A great body of evidence shows that the recollection process of long -term memory is dynamic and requires de novo protein synthesis. Memory retrieval is also one way to incorporate new information into preexisting memories. Indeed, long-term memory is not that solid, but becomes labile particularly during its retrieval. We have investigated whether or not protein degradation is involved in the reorganization of retrieved memory. In this talk I will show the evidence that postsynaptic proteins are degraded in the hippocampus by polyubiquiti -nation after retrieval of contextual fear memory. We also found that the infusion of proteasome inhibitor into the hippocampus immediately after the memory retrieval prevented anisomycin (protein synthesis inhibitor)-induced memory impairment, as well as the extinction of fear memory. This indicates that ubiquitin/proteasome-dependent protein degradation underlies destabilization processes after the memory retrieval. It also suggests preexisting memory is disrupted by proteasome-mediated protein degradation, and that updated memory is reconsolidated or strengthened by protein synthesis.