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Sci Rep. 2016 Feb 16;6:21007. doi: 10.1038/srep21007.

Late Arc/Arg3.1 expression in the basolateral amygdala is essential for persistence of newly-acquired and reactivated contextual fear memories.

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Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, Japan.
Center for Information and Neural Networks, Suita City, Osaka, Japan.


A feature of fear memory is its persistence, which could be a factor for affective disorders. Memory retrieval destabilizes consolidated memories, and then rapid molecular cascades contribute to early stabilization of reactivated memories. However, persistence of reactivated memories has been poorly understood. Here, we discover that late Arc (also known as Arg3.1) expression in the mouse basolateral amygdala (BLA) is involved in persistence of newly-acquired and reactivated fear memories. After both fear learning and retrieval, Arc levels increased at 2 h, returned to basal levels at 6 h but increased again at 12 h. Inhibiting late Arc expression impaired memory retention 7 d, but not 2 d, after fear learning and retrieval. Moreover, blockade of NR2B-containing N-methyl-D-aspartate receptors (NMDARs) prevented memory destabilization and inhibited late Arc expression. These findings indicate that NR2B-NMDAR and late Arc expression plays a critical role in the destabilization and persistence of reactivated memories.

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