Cellular and systems mechanisms of memory strength as a constraint on auditory fear reconsolidation
Cellular and systems mechanisms of memory strength as a constraint on auditory fear reconsolidation
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DOI：
10.1038/nn.2350
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发表时间：
2009-07-01
影响因子：
25
通讯作者：
Nader, Karim
中科院分区：
文献类型：
--
作者：
Wang, Szu-Han;Alvares, Lucas de Oliveira;Nader, Karim
记忆再巩固已在各种任务和物种中得到证实，这表明它是一个基本过程。然而，有一些实验参数可以抑制再固结的发生（边界条件）。这些条件及其机制仍然不明确。在这里，我们描述了强训练在行为、系统和分子水平上抑制再巩固的能力。我们证明，在大鼠的强大的记忆最初是抵抗再巩固，但经过足够的时间将进行再巩固，这表明边界条件可以是短暂的。在系统水平上，我们表明，海马是必要的抑制杏仁核的再巩固。在分子水平上，我们证明了NR2B NMDA受体亚基，这是至关重要的诱导杏仁核中的听觉记忆的再巩固，下调只有在条件下，当强大的记忆不经历再巩固。这表明介导边界条件的一种分子机制是通过下调再固结诱导机制。
Memory reconsolidation has been demonstrated in various tasks and species, suggesting it is a fundamental process. However, there are experimental parameters that can inhibit reconsolidation from occurring (boundary conditions). These conditions and their mechanisms remain poorly defined. Here, we characterize the ability of strong training to inhibit reconsolidation at the behavioral, systems and molecular levels. We demonstrate that strong memories in rats initially are resistant to reconsolidation, but after sufficient time will undergo reconsolidation, suggesting that boundary conditions can be transient. At the systems level, we show that the hippocampus is necessary for inhibiting reconsolidation in the amygdala. At the molecular level, we demonstrate that NR2B NMDA-receptor subunits which are critical for the induction of reconsolidation of auditory memories in the amygdala, are downregulated only under conditions when strong memories do not undergo reconsolidation. This suggests that one molecular mechanism for mediating boundary conditions is through downregulation of reconsolidation induction mechanisms.