Department of Neuroscience and Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Science. 2010 Nov 19;330(6007):1108-12. doi: 10.1126/science.1195298. Epub 2010 Oct 28.
Traumatic fear memories can be inhibited by behavioral therapy for humans, or by extinction training in rodent models, but are prone to recur. Under some conditions, however, these treatments generate a permanent effect on behavior, which suggests that emotional memory erasure has occurred. The neural basis for such disparate outcomes is unknown. We found that a central component of extinction-induced erasure is the synaptic removal of calcium-permeable α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPARs) in the lateral amygdala. A transient up-regulation of this form of plasticity, which involves phosphorylation of the glutamate receptor 1 subunit of the AMPA receptor, defines a temporal window in which fear memory can be degraded by behavioral experience. These results reveal a molecular mechanism for fear erasure and the relative instability of recent memory.
创伤性恐惧记忆可以通过人类的行为疗法或啮齿动物模型的消退训练来抑制，但容易复发。然而，在某些条件下，这些治疗方法会对行为产生永久性的影响，这表明情绪记忆已经被抹去。这种截然不同结果的神经基础尚不清楚。我们发现，消退诱导的遗忘的一个核心组成部分是外侧杏仁核中钙通透性 α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体 (AMPAR) 的突触去除。这种形式的可塑性的短暂上调，涉及 AMPA 受体谷氨酸受体 1 亚基的磷酸化，定义了一个时间窗口，在这个窗口内，通过行为经验可以降解恐惧记忆。这些结果揭示了恐惧消除的分子机制和近期记忆的相对不稳定性。
