"Dynamic protein changes in aversive taste conditioning: insights from GAP-43 and synaptophysin in memory retrieval and extinction".

Understanding the neural mechanisms underlying the formation, retrieval, and extinction of taste memory is crucial for elucidating learning and memory processes. Using the conditioned taste aversion (CTA) model, we investigated the roles of the amygdala and gustatory cortex (GC), key structures consistently implicated in taste memory. Our study focused on the plastic changes associated with both appetitive and aversive taste memories, emphasizing the importance of extinction in promoting adaptive behavior and counteracting maladaptive responses. Memory processes elicit synaptic plasticity, often reflected in increased expression of neuronal remodeling markers such as growth-associated protein 43 (GAP-43) and synaptophysin (SYN). We examined the involvement of GAP-43 and SYN in taste memory by immunohistochemical analysis in male rats subjected to the formation of appetitive and aversive memories. During memory retrieval, GAP-43 expression was significantly upregulated in the basolateral amygdala (BLA), particularly under aversive conditions. In contrast, memory extinction induced a robust increase in GAP-43 expression in the central amygdala of overtrained animals, accompanied by elevated SYN expression in both the basolateral and central nuclei. These findings highlight the critical roles of GAP-43 and SYN in mediating synaptic changes during memory extinction, supporting the view of extinction as a dynamic, plastic process essential for behavioral adaptation. Our results advance understanding of the molecular substrates of taste memory and suggest potential targets for interventions aimed at modifying maladaptive memory traces, with implications for therapeutic strategies addressing aversive experiences and enhancing adaptive learning.