• M C Krawczyk, M G Blake, C M Baratti, A Romano, M M Boccia, and M Feld.
• Laboratorio de Neurofarmacología de los Procesos de Memoria, Cátedra de Farmacología, Fac. Farmacia y Bioquímica, UBA, Argentina.
• Neuroscience. 2015 May 21;294:227-37.

AbstractReconsolidation has been defined as the process of memory stabilization after retrieval involving, among others, gene expression regulation and post-translational modifications. Many of these mechanisms are shared with memory consolidation. Here, we studied hippocampal ERK participation on memory reconsolidation of an inhibitory avoidance task in CF-1 mice. We found a retrieval-induced cytosolic ERK2 activation in the hippocampus (HIP) 15 min after memory reactivation, and an inhibition at 45 min. PD098059, a MEK1/2 (MAPK/ERK kinase) inhibitor, administered in the HIP immediately after retrieval impaired memory in a dose-dependent fashion. However, infusions of the highest dose of PD098059 performed 40 min after retrieval enhanced memory in mice trained with a weaker footshock. These results suggest for the first time that ERK2 is involved in memory reconsolidation in a biphasic fashion. Furthermore, the inhibition of ERK could either impair or enhance mice performance depending on ERK state of activation.Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

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