NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice

Autores
Freudenthal, Ramiro A. M.; Boccia, Mariano Martín; Acosta, Gabriela Beatriz; Blake, Mariano Guillermo; Merlo, Emiliano; Baratti, Carlos Maria; Romano, Arturo Gabriel
Año de publicación
2005
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Although it is generally accepted that memory consolidation requires regulation of gene expression, only a few transcription factors (TFs) have been clearly demonstrated to be specifically involved in this process. Increasing research data point to the participation of the Rel/nuclear factor‐κB (NF‐κB) family of TFs in memory and neural plasticity. Here we found that two independent inhibitors of NF‐κB induced memory impairment in the one‐trial step‐through inhibitory avoidance paradigm in mice: post‐training administration of the drug sulfasalazine and 2 h pretraining administration of a double‐stranded DNA oligonucleotide containing the NF‐κB consensus sequence (κB decoy). Conversely, one base mutation of the κB decoy (mut‐κB decoy) injection did not affect long‐term memory. Accordingly, the κB decoy inhibited NF‐κB in hippocampus 2 h after injection but no inhibition was found with mut‐κB decoy administration. A temporal course of hippocampal NF‐κB activity after training was determined. Unexpectedly, an inhibition of NF‐κB was found 15 min after training in shocked and unshocked groups when compared with the naïve group. Hippocampal NF‐κB was activated 45 min after training in both shocked and unshocked groups, decreasing 1 h after training and returning to basal levels 2 and 4 h after training. On the basis of the latter results, we propose that activation of NF‐κB in hippocampus is part of the molecular mechanism involved in the storage of contextual features that constitute the conditioned stimulus representation. The results presented here provide the first evidence to support NF‐κB activity being regulated in hippocampus during consolidation, stressing the role of this TF as a conserved molecular mechanism for memory storage.
Fil: Freudenthal, Ramiro A. M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
Fil: Boccia, Mariano Martín. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Acosta, Gabriela Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Blake, Mariano Guillermo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Merlo, Emiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
Fil: Baratti, Carlos Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Romano, Arturo Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
Materia
ΚB DECOY
GEL SHIFT
HIPPOCAMPUS
SULFASALAZINE
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/94693
Acceder
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network_acronym_str CONICETDig
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network_name_str CONICET Digital (CONICET)
spelling NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in miceFreudenthal, Ramiro A. M.Boccia, Mariano MartínAcosta, Gabriela BeatrizBlake, Mariano GuillermoMerlo, EmilianoBaratti, Carlos MariaRomano, Arturo GabrielΚB DECOYGEL SHIFTHIPPOCAMPUSSULFASALAZINEhttps://purl.org/becyt/ford/3.5https://purl.org/becyt/ford/3Although it is generally accepted that memory consolidation requires regulation of gene expression, only a few transcription factors (TFs) have been clearly demonstrated to be specifically involved in this process. Increasing research data point to the participation of the Rel/nuclear factor‐κB (NF‐κB) family of TFs in memory and neural plasticity. Here we found that two independent inhibitors of NF‐κB induced memory impairment in the one‐trial step‐through inhibitory avoidance paradigm in mice: post‐training administration of the drug sulfasalazine and 2 h pretraining administration of a double‐stranded DNA oligonucleotide containing the NF‐κB consensus sequence (κB decoy). Conversely, one base mutation of the κB decoy (mut‐κB decoy) injection did not affect long‐term memory. Accordingly, the κB decoy inhibited NF‐κB in hippocampus 2 h after injection but no inhibition was found with mut‐κB decoy administration. A temporal course of hippocampal NF‐κB activity after training was determined. Unexpectedly, an inhibition of NF‐κB was found 15 min after training in shocked and unshocked groups when compared with the naïve group. Hippocampal NF‐κB was activated 45 min after training in both shocked and unshocked groups, decreasing 1 h after training and returning to basal levels 2 and 4 h after training. On the basis of the latter results, we propose that activation of NF‐κB in hippocampus is part of the molecular mechanism involved in the storage of contextual features that constitute the conditioned stimulus representation. The results presented here provide the first evidence to support NF‐κB activity being regulated in hippocampus during consolidation, stressing the role of this TF as a conserved molecular mechanism for memory storage.Fil: Freudenthal, Ramiro A. M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaFil: Boccia, Mariano Martín. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Acosta, Gabriela Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; ArgentinaFil: Blake, Mariano Guillermo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Merlo, Emiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaFil: Baratti, Carlos Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Romano, Arturo Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; ArgentinaWiley Blackwell Publishing, Inc2005-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/94693Freudenthal, Ramiro A. M.; Boccia, Mariano Martín; Acosta, Gabriela Beatriz; Blake, Mariano Guillermo; Merlo, Emiliano; et al.; NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice; Wiley Blackwell Publishing, Inc; European Journal Of Neuroscience; 21; 10; 5-2005; 2845-28520953-816XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/full/10.1111/j.1460-9568.2005.04126.xinfo:eu-repo/semantics/altIdentifier/doi/10.1111/j.1460-9568.2005.04126.xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:56:34Zoai:ri.conicet.gov.ar:11336/94693instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 14:56:34.927CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
title NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
spellingShingle NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
Freudenthal, Ramiro A. M.
ΚB DECOY
GEL SHIFT
HIPPOCAMPUS
SULFASALAZINE
title_short NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
title_full NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
title_fullStr NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
title_full_unstemmed NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
title_sort NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice
dc.creator.none.fl_str_mv Freudenthal, Ramiro A. M.
Boccia, Mariano Martín
Acosta, Gabriela Beatriz
Blake, Mariano Guillermo
Merlo, Emiliano
Baratti, Carlos Maria
Romano, Arturo Gabriel
author Freudenthal, Ramiro A. M.
author_facet Freudenthal, Ramiro A. M.
Boccia, Mariano Martín
Acosta, Gabriela Beatriz
Blake, Mariano Guillermo
Merlo, Emiliano
Baratti, Carlos Maria
Romano, Arturo Gabriel
author_role author
author2 Boccia, Mariano Martín
Acosta, Gabriela Beatriz
Blake, Mariano Guillermo
Merlo, Emiliano
Baratti, Carlos Maria
Romano, Arturo Gabriel
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv ΚB DECOY
GEL SHIFT
HIPPOCAMPUS
SULFASALAZINE
topic ΚB DECOY
GEL SHIFT
HIPPOCAMPUS
SULFASALAZINE
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.5
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Although it is generally accepted that memory consolidation requires regulation of gene expression, only a few transcription factors (TFs) have been clearly demonstrated to be specifically involved in this process. Increasing research data point to the participation of the Rel/nuclear factor‐κB (NF‐κB) family of TFs in memory and neural plasticity. Here we found that two independent inhibitors of NF‐κB induced memory impairment in the one‐trial step‐through inhibitory avoidance paradigm in mice: post‐training administration of the drug sulfasalazine and 2 h pretraining administration of a double‐stranded DNA oligonucleotide containing the NF‐κB consensus sequence (κB decoy). Conversely, one base mutation of the κB decoy (mut‐κB decoy) injection did not affect long‐term memory. Accordingly, the κB decoy inhibited NF‐κB in hippocampus 2 h after injection but no inhibition was found with mut‐κB decoy administration. A temporal course of hippocampal NF‐κB activity after training was determined. Unexpectedly, an inhibition of NF‐κB was found 15 min after training in shocked and unshocked groups when compared with the naïve group. Hippocampal NF‐κB was activated 45 min after training in both shocked and unshocked groups, decreasing 1 h after training and returning to basal levels 2 and 4 h after training. On the basis of the latter results, we propose that activation of NF‐κB in hippocampus is part of the molecular mechanism involved in the storage of contextual features that constitute the conditioned stimulus representation. The results presented here provide the first evidence to support NF‐κB activity being regulated in hippocampus during consolidation, stressing the role of this TF as a conserved molecular mechanism for memory storage.
Fil: Freudenthal, Ramiro A. M.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
Fil: Boccia, Mariano Martín. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Acosta, Gabriela Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Farmacológicas. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Investigaciones Farmacológicas; Argentina
Fil: Blake, Mariano Guillermo. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Merlo, Emiliano. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
Fil: Baratti, Carlos Maria. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Farmacología. Cátedra de Farmacología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Romano, Arturo Gabriel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Fisiología, Biología Molecular y Neurociencias. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Fisiología, Biología Molecular y Neurociencias; Argentina
description Although it is generally accepted that memory consolidation requires regulation of gene expression, only a few transcription factors (TFs) have been clearly demonstrated to be specifically involved in this process. Increasing research data point to the participation of the Rel/nuclear factor‐κB (NF‐κB) family of TFs in memory and neural plasticity. Here we found that two independent inhibitors of NF‐κB induced memory impairment in the one‐trial step‐through inhibitory avoidance paradigm in mice: post‐training administration of the drug sulfasalazine and 2 h pretraining administration of a double‐stranded DNA oligonucleotide containing the NF‐κB consensus sequence (κB decoy). Conversely, one base mutation of the κB decoy (mut‐κB decoy) injection did not affect long‐term memory. Accordingly, the κB decoy inhibited NF‐κB in hippocampus 2 h after injection but no inhibition was found with mut‐κB decoy administration. A temporal course of hippocampal NF‐κB activity after training was determined. Unexpectedly, an inhibition of NF‐κB was found 15 min after training in shocked and unshocked groups when compared with the naïve group. Hippocampal NF‐κB was activated 45 min after training in both shocked and unshocked groups, decreasing 1 h after training and returning to basal levels 2 and 4 h after training. On the basis of the latter results, we propose that activation of NF‐κB in hippocampus is part of the molecular mechanism involved in the storage of contextual features that constitute the conditioned stimulus representation. The results presented here provide the first evidence to support NF‐κB activity being regulated in hippocampus during consolidation, stressing the role of this TF as a conserved molecular mechanism for memory storage.
publishDate 2005
dc.date.none.fl_str_mv 2005-05
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/94693
Freudenthal, Ramiro A. M.; Boccia, Mariano Martín; Acosta, Gabriela Beatriz; Blake, Mariano Guillermo; Merlo, Emiliano; et al.; NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice; Wiley Blackwell Publishing, Inc; European Journal Of Neuroscience; 21; 10; 5-2005; 2845-2852
0953-816X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/94693
identifier_str_mv Freudenthal, Ramiro A. M.; Boccia, Mariano Martín; Acosta, Gabriela Beatriz; Blake, Mariano Guillermo; Merlo, Emiliano; et al.; NF‐κB transcription factor is required for inhibitory avoidance long‐term memory in mice; Wiley Blackwell Publishing, Inc; European Journal Of Neuroscience; 21; 10; 5-2005; 2845-2852
0953-816X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1460-9568.2005.04126.x
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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