Abstract
Consolidated memory can re-enter states of transient instability following reactivation, which is referred to as reconsolidation, and the exact molecular mechanisms underlying this process remain unexplored. Brain-derived neurotrophic factor (BDNF) plays a critical role in synaptic plasticity and memory processes. We have recently observed that BDNF signaling in the central nuclei of the amygdala (CeA) and insular cortex (IC) was involved in the consolidation of conditioned taste aversion (CTA) memory. However, whether BDNF in the CeA or IC is required for memory reconsolidation is still unclear. In the present study, using a CTA memory paradigm, we observed increased BDNF expression in the IC but not in the CeA during CTA reconsolidation. We further determined that BDNF synthesis and signaling in the IC but not in the CeA was required for memory reconsolidation. The differential, spatial-specific roles of BDNF in memory consolidation and reconsolidation suggest that dissociative molecular mechanisms underlie reconsolidation and consolidation, which might provide novel targets for manipulating newly encoded and reactivated memories without causing universal amnesia.
Highlights
The traditional theories of how the brain forms new memories consider that a consolidation process fixes initially fragile memories over time until they undergo ‘stabilization’ in the brain
We previously observed that Brain-derived neurotrophic factor (BDNF) mRNA levels in both the insular cortex (IC) and central nuclei of the amygdala (CeA) increased after conditioned taste aversion (CTA) acquisition and showed that BDNF synthesis in these two areas is required for CTA consolidation [19]
To further establish that the changes in the BDNF mRNA levels in the IC were induced through the process of memory reconsolidation, a no reconsolidation group was subjected to double trial CTA training and no retrieval on the test day
Summary
The traditional theories of how the brain forms new memories consider that a consolidation process fixes initially fragile memories over time until they undergo ‘stabilization’ in the brain. Other data challenge this claim, indicating that the retrieval of memory traces can induce an additional labile phase that requires an active process to stabilize memory after retrieval [2,3,4]. This process has been referred to as reconsolidation and has recently been considered an important component of long-term memory processing [5,6,7]. Investigating the detailed molecular mechanisms involved in reconsolidation is important to further understand the process of memory and for future clinical therapy
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