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Recent studies have shown that retrieved memory becomes labile and is re-stabilized through a gene expression-dependent re-stabilization process known as reconsolidation.in addition, the activation of proteasome-dependent protein degradation has been shown to be required for the induction of reconsolidation of retrieved fear memory.However, it still remains unclear whether reconsolidation strengthens original memory.We have asked this using light-dark inhibitory avoidance (IA) task because this task allows to induce reconsolidation without inducing extinction when mice is re-exposed to the light box.We first found that the re-exposure to the light box enhances IA memory.We next examined roles of amygdala (AMY), hippocampus (HP) and medial prefrontal cortex (mPFC) on enhancement of reactivated IA memory.Protein synthesis inhibition in AMY disrupted reactivated IA memory.Interestingly, the inhibition of proteasome-dependent protein degradation in AMY blocked the enhancement of reactivated IA memory and the disruption of reactivated IA memory by protein synthesis inhibition.These results suggest that IA memory is reconsolidated and enhanced in AMY through protein degradation and synthesis.Furthermore, protein synthesis inhibition in the HP or mPFC blocked enhancement of reactivated IA memory without disrupting IA memory, whereasa micro-infusion ofproteasome inhibitor into HP or mPFCblocked the enhancement of reactivated IA memory, suggesting that protein degradation and synthesis in HP/mPFC are required for enhancement, but not reconsolidation, of IA memory.Taken together, our observations suggest that reactivated fear memory is reconsolidated/enhanced and enhanced in the AMY and HP/mPFC, respectively,through protein degradation and synthesis.