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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todo:paper_0953816X_v21_n10_p2845_Freudenthal2023-10-03T15:51:16Z NF-κB transcription factor is required for inhibitory avoidance long-term memory in mice Freudenthal, R. Boccia, M.M. Acosta, G.B. Blake, M.G. Merlo, E. Baratti, C.M. Romano, A. 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. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar 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, R. Boccia, M.M. Acosta, G.B. Blake, M.G. Merlo, E. Baratti, C.M. Romano, A. 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. |
| format |
JOUR |
| author |
Freudenthal, R. Boccia, M.M. Acosta, G.B. Blake, M.G. Merlo, E. Baratti, C.M. Romano, A. |
| author_facet |
Freudenthal, R. Boccia, M.M. Acosta, G.B. Blake, M.G. Merlo, E. Baratti, C.M. Romano, A. |
| author_sort |
Freudenthal, R. |
| 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 |
| url |
http://hdl.handle.net/20.500.12110/paper_0953816X_v21_n10_p2845_Freudenthal |
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