Gräff, JohannesJoseph, Nadine F.Horn, Meryl E.Samiei, AlirezaMeng, JiaSeo, JinsooRei, DamienBero, Adam W.Phan, Trongha X.Wagner, FlorenceHolson, EdwardXu, JinbinSun, JianjunNeve, Rachael L.Mach, Robert H.Haggarty, Stephen J.Tsai, Li-Huei2014-01-282014-01-282014-01-28201410.1016/j.cell.2013.12.020https://infoscience.epfl.ch/handle/20.500.14299/100204Traumatic events generate some of the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating mechanisms during reconsolidation that are initiated upon memory recall. Here, we show that, in mice, successful reconsolidation-updating paradigms for recent memories fail to attenuate remote (i.e., month-old) ones. We find that, whereas recent memory recall induces a limited period of hippocampal neuroplasticity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent for remote memories. However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation, even remote memories can be persistently attenuated. This intervention epigenetically primes the expression of neuroplasticity-related genes, which is accompanied by higher metabolic, synaptic, and structural plasticity. Thus, applying HDACis during memory reconsolidation might constitute a treatment option for remote traumata.text::journal::journal article::research article