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

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-...

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Autores principales: Freudenthal, Ramiro Angel María, Merlo, Emiliano, Romano, Arturo Gabriel
Publicado: 2005
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0953816X_v21_n10_p2845_Freudenthal
http://hdl.handle.net/20.500.12110/paper_0953816X_v21_n10_p2845_Freudenthal
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spelling paper:paper_0953816X_v21_n10_p2845_Freudenthal2023-06-08T15:55:28Z NF-κB transcription factor is required for inhibitory avoidance long-term memory in mice Freudenthal, Ramiro Angel María Merlo, Emiliano Romano, Arturo Gabriel κB decoy Gel shift Hippocampus Sulfasalazine double stranded DNA immunoglobulin enhancer binding protein oligonucleotide salazosulfapyridine transcription factor indometacin salazosulfapyridine animal behavior animal experiment animal tissue article avoidance behavior controlled study darkness gene expression regulation gene mutation habituation hippocampus inhibitory avoidance behavior long term memory male memory consolidation mouse nerve cell plasticity neuropathology nonhuman priority journal signal transduction task performance training animal drug effect electric shock memory metabolism physiology Animals Avoidance Learning Electroshock Indomethacin Male Memory Mice Neuronal Plasticity NF-kappa B Sulfasalazine Transcription Factors 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. © Federation of European Neuroscience Societies. Fil:Freudenthal, R. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Merlo, E. 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. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0953816X_v21_n10_p2845_Freudenthal http://hdl.handle.net/20.500.12110/paper_0953816X_v21_n10_p2845_Freudenthal
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic κB decoy
Gel shift
Hippocampus
Sulfasalazine
double stranded DNA
immunoglobulin enhancer binding protein
oligonucleotide
salazosulfapyridine
transcription factor
indometacin
salazosulfapyridine
animal behavior
animal experiment
animal tissue
article
avoidance behavior
controlled study
darkness
gene expression regulation
gene mutation
habituation
hippocampus
inhibitory avoidance behavior
long term memory
male
memory consolidation
mouse
nerve cell plasticity
neuropathology
nonhuman
priority journal
signal transduction
task performance
training
animal
drug effect
electric shock
memory
metabolism
physiology
Animals
Avoidance Learning
Electroshock
Indomethacin
Male
Memory
Mice
Neuronal Plasticity
NF-kappa B
Sulfasalazine
Transcription Factors
spellingShingle κB decoy
Gel shift
Hippocampus
Sulfasalazine
double stranded DNA
immunoglobulin enhancer binding protein
oligonucleotide
salazosulfapyridine
transcription factor
indometacin
salazosulfapyridine
animal behavior
animal experiment
animal tissue
article
avoidance behavior
controlled study
darkness
gene expression regulation
gene mutation
habituation
hippocampus
inhibitory avoidance behavior
long term memory
male
memory consolidation
mouse
nerve cell plasticity
neuropathology
nonhuman
priority journal
signal transduction
task performance
training
animal
drug effect
electric shock
memory
metabolism
physiology
Animals
Avoidance Learning
Electroshock
Indomethacin
Male
Memory
Mice
Neuronal Plasticity
NF-kappa B
Sulfasalazine
Transcription Factors
Freudenthal, Ramiro Angel María
Merlo, Emiliano
Romano, Arturo Gabriel
NF-κB transcription factor is required for inhibitory avoidance long-term memory in mice
topic_facet κB decoy
Gel shift
Hippocampus
Sulfasalazine
double stranded DNA
immunoglobulin enhancer binding protein
oligonucleotide
salazosulfapyridine
transcription factor
indometacin
salazosulfapyridine
animal behavior
animal experiment
animal tissue
article
avoidance behavior
controlled study
darkness
gene expression regulation
gene mutation
habituation
hippocampus
inhibitory avoidance behavior
long term memory
male
memory consolidation
mouse
nerve cell plasticity
neuropathology
nonhuman
priority journal
signal transduction
task performance
training
animal
drug effect
electric shock
memory
metabolism
physiology
Animals
Avoidance Learning
Electroshock
Indomethacin
Male
Memory
Mice
Neuronal Plasticity
NF-kappa B
Sulfasalazine
Transcription Factors
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. © Federation of European Neuroscience Societies.
author Freudenthal, Ramiro Angel María
Merlo, Emiliano
Romano, Arturo Gabriel
author_facet Freudenthal, Ramiro Angel María
Merlo, Emiliano
Romano, Arturo Gabriel
author_sort Freudenthal, Ramiro Angel María
title NF-κB transcription factor is required for inhibitory avoidance long-term memory in mice
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
publishDate 2005
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_0953816X_v21_n10_p2845_Freudenthal
http://hdl.handle.net/20.500.12110/paper_0953816X_v21_n10_p2845_Freudenthal
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AT merloemiliano nfkbtranscriptionfactorisrequiredforinhibitoryavoidancelongtermmemoryinmice
AT romanoarturogabriel nfkbtranscriptionfactorisrequiredforinhibitoryavoidancelongtermmemoryinmice
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