Long-term aversive taste memory requires insular and amygdala protein degradation.

Some reports have shown that the ubiquitin-proteasome system (UPS) is necessary to degrade repressor factors to produce new proteins essential to memory consolidation. Furthermore, recent evidence suggests that memory updating also relies on protein degradation through the UPS. To evaluate whether degradation of proteins is part of the cellular events needed for long-term storage of taste aversion, we injected lactacystin--an UPS inhibitor--into the amygdala and/or insular cortex 30 min before the first or second training trials. The results revealed that degradation of proteins in either the amygdala or insular cortex suffices for long-term stabilization of first-time encounter taste aversion. On the other hand, lactacystin applied in the insula, but not in the amygdala, before the second training prevented long-term storage of updated information. Our results support that degradation of proteins by means of the UPS is required every time taste aversion is to be stored in long-term memory.

Simultaneous but not independent anisomycin infusions in insular cortex and amygdala hinder stabilization of taste memory when updated.

Reconsolidation has been described as a process where a consolidated memory returns to a labile state when retrieved. Growing evidence suggests that reconsolidation is, in fact, a destabilization/stabilization process that incorporates updated information to a previously consolidated memory. We used the conditioned taste aversion (CTA) task in order to test this theory. On the first trial, the conditioned stimulus (CS) (saccharin) was associated to the unconditioned stimulus (US) (LiCl injection), and as a result, aversion to saccharin was obtained. The following day, animals were injected with anisomycin in either the insular cortex (IC), central amygdala (CeA), basolateral amygdala (BLA), or simultaneously in IC and CeA or IC and BLA, and a second CTA trial was carried out in which updated information was acquired. Animals were tested 24 h later. When protein synthesis was inhibited in either the IC or CeA, consolidation was affected and previously consolidated memory was unimpaired. However, when both the IC and CeA were simultaneously anisomycin injected, the previously consolidated memory was affected. After repeated association trials, protein synthesis inhibition in the IC and CeA did not have an effect on taste memory. These results suggest that the IC and the CeA are necessary for taste-aversion consolidation, and that both share the previously consolidated memory trace. In addition, our data demonstrated that protein synthesis in either the IC or the CeA suffices to stabilize previously consolidated taste memory when destabilized by incorporation of updated information.