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Activation of hippocampal nuclear factor-κB by retrieval is required for memory reconsolidation

Boccia, M. - Freudenthal, R. - Blake, M. - De La Fuente, V. - Acosta, G. - Baratti, C. - Romano, A.
   
Fecha:
2007
Tipo de documento: 
info:eu-repo/semantics/article
info:ar-repo/semantics/artículo
info:eu-repo/semantics/publishedVersion
Formato:
application/pdf
Temas:
κB decoy - Hippocampus - Inhibitory avoidance - NF-κB - Reconsolidation - Sulfasalazine - double stranded DNA - immunoglobulin enhancer binding protein - salazosulfapyridine - animal experiment - article - avoidance behavior - brain function - controlled study - hippocampus - information processing - male - memory - memory consolidation - mouse - nonhuman - priority journal - task performance - Animals - Hippocampus - Injections, Intraventricular - Male - Memory - Mice - NF-kappa B - Sulfasalazine
Descripción:
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-κB (NF-κB) in memory consolidation. Here, we demonstrate that the inhibition of NF-κB 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 (IκB kinase), the kinase that activates NF-κB. Second, we infused intracerebroventricular or intrahippocampal κB decoy, a direct inhibitor of NF-κB consisting of a double-stranded DNA oligonucleotide that contains the κB consensus sequence. When injected immediately after memory retrieval, sulfasalazine or κB decoy (Decoy) impaired long-term retention. In contrast, a one base mutated κB decoy (mDecoy) had no effect. Furthermore, we also found NF-κB 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-κB is an important transcriptional regulator in memory consolidation and reconsolidation in hippocampus, although the temporal kinetics of activation differs between the two processes. Copyright © 2007 Society for Neuroscience.
Fil:Freudenthal, R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:De La Fuente, V. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fil:Romano, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.
Fuente:
J. Neurosci. 2007;27(49):13436-13445
Identificador:
http://hdl.handle.net/20.500.12110/paper_02706474_v27_n49_p13436_Boccia
http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_02706474_v27_n49_p13436_Boccia_oai
Derechos:
info:eu-repo/semantics/openAccess

Cita bibliográfica:

Boccia, M. ; Freudenthal, R. ; Blake, M. ; et al. (2007).  Activation of hippocampal nuclear factor-κB by retrieval is required for memory reconsolidation.  (info:eu-repo/semantics/article).  [consultado:  ] Disponible en el Repositorio Digital Institucional de la Universidad de Buenos Aires:  <http://hdl.handle.net/20.500.12110/paper_02706474_v27_n49_p13436_Boccia>