Role of histone acetylation in memory reconsolidation

FEDERMAN, NOEL; ROMANO, ARTURO

Amsterdam

Congreso; FENS forum 2010; 2010

Federation of European Neuroscience Societies

Gene expression is a critical requirement for the conversion of a labile short-term memory into a consolidated long-term memory. Recently, the participation of epigenetic mechanisms, like histone acetylation, was evidenced in memory consolidation. However, the training strength required and the persistence of the chromatin acetylation recruited are not well characterized. In the present work we studied whether histone acetylation is involved in consolidation and reconsolidation in invertebrates, if its participation depends on the training strength and if it is a permanent or transient mechanism. We used a well characterized memory model in invertebrates, the context-signal memory in crabs. Our results show no changes in histone 3 (H3) acetylation during consolidation of a standard training protocol. However, a stronger training session induced a significant increase in H3 acetylation 1 h post-training, returning to basal levels afterward. A similar H3 acetylation increment was found in the reconsolidation phase of a memory induced by a strong training protocol. Furthermore, administration of the histone deacetylase inhibitor sodium butyrate (NaB) allowed a weak training to induce long-term memory in two phases during consolidation, probably by transforming a weak memory trace in a stronger long-term memory one.  Moreover, in spite of the fact that weak training protocol did not induce histone H3 acetylation in animals injected with saline solution, the injection of NaB increased H3 acetylation 1 h after weak training, as the increment found after strong training protocol without any injection. These findings support that H3 acetylation 1) is an evolutionarily-conserved mechanism involved in memory consolidation and reconsolidation; 2) occurs only after strong training; 3) is a transient process; and that 4) NaB enhances memory in two phases by means of, at least in part, increasing histone acetylation. The time coincidence of this epigenetic mechanism with other molecular processes participating in memory formation is fully discussed in the framework of gene expression regulation during memory consolidation and strength.