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演題詳細

Poster

学習・長期記憶
Learning and Long-term Memory

開催日 2014/9/12
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

古い恐怖条件付け文脈記憶の安定性制御機構の解析
Analysis of regulatory mechanisms of stability of remote contextual fear memory

  • P2-245
  • 福島 穂高 / Hotaka Fukushima:1,2 金 亮 / Ryang KIM:1 喜田 聡 / Satoshi KIDA:1,2 
  • 1:東農大・応生科・バイオ / Dept. Biosci., Tokyo Univ. of Agric., Tokyo, Japan 2:科学技術振興機構・CREST / JST, CREST, Tokyo, Japan  

Recent studies have shown that reactivated contextual fear memory becomes labile and is re-stabilized through memory reconsolidation that requires CREB-mediated transcription in the hippocampus (HP) (Suzuki et al., 2004; Mamiya et al., 2009). We previously found that short re-exposure to conditioned stimulus (CS; context) for 3 min induced reconsolidation on recent, but not remote, contextual fear memory. Interestingly, we also found that long re-exposure to the CS for 10 min enabled to induce reconsolidation of remote contextual fear memory. In this study, we tried to understand mechanisms by which the stability of remote contextual fear memory is regulated. Mice were trained with a single footshock and re-exposed to training context for 3 or 10 min 1 or 30 days later. To identify which brain regions were activated when remote contextual fear memory is reconsolidated, we first performed immunohistochemistry to measure the expression levels of c-fos, a target gene of CREB. Similarly with our previous finding, re-exposure to CS for both 3 and 10 min 1 day after training led to increase in c-fos expression in the HP. Interestingly, re-exposure to CS for 10 min, but not 3 min, 30 days after training led to increase in c-fos expression in the HP, suggesting that long re-exposure to CS enables to induce gene expression in the HP even when memory is remote. Next, to understand roles of gene expression in the HP following re-exposure to CS in remote contextual fear memory, mice were micro-infused with a protein synthesis inhibitor, anisomycin (ANI) into the HP immediately after re-exposure. ANI treatment disrupted reactivated fear memory in re-exposure to CS for 3 or 10 min 1 and 30 days, respectively, after training, suggesting that gene expression in the HP is required for reconsolidation of both recent and remote contextual fear memory. Our observations suggest that remote contextual fear memory becomes labile following long re-exposure to CS and then is reconsolidated through gene expression in the HP.

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