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

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

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Basolateral Nuclear Complex / physiology*
  • Cytoskeletal Proteins / genetics*
  • Cytoskeletal Proteins / metabolism
  • Fear*
  • Gene Expression*
  • Learning
  • Male
  • Memory*
  • Mental Recall
  • Mice
  • Models, Animal
  • Nerve Tissue Proteins / genetics*
  • Nerve Tissue Proteins / metabolism
  • Receptors, N-Methyl-D-Aspartate / metabolism

Substances

  • Cytoskeletal Proteins
  • NR2B NMDA receptor
  • Nerve Tissue Proteins
  • Receptors, N-Methyl-D-Aspartate
  • activity regulated cytoskeletal-associated protein