| Summary: | 碩士 === 國立成功大學 === 行為醫學研究所 === 97 === Basolateral nuclei of amygdala (BLA) are thought to play a critical role in mediating both positive and negative emotion-supported learning and memory. We hereby demonstrate that intra-BLA lidocaine infusion immediately after the reactivation of cocaine-induced conditioned place preference (CPP) or passive avoidance (PA) memory selectively diminishes the expression magnitude of the reactivated memory in subsequent tests. In contrast, intra-BLA infusion of lidocaine alone does not affect the memory expression. We attempt to test the hypothesis that a non-reactivated memory can never return to a labile state susceptible to modification. Some mice were trained to acquire both cocaine-induced CPP and PA memory. Intra-BLA lidocaine infusion was given immediately after the reactivation of one of the acquired memory, and the performance of these memories was measured in subsequent retests for the maintenance of these memories. Here we show that intra-BLA lidocaine infusion immediately following the reactivation of passive avoidance memory diminishes the performance of both PA and cocaine-induced CPP memories in subsequent retests. Likewise, intra-BLA lidocaine infusion immediately following the reactivation of cocaine-induced CPP memory diminishes the performance of both cocaine-induced CPP and PA memories in subsequent retests. We conclude that reactivation of one memory can make the other storage-related memories susceptible to modification. In addition, numerous studies have demonstrated that specific intracellular signaling pathways are involved in the reconsolidation of various memories. Of these numerous pathways, one in particular has been vigorously studied for the role in synaptic plasticity and memory formation, the mitogen-activated protein kinase (MAPK) pathway. Previously, we demonstrated that U0126, an inhibitor of MAPK/ERK kinase (MEK), disrupted the reconsolidation of cocaine-induced CPP memory. In our preliminary results, we found that intra-BLA infusion with U0126 after the reactivation of passive avoidance memory effectively impaired subsequent retrieval of this memory. In contrast with the results of lidocaine, we found that injection of U0126 into the BLA impaired neither cocaine-induced CPP nor PA memory regardless which memory was reactivated.
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