CONICET | Buscador de Institutos y Recursos Humanos

Diapositiva 1 .O {font-size:149%;}   Gene expression has been implicated as a necessary molecular process for the time dependent phase of memory stabilization following its re-activation, a process known as reconsolidation. However, the transcription regulation mechanisms engaged in memory reconsolidation, and its associated function at the memory process, have been less studied. Histone modification is a fundamental mechanism involved in epigenetic regulation of gene expression and it has been implicated in memory consolidation. Particularly, acetylation of histones, which is thoroughly related with transcriptional activation, it has been demonstrated to increase by learning. Furthermore, pharmacologically histone acetylation increment induced by KDACs inhibitors administration during consolidation lead to memory enhancement. Nevertheless, there are a few evidences showing this molecular process participating in gene activation induced after retrieval. Therefore, we ask: ¿Is the histone acetylation process, already implicated in consolidation, induced during the reconsolidation phase? ¿Which is the role of this epigenetic mechanism associated at this phase? Using the context signal memory paradigm in Chasmagnathus crab, we found a histone H3 acetylation increment 1 hour post- reactivation of a memory induced by strong training protocol, but not during the reconsolidation phase of a memory formed by a weak training (Figure 1). In other hand, brain histone acetylation increment, induced by a KDAC inhibitor (NaB) administration, during reconsolidation is not sufficient to enhance a weak memory(Figure 3), different from the effects of the administration of this drug during consolidation (Federman et al.2009). Our results suggest that this molecular marking of the genome is a process necessary for the activation of transcription during the re-stabilization of stronger memories, functioning as molecular feature of them.