Differential Protein Expression in the Insular Cortex and the Amygdala after Taste Memory Acquisition and Retrieval



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Long-term memories turn labile with reactivation and undergo a re-stabilization process, termed reconsolidation, involving molecular changes that allow updating of an existing memory trace. Such molecular changes may involve the activation of kinases and expression of proteins related to the increase of synaptic plasticity and memory formation. A kinase reported to have a role in a variety of memory tasks is the extracellular signal-regulated kinase 1/2 (ERK1/2). The downstream activation of ERK targets other regulatory enzymes, transcription factors and cytoskeletal proteins, which allow structural changes in the neuron due to protein synthesis up-regulation. Among the proteins up-regulated by ERK activity is the activity-regulated cytoskeleton-associated protein (ARC), an immediate early gene related to synaptic plasticity. The phase-dependent roles of ERK and ARC have not been examined as part of the molecular mechanisms triggered after a learning experience. In this study I used conditioned taste aversion (CTA) as the learning paradigm and investigated the expression of pERK and ARC in brain regions critical for taste information processing such as the insular cortex and the amygdala.

A differential pattern of protein expression was observed in the insular cortex (IC) two hours after taste memory acquisition: pERK activity increased in the aversively conditioned group while ARC increased in the group that received only the novel taste. The central amygdala (CeA) showed a significant increase in pERK, but not ARC activity after CTA training. Immunoblotting experiments performed after memory retrieval in the appetitive group show that pERK continues to signal aversive taste to the IC with ARC exhibiting heightened expression an hour later. An increase in ARC expression 30 minutes after reactivation of the aversive taste was seen in the basolateral amygdala and the CeA exhibited a similar increase at 60 and 90 minutes. Local infusion of ARC antisense oligonucleotides within the IC interfered with the consolidation of safe taste memories, but not with their acquisition. Trace update experiments showed that ARC influences the memory switch from aversive to safe, but not the reverse. Our results indicate that ARC plays a critical role in consolidation and updating of safe taste memories, and the ARC signaling could possibly elicit ERK activation.