Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval
Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval
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DOI：
10.1038/35021052
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发表时间：
2000-08-17
期刊：
影响因子：
64.8
通讯作者：
Le Doux, JE
中科院分区：
文献类型：
--
作者：
Nader, K;Schafe, GE;Le Doux, JE
“新”记忆最初是不稳定的，在被巩固为稳定的长期记忆之前对破坏很敏感（1-5）。许多证据表明，这种巩固涉及神经元中新蛋白质的合成（6-9）。杏仁核的外侧核和基底核（LBA）被认为是恐惧学习中记忆储存的部位（10）。在训练后不久将蛋白质合成抑制剂茴香霉素注入LBA可以防止恐惧记忆的巩固（11）。在这里，我们表明，巩固的恐惧记忆，当在检索过程中重新激活，返回到一个不稳定的状态，其中茴香霉素的输液后不久，记忆重新激活产生健忘症在以后的测试，无论是否重新激活后进行1或14天的条件反射。用茴香霉素进行同样的治疗，在没有记忆激活的情况下，记忆完好无损。与巩固过程中蛋白质合成产生的时间限制作用一致，将输注延迟至记忆再激活后6小时不会产生健忘症。我们的数据表明，巩固的恐惧记忆，当重新激活，返回到一个不稳定的状态，需要从头蛋白质合成重新巩固。这些发现并不是传统的记忆巩固理论所预测的。
'New' memories are initially labile and sensitive to disruption before being consolidated into stable long-term memories(1-5). Much evidence indicates that this consolidation involves the synthesis of new proteins in neurons(6-9). The lateral and basal nuclei of the amygdala (LBA) are believed to be a site of memory storage in fear learning(10). Infusion of the protein synthesis inhibitor anisomycin into the LBA shortly after training prevents consolidation of fear memories(11). Here we show that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning. The same treatment with anisomycin, in the absence of memory reactivation, left memory intact. Consistent with a time-limited role for protein synthesis production in consolidation, delay of the infusion until six hours after memory reactivation produced no amnesia. Our data show that consolidated fear memories, when reactivated, return to a labile state that requires de novo protein synthesis for reconsolidation. These findings are not predicted by traditional theories of memory consolidation.