title: Activation of the transcription factor NF-kappaB by retrieval is required for long-term memory reconsolidation.
abstract: Several studies support that stored memories undergo a new period of consolidation after retrieval. It is not known whether this process, termed reconsolidation, requires the same transcriptional mechanisms involved in consolidation. Increasing evidence supports the participation of the transcription factor NF-kappaB in memory. This was initially demonstrated in the crab Chasmagnathus model of associative contextual memory, in which re-exposure to the training context induces a well characterized reconsolidation process. Here we studied the role of NF-kappaB in reconsolidation. NF-kappaB was specifically activated in trained animals re-exposed to the training context but not to a different context. NF-kappaB was not activated when animals were re-exposed to the context after a weak training protocol insufficient to induce long-term memory. A specific inhibitor of the NF-kappaB pathway, sulfasalazine, impaired reconsolidation when administered 20 min before re-exposure to the training context but was not effective when a different context was used. These findings indicate for the first time that NF-kappaB is activated specifically by retrieval and that this activation is required for memory reconsolidation, supporting the view that this molecular mechanism is required in both consolidation and reconsolidation.
authors.affiliation: Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, IFIByNE, CONICET, Ciudad Universitaria, Buenos Aires, Argentina.
authors.forename: Emiliano
authors.initials: E
authors.lastname: Merlo
authors.forename: Ramiro
authors.initials: R
authors.lastname: Freudenthal
authors.forename: Héctor
authors.initials: H
authors.lastname: Maldonado
authors.forename: Arturo
authors.initials: A
authors.lastname: Romano
mesh_terms: D000647:Amnesia / Q000523:psychology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D003386:Brachyura / Q000502:physiology*; D001923:Brain Chemistry / Q000502:physiology; D003214:Conditioning, Classical / Q000187:drug effects; D024202:Electrophoretic Mobility Shift Assay; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008568:Memory / Q000502:physiology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000502:physiology*; D010775:Photic Stimulation; D012460:Sulfasalazine / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016328:NF-kappa B; D012460:Sulfasalazine; D007213:Indomethacin