Disruption of memory reconsolidation impairs storage of other, non-reactivated memory.

Two hypotheses were tested in this study. First, blockade of neural activity by lidocaine immediately following the retrieval of a memory may impair the reconsolidation and subsequent expression of that memory. Second, a non-retrieved memory would not be affected by this lidocaine treatment. Since the basolateral nucleus of the amygdala (BLA) is involved in emotion-related memory, an intra-BLA lidocaine infusion was used immediately after the retrieval of two emotion-related memories, the step-through passive avoidance response (PA) and cocaine-induced conditioned place preference (CPP). Intra-BLA lidocaine infusion immediately after cocaine-induced CPP retrieval diminished CPP magnitude in retests. However, intra-BLA lidocaine infusion alone did not affect cocaine-induced CPP performance. Intra-BLA lidocaine infusion immediately after PA retrieval decreased PA performance in retests. Omission of PA retrieval procedure, intra-BLA lidocaine infusion did not affect subsequent PA performance. Surprisingly, intra-BLA lidocaine infusion immediately following the retrieval of PA or cocaine-induced CPP diminished both PA and cocaine-induced CPP performance in the retests. Finally, Fos-staining results revealed that a number of BLA neurons were activated by the retrieval of both cocaine-induced CPP and PA. We conclude that inactivation of neural activity in BLA immediately following retrieval of a fear or cocaine-conditioned memory can impair subsequent expression of both memories. More importantly, retrieval of a memory does not seem to be an absolute condition for rapidly changing the memory.

Involvement of amygdaloid protein synthesis in early- and late-phase reconsolidation of emotion-related memories.

This study was undertaken to test whether de novo protein synthesis in the basolateral (BLA) and central (CeA) nucleus of amygdala was required for reconsolidation of emotion-related memories. Mice were trained to sequentially acquire both cocaine-induced conditioned place preference (CPP) and step through passive avoidance (PA) memories. Immediately following PA retrieval, intra-BLA anisomycin infusion was found to decrease subsequent PA performance in retests. Immediately following PA retrieval, intra-CeA anisomycin infusion did not acutely affect PA performance but decreased such a PA memory 5 days later. Given PA retrieval procedure was omitted, intra-BLA and intra-CeA anisomycin infusion did not affect PA memory. Likewise, intra-BLA anisomycin infusion immediately following cocaine-induced CPP retrieval was found to decrease cocaine-induced CPP magnitude in early and late retests. Immediately after cocaine-induced CPP retrieval, intra-CeA anisomycin infusion did not acutely affect cocaine-induced CPP but decreased this memory 5 days later. Given the cocaine-induced CPP retrieval procedure was omitted, intra-BLA and intra-CeA anisomycin infusion did not affect cocaine-induced CPP in subsequent retests. These results, taken together, imply that de novo protein synthesis in amygdala plays an important role in modulating reconsolidation of emotion-related memory. More importantly, de novo protein synthesis in the BLA is essential for early phase reconsolidation of retrieved emotion-related memories. Protein synthesis in the CeA is required for late phase reconsolidation of retrieved emotion-related memories.