2026-03-04 理化学研究所
嫌悪記憶の再固定化に関わる脳回路
＜関連情報＞
- https://www.riken.jp/press/2026/20260304_1/index.html
- https://www.cell.com/neuron/abstract/S0896-6273(26)00006-1
想起中に嫌悪記憶を再フォーマットするための神経調節回路から分子への経路 A neuromodulatory circuit-to-molecular pathway for reformatting aversive memories during recall
Bao Zhen Tan ∙ Jessica Natali Sulkes Cuevas ∙ Reiko Yoshida, ∙ … ∙ Yuri Ishizu ∙ Yukiko Goda ∙ Joshua P. Johansen
Neuron Published:March 3, 2026
DOI:https://doi.org/10.1016/j.neuron.2026.01.006
Highlights
- Locus coeruleus inputs to amygdala are required for aversive memory reconsolidation
- Blocking LC or β2-ARs prevents reconsolidation-induced CRTC1 nuclear translocation
- β2-AR and CRTC1 in a specific amygdala cell type are required for reconsolidation
- Stress or optogenetic β2-AR activation strengthens aversive memory reconsolidation
Summary
Memories can be altered when they are recalled through the process of reconsolidation, requiring gene expression in brain cells that store these memories. How brain circuits reformat memories during recall by directing molecular signaling in specific neuronal populations is not known. Here, we show that brainstem noradrenaline projections to the amygdala, a brain region that stores aversive emotional memories, control memory reconsolidation in rats. During reconsolidation, this circuit regulates the nuclear translocation of CREB-regulated transcriptional coactivator-1 (CRTC1), a molecule important for synapse-to-nucleus transcriptional regulation, through β2-adrenergic receptor (β2-AR) signaling. Cell-type-specific molecular manipulations revealed that reconsolidation requires both β2-AR signaling and CRTC1 in an anatomically and genetically defined amygdala cell population. Finally, increasing stress prior to memory recall enhanced reconsolidation, an effect that was mimicked by amygdala cell-type-specific upregulation of noradrenaline signaling. These results reveal a circuit-to-molecular pathway for state-dependent modification of emotional memories during recall.
