. Yet, cell-by-cell analyses disclosed large but heterogeneous CS-evoked responses in CeL. By the end of fear conditioning, roughly equal proportions of CeL cells exhibited excitatory (CeL+) or inhibitory (CeL−) CS-evoked responses (≈10%). The next day, the proportion of CeL− cells tripled with no change in the incidence of CeL+ cells, suggesting that conditioning leads to overnight synaptic plasticity in an inhibitory input to CeL− cells. As in CeM, extinction training caused the disappearance of CS-evoked activity in CeL. Overall, these findings suggest that conditioned freezing depends on increased CeM responses to the CS. The large increase in the incidence of CeL− but not CeL+ cells from conditioning to recall leads us to propose a model of fear conditioning involving the potentiation of an extrinsic inhibitory input (from the amygdala or elsewhere) to CeL, ultimately leading to disinhibition of CeM neurons.