“…According to this hypothesis, HDAC inhibitors, that are able to prevent the reduction of acetylation in models of cerebral ischemia, up-regulate protein levels of Bcl-2, Hsp70, pCREB, BDNF, GFAP, pAKT and reduce the ischemia-induced increase in expression of p53, NOS, COX-2, TNF-a and IL-b; (Faraco et al, 2006;Kim et al, 2007Kim et al, , 2009. In this study, we show that the mild increase in acetylation induced by NMDA preconditioning is associated with a downstream increase in ERK 1/2 phosphorylation, a crucial prosurvival signaling pathway in models of ischemic tolerance (Shamloo et al, 1999;Choi et al, 2006;Gao et al, 2010;Gerace et al, 2012). Similarly, Sinn and colleagues (Sinn et al, 2007) have reported that increased acetylation by the HDAC inhibitor valproate activates the translation of pERK in a model of intracerebral hemorrhage.…”