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Memory traces and tags in the brain

開催日 2014/9/11
時間 9:00 - 11:00
会場 Room B(501)
Chairperson(s) 奥野 浩行 / Hiroyuki Okuno (京都大学大学院 医学研究科 メディカルイノベーションセンター / Medical Innovation Center, Kyoto University Graduate School of Medicine, Japan)
尾藤 晴彦 / Haruhiko Bito (東京大学大学院 医学系研究科 神経生化学分野 / Department of Neurochemistry, The University of Tokyo Graduate School of Medicine, Japan)

Memory traces regulating reconsolidation and extinction after retrieval

  • S1-B-1-4
  • 喜田 聡 / Satoshi Kida:1 
  • 1:東京農業大学 / Dept.of Biosci., Tokyo Univ.of Agriculture, Japan 

Memory retrieval is not a passive phenomenon. Previous studies have presented evidence that memory retrieval is a dynamic process during which memories can be made stronger, weaker, or their content can be altered. Recent studies have shown that reactivated memory becomes labile after retrieval and is re-stabilized through a gene expression-dependent process known as memory reconsolidation. Memory reconsolidation after retrieval may be used to maintain or update long-term memories, reinforcing or integrating new information into them. In classical Pavlovian fear conditioning paradigms, the reactivation of conditioned fear memory by re-exposure to the conditioned stimulus (CS) in the absence of the unconditioned stimulus (US) also initiates extinction as a form of new learning that weakens fear memory expression (i.e., a new CS-no US inhibitory memory that competes with the original CS-US memory trace12-14). Thus, in the fear conditioning paradigms, memory retrieval also includes extinction learning. Therefore, when fear memory is retrieved, the dominance of the original (fear) or new (extinction) memory traces is thought to determine the fate of memory through their competition. To understand mechanisms by which the fate of retrieved fear memory is determined, we have tried to identify traces inducing reconsolidation and extinction of contextual fear memory. Our behavioral results showed that CREB-mediated gene expression and proteasome-dependent protein degradation are required for both reconsolidation and extinction. We next found populations of neurons inducing both CREB-mediated gene expression and proteasome-dependent protein degradation in the mPFC and amygdala during the reconsolidation and extinction phases. These neurons are thought to be winners of the competition between reconsolidation and extinction.

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