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The Journal of Neuroscience, December 5, 2007, 27(49):13436-13445; doi:10.1523/JNEUROSCI.4430-07.2007

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Behavioral/Systems/Cognitive
Activation of Hippocampal Nuclear Factor-B by Retrieval Is Required for Memory Reconsolidation

Mariano Boccia,^1 * Ramiro Freudenthal,^2 * Mariano Blake,¹ Veronica de la Fuente,² Gabriela Acosta,³ Carlos Baratti,¹ and Arturo Romano²

¹Laboratorio de Neurofarmacología de Procesos de Memoria, Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina, ²Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Instituto de Fisiología, Biología Molecular y Neurociencias, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), 1428 EHA Buenos Aires, Argentina, and ³Instituto de Investigaciones Farmacológicas–CONICET, 1113 Buenos Aires, Argentina

Correspondence should be addressed to Arturo Romano, 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, Pabellón II, 2do piso (C1428EHA), Buenos Aires, Argentina. Email: aromano{at}fbmc.fcen.uba.ar

Initially, memory is labile and requires consolidation to become stable. However, several studies support that consolidated memories can undergo a new period of lability after retrieval. The mechanistic differences of this process, termed reconsolidation, with the consolidation process are under debate, including the participation of hippocampus. Up to this point, few reports describe molecular changes and, in particular, transcription factor (TF) involvement in memory restabilization. Increasing evidence supports the participation of the TF nuclear factor-B (NF-B) in memory consolidation. Here, we demonstrate that the inhibition of NF-B after memory reactivation impairs retention of a hippocampal-dependent inhibitory avoidance task in mice. We used two independent disruptive strategies to reach this conclusion. First, we administered intracerebroventricular or intrahippocampal sulfasalazine, an inhibitor of IKK (IB kinase), the kinase that activates NF-B. Second, we infused intracerebroventricular or intrahippocampal B decoy, a direct inhibitor of NF-B consisting of a double-stranded DNA oligonucleotide that contains the B consensus sequence. When injected immediately after memory retrieval, sulfasalazine or B decoy (Decoy) impaired long-term retention. In contrast, a one base mutated B decoy (mDecoy) had no effect. Furthermore, we also found NF-B activation in the hippocampus, with a peak 15 min after memory retrieval. This activation was earlier than that found during consolidation. Together, these results indicate that NF-B is an important transcriptional regulator in memory consolidation and reconsolidation in hippocampus, although the temporal kinetics of activation differs between the two processes.

Key words: reconsolidation; hippocampus; NF-B; B decoy; sulfasalazine; inhibitory avoidance

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Received March 10, 2007; revised Oct. 18, 2007; accepted Oct. 18, 2007.

Correspondence should be addressed to Arturo Romano, 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, Pabellón II, 2do piso (C1428EHA), Buenos Aires, Argentina. Email: aromano{at}fbmc.fcen.uba.ar

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