Memory extinction entails the inhibition of the transcription factor NF-κB

Autores
Merlo, E.; Romano, A.
Año de publicación
2008
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
In contextual memories, an association between a positive or negative reinforcement and the contextual cues where the reinforcement occurs is formed. The re-exposure to the context without reinforcement can lead to memory extinction or reconsolidation, depending on the number of events or duration of a single event of context re-exposure. Extinction involves the temporary waning of the previously acquired conditioned response. The molecular processes underlying extinction and the mechanisms which determine if memory will reconsolidate or extinguish after retrieval are not well characterized, particularly the role of transcription factors and gene expression. Here we studied the participation of a transcription factor, NF-κB, in memory extinction. In the crab context-signal memory, the activation of NF-κB plays a critical role in consolidation and reconsolidation, memory processes that are well characterized in this model. The administration of a NF-κB inhibitor, sulfasalazine prior to extinction session impeded spontaneous recovery. Moreover, reinstatement experiments showed that the original memory was not affected and that NF-κB inhibition by sulfasalazine impaired spontaneous recovery strengthening the ongoing memory extinction process. Interestingly, in animals with fully consolidated memory, a brief re-exposure to the training context induced neuronal NF-κB activation and reconsolidation, while prolonged re-exposure induced NF-κB inhibition and memory extinction. These data constitutes a novel insight into the molecular mechanisms involved in the switch between memory reconsolidation and extinction. Moreover, we propose the inhibition of NF-κB as the engaged mechanism underlying extinction, supporting a novel approach for the pharmacological enhancement of this memory process. The accurate description of the molecular mechanisms that support memory extinction is potentially useful for developing new strategies and drug candidates for therapeutic treatments of the maladaptive memory disorders such as post-traumatic stress, phobias, and drug addiction. © 2008 Merlo, Romano.
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.
Fuente
PLoS ONE 2008;3(11)
Materia
immunoglobulin enhancer binding protein
salazosulfapyridine
immunoglobulin enhancer binding protein
article
brain function
controlled study
gene expression
memory consolidation
memory disorder
molecular mechanics
nonhuman
pharmacological blocking
transcription initiation
working memory
animal
Brachyura
drug antagonism
long term memory
male
memory
metabolism
physiology
reinforcement
Animalia
Decapoda (Crustacea)
Animals
Brachyura
Extinction, Psychological
Male
Memory
NF-kappa B
Retention (Psychology)
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/2.5/ar
Repositorio
Biblioteca Digital (UBA-FCEN)
Institución
Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
OAI Identificador
paperaa:paper_19326203_v3_n11_p_Merlo

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oai_identifier_str paperaa:paper_19326203_v3_n11_p_Merlo
network_acronym_str BDUBAFCEN
repository_id_str 1896
network_name_str Biblioteca Digital (UBA-FCEN)
spelling Memory extinction entails the inhibition of the transcription factor NF-κBMerlo, E.Romano, A.immunoglobulin enhancer binding proteinsalazosulfapyridineimmunoglobulin enhancer binding proteinarticlebrain functioncontrolled studygene expressionmemory consolidationmemory disordermolecular mechanicsnonhumanpharmacological blockingtranscription initiationworking memoryanimalBrachyuradrug antagonismlong term memorymalememorymetabolismphysiologyreinforcementAnimaliaDecapoda (Crustacea)AnimalsBrachyuraExtinction, PsychologicalMaleMemoryNF-kappa BRetention (Psychology)In contextual memories, an association between a positive or negative reinforcement and the contextual cues where the reinforcement occurs is formed. The re-exposure to the context without reinforcement can lead to memory extinction or reconsolidation, depending on the number of events or duration of a single event of context re-exposure. Extinction involves the temporary waning of the previously acquired conditioned response. The molecular processes underlying extinction and the mechanisms which determine if memory will reconsolidate or extinguish after retrieval are not well characterized, particularly the role of transcription factors and gene expression. Here we studied the participation of a transcription factor, NF-κB, in memory extinction. In the crab context-signal memory, the activation of NF-κB plays a critical role in consolidation and reconsolidation, memory processes that are well characterized in this model. The administration of a NF-κB inhibitor, sulfasalazine prior to extinction session impeded spontaneous recovery. Moreover, reinstatement experiments showed that the original memory was not affected and that NF-κB inhibition by sulfasalazine impaired spontaneous recovery strengthening the ongoing memory extinction process. Interestingly, in animals with fully consolidated memory, a brief re-exposure to the training context induced neuronal NF-κB activation and reconsolidation, while prolonged re-exposure induced NF-κB inhibition and memory extinction. These data constitutes a novel insight into the molecular mechanisms involved in the switch between memory reconsolidation and extinction. Moreover, we propose the inhibition of NF-κB as the engaged mechanism underlying extinction, supporting a novel approach for the pharmacological enhancement of this memory process. The accurate description of the molecular mechanisms that support memory extinction is potentially useful for developing new strategies and drug candidates for therapeutic treatments of the maladaptive memory disorders such as post-traumatic stress, phobias, and drug addiction. © 2008 Merlo, Romano.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.2008info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttp://hdl.handle.net/20.500.12110/paper_19326203_v3_n11_p_MerloPLoS ONE 2008;3(11)reponame:Biblioteca Digital (UBA-FCEN)instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesinstacron:UBA-FCENenginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/2.5/ar2025-10-23T11:18:31Zpaperaa:paper_19326203_v3_n11_p_MerloInstitucionalhttps://digital.bl.fcen.uba.ar/Universidad públicaNo correspondehttps://digital.bl.fcen.uba.ar/cgi-bin/oaiserver.cgiana@bl.fcen.uba.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:18962025-10-23 11:18:32.934Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesfalse
dc.title.none.fl_str_mv Memory extinction entails the inhibition of the transcription factor NF-κB
title Memory extinction entails the inhibition of the transcription factor NF-κB
spellingShingle Memory extinction entails the inhibition of the transcription factor NF-κB
Merlo, E.
immunoglobulin enhancer binding protein
salazosulfapyridine
immunoglobulin enhancer binding protein
article
brain function
controlled study
gene expression
memory consolidation
memory disorder
molecular mechanics
nonhuman
pharmacological blocking
transcription initiation
working memory
animal
Brachyura
drug antagonism
long term memory
male
memory
metabolism
physiology
reinforcement
Animalia
Decapoda (Crustacea)
Animals
Brachyura
Extinction, Psychological
Male
Memory
NF-kappa B
Retention (Psychology)
title_short Memory extinction entails the inhibition of the transcription factor NF-κB
title_full Memory extinction entails the inhibition of the transcription factor NF-κB
title_fullStr Memory extinction entails the inhibition of the transcription factor NF-κB
title_full_unstemmed Memory extinction entails the inhibition of the transcription factor NF-κB
title_sort Memory extinction entails the inhibition of the transcription factor NF-κB
dc.creator.none.fl_str_mv Merlo, E.
Romano, A.
author Merlo, E.
author_facet Merlo, E.
Romano, A.
author_role author
author2 Romano, A.
author2_role author
dc.subject.none.fl_str_mv immunoglobulin enhancer binding protein
salazosulfapyridine
immunoglobulin enhancer binding protein
article
brain function
controlled study
gene expression
memory consolidation
memory disorder
molecular mechanics
nonhuman
pharmacological blocking
transcription initiation
working memory
animal
Brachyura
drug antagonism
long term memory
male
memory
metabolism
physiology
reinforcement
Animalia
Decapoda (Crustacea)
Animals
Brachyura
Extinction, Psychological
Male
Memory
NF-kappa B
Retention (Psychology)
topic immunoglobulin enhancer binding protein
salazosulfapyridine
immunoglobulin enhancer binding protein
article
brain function
controlled study
gene expression
memory consolidation
memory disorder
molecular mechanics
nonhuman
pharmacological blocking
transcription initiation
working memory
animal
Brachyura
drug antagonism
long term memory
male
memory
metabolism
physiology
reinforcement
Animalia
Decapoda (Crustacea)
Animals
Brachyura
Extinction, Psychological
Male
Memory
NF-kappa B
Retention (Psychology)
dc.description.none.fl_txt_mv In contextual memories, an association between a positive or negative reinforcement and the contextual cues where the reinforcement occurs is formed. The re-exposure to the context without reinforcement can lead to memory extinction or reconsolidation, depending on the number of events or duration of a single event of context re-exposure. Extinction involves the temporary waning of the previously acquired conditioned response. The molecular processes underlying extinction and the mechanisms which determine if memory will reconsolidate or extinguish after retrieval are not well characterized, particularly the role of transcription factors and gene expression. Here we studied the participation of a transcription factor, NF-κB, in memory extinction. In the crab context-signal memory, the activation of NF-κB plays a critical role in consolidation and reconsolidation, memory processes that are well characterized in this model. The administration of a NF-κB inhibitor, sulfasalazine prior to extinction session impeded spontaneous recovery. Moreover, reinstatement experiments showed that the original memory was not affected and that NF-κB inhibition by sulfasalazine impaired spontaneous recovery strengthening the ongoing memory extinction process. Interestingly, in animals with fully consolidated memory, a brief re-exposure to the training context induced neuronal NF-κB activation and reconsolidation, while prolonged re-exposure induced NF-κB inhibition and memory extinction. These data constitutes a novel insight into the molecular mechanisms involved in the switch between memory reconsolidation and extinction. Moreover, we propose the inhibition of NF-κB as the engaged mechanism underlying extinction, supporting a novel approach for the pharmacological enhancement of this memory process. The accurate description of the molecular mechanisms that support memory extinction is potentially useful for developing new strategies and drug candidates for therapeutic treatments of the maladaptive memory disorders such as post-traumatic stress, phobias, and drug addiction. © 2008 Merlo, Romano.
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.
description In contextual memories, an association between a positive or negative reinforcement and the contextual cues where the reinforcement occurs is formed. The re-exposure to the context without reinforcement can lead to memory extinction or reconsolidation, depending on the number of events or duration of a single event of context re-exposure. Extinction involves the temporary waning of the previously acquired conditioned response. The molecular processes underlying extinction and the mechanisms which determine if memory will reconsolidate or extinguish after retrieval are not well characterized, particularly the role of transcription factors and gene expression. Here we studied the participation of a transcription factor, NF-κB, in memory extinction. In the crab context-signal memory, the activation of NF-κB plays a critical role in consolidation and reconsolidation, memory processes that are well characterized in this model. The administration of a NF-κB inhibitor, sulfasalazine prior to extinction session impeded spontaneous recovery. Moreover, reinstatement experiments showed that the original memory was not affected and that NF-κB inhibition by sulfasalazine impaired spontaneous recovery strengthening the ongoing memory extinction process. Interestingly, in animals with fully consolidated memory, a brief re-exposure to the training context induced neuronal NF-κB activation and reconsolidation, while prolonged re-exposure induced NF-κB inhibition and memory extinction. These data constitutes a novel insight into the molecular mechanisms involved in the switch between memory reconsolidation and extinction. Moreover, we propose the inhibition of NF-κB as the engaged mechanism underlying extinction, supporting a novel approach for the pharmacological enhancement of this memory process. The accurate description of the molecular mechanisms that support memory extinction is potentially useful for developing new strategies and drug candidates for therapeutic treatments of the maladaptive memory disorders such as post-traumatic stress, phobias, and drug addiction. © 2008 Merlo, Romano.
publishDate 2008
dc.date.none.fl_str_mv 2008
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/20.500.12110/paper_19326203_v3_n11_p_Merlo
url http://hdl.handle.net/20.500.12110/paper_19326203_v3_n11_p_Merlo
dc.language.none.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/2.5/ar
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/2.5/ar
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv PLoS ONE 2008;3(11)
reponame:Biblioteca Digital (UBA-FCEN)
instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron:UBA-FCEN
reponame_str Biblioteca Digital (UBA-FCEN)
collection Biblioteca Digital (UBA-FCEN)
instname_str Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
instacron_str UBA-FCEN
institution UBA-FCEN
repository.name.fl_str_mv Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
repository.mail.fl_str_mv ana@bl.fcen.uba.ar
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