α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体通过一种依赖于Arc的机制控制恐惧消退。
AMPA receptors control fear extinction through an Arc-dependent mechanism.
作者信息
Trent Simon, Barnes Philip, Hall Jeremy, Thomas Kerrie L
机构信息
Neuroscience and Mental Health Research Institute, Cardiff University, Haydn Ellis Building, Cardiff CF24 4HQ, United Kingdom.
Cardiff School of Biosciences, Cardiff University, Park Place, Cardiff CF10 3AX, United Kingdom.
出版信息
Learn Mem. 2017 Jul 17;24(8):375-380. doi: 10.1101/lm.045013.117. Print 2017 Aug.
Activity-regulated cytoskeleton-associated protein (Arc) supports fear memory through synaptic plasticity events requiring actin cytoskeleton rearrangements. We have previously shown that reducing hippocampal Arc levels through antisense knockdown leads to the premature extinction of contextual fear. Here we show that the AMPA receptor antagonist CNQX elevates hippocampal Arc levels during extinction and blocks extinction that can be rescued by reducing Arc. Increasing Arc levels with CNQX also overcomes the actin-destabilizing properties of cytochalasin D and promotes extinction. Therefore, extinction is dependent on AMPA-mediated reductions of Arc via a mechanism consistent with a role for Arc in stabilizing the actin cytoskeleton to constrain extinction.
活性调节细胞骨架相关蛋白（Arc）通过需要肌动蛋白细胞骨架重排的突触可塑性事件来支持恐惧记忆。我们之前已经表明，通过反义敲低降低海马体中Arc的水平会导致情境恐惧的过早消退。在这里我们表明，AMPA受体拮抗剂CNQX在消退过程中会提高海马体中Arc的水平，并阻断可以通过降低Arc来挽救的消退。用CNQX提高Arc水平也能克服细胞松弛素D的肌动蛋白去稳定特性并促进消退。因此，消退依赖于AMPA介导的Arc减少，其机制与Arc在稳定肌动蛋白细胞骨架以抑制消退中的作用一致。
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