HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons

Autores
Calfa, Gaston Diego; Chapleau, Christopher A.; Campbell, Susan; Inoue, Takafumi; Morse, Sarah J.; Lubin, Farah D.; Pozzo-Miller, Lucas
Año de publicación
2012
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Molecular mechanisms involved in the strengthening and formation of synapses include the activation and repression of specific genes or subsets of genes by epigenetic modifications that do not alter the genetic code itself. Chromatin modifications mediated by histone acetylation have been shown to be critical for synaptic plasticity at hippocampal excitatory synapses and hippocampal-dependent memory formation. Considering that brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity and behavioral adaptations, it is not surprising that regulation of this gene is subject to histone acetylation changes during synaptic plasticity and hippocampal-dependent memory formation. Whether the effects of BDNF on dendritic spines and quantal transmitter release require histone modifications remains less known. By using two different inhibitors of histone deacetylases (HDACs), we describe here that their activity is required for BDNF to increase dendritic spine density and excitatory quantal transmitter release onto CA1 pyramidal neurons in hippocampal slice cultures. These results suggest that histone acetylation/deacetylation is a critical step in the modulation of hippocampal synapses by BDNF. Thus, mechanisms ofepigenetic modulation of synapse formation and function are novel targets to consider for the amelioration of symptoms of intellectual disabilities and neurodegenerative disorders associated with cognitive and memory deficits. © 2011 Wiley Periodicals, Inc.
Fil: Calfa, Gaston Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Chapleau, Christopher A.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Campbell, Susan. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
Fil: Inoue, Takafumi. Waseda University. Faculty of Science and Engineering. Department of Life Science and Medical Bioscience; Japón
Fil: Morse, Sarah J.. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
Fil: Lubin, Farah D.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Pozzo-Miller, Lucas. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
Materia
BDNF
DENDRITIC SPINES
EPIGENETICS
HIPPOCAMPAL SLICE CULTURES
HISTONE DEACETYLASE
QUANTAL RELEASE
SAHA
TSA
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:11336/198382
Acceder
id CONICETDig_85a1541c21523064ebd64c2b3800e274
oai_identifier_str oai:ri.conicet.gov.ar:11336/198382
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neuronsCalfa, Gaston DiegoChapleau, Christopher A.Campbell, SusanInoue, TakafumiMorse, Sarah J.Lubin, Farah D.Pozzo-Miller, LucasBDNFDENDRITIC SPINESEPIGENETICSHIPPOCAMPAL SLICE CULTURESHISTONE DEACETYLASEQUANTAL RELEASESAHATSAhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Molecular mechanisms involved in the strengthening and formation of synapses include the activation and repression of specific genes or subsets of genes by epigenetic modifications that do not alter the genetic code itself. Chromatin modifications mediated by histone acetylation have been shown to be critical for synaptic plasticity at hippocampal excitatory synapses and hippocampal-dependent memory formation. Considering that brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity and behavioral adaptations, it is not surprising that regulation of this gene is subject to histone acetylation changes during synaptic plasticity and hippocampal-dependent memory formation. Whether the effects of BDNF on dendritic spines and quantal transmitter release require histone modifications remains less known. By using two different inhibitors of histone deacetylases (HDACs), we describe here that their activity is required for BDNF to increase dendritic spine density and excitatory quantal transmitter release onto CA1 pyramidal neurons in hippocampal slice cultures. These results suggest that histone acetylation/deacetylation is a critical step in the modulation of hippocampal synapses by BDNF. Thus, mechanisms ofepigenetic modulation of synapse formation and function are novel targets to consider for the amelioration of symptoms of intellectual disabilities and neurodegenerative disorders associated with cognitive and memory deficits. © 2011 Wiley Periodicals, Inc.Fil: Calfa, Gaston Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados UnidosFil: Chapleau, Christopher A.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados UnidosFil: Campbell, Susan. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados UnidosFil: Inoue, Takafumi. Waseda University. Faculty of Science and Engineering. Department of Life Science and Medical Bioscience; JapónFil: Morse, Sarah J.. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados UnidosFil: Lubin, Farah D.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados UnidosFil: Pozzo-Miller, Lucas. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados UnidosWiley-liss, div John Wiley & Sons Inc.2012-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/198382Calfa, Gaston Diego; Chapleau, Christopher A.; Campbell, Susan; Inoue, Takafumi; Morse, Sarah J.; et al.; HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons; Wiley-liss, div John Wiley & Sons Inc.; Hippocampus; 22; 7; 7-2012; 1493-15001050-96311098-1063CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/hipo.20990info:eu-repo/semantics/altIdentifier/url/https://pubmed.ncbi.nlm.nih.gov/22161912/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-17T11:23:08Zoai:ri.conicet.gov.ar:11336/198382instacron: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:34982025-09-17 11:23:09.252CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
title HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
spellingShingle HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
Calfa, Gaston Diego
BDNF
DENDRITIC SPINES
EPIGENETICS
HIPPOCAMPAL SLICE CULTURES
HISTONE DEACETYLASE
QUANTAL RELEASE
SAHA
TSA
title_short HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
title_full HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
title_fullStr HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
title_full_unstemmed HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
title_sort HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons
dc.creator.none.fl_str_mv Calfa, Gaston Diego
Chapleau, Christopher A.
Campbell, Susan
Inoue, Takafumi
Morse, Sarah J.
Lubin, Farah D.
Pozzo-Miller, Lucas
author Calfa, Gaston Diego
author_facet Calfa, Gaston Diego
Chapleau, Christopher A.
Campbell, Susan
Inoue, Takafumi
Morse, Sarah J.
Lubin, Farah D.
Pozzo-Miller, Lucas
author_role author
author2 Chapleau, Christopher A.
Campbell, Susan
Inoue, Takafumi
Morse, Sarah J.
Lubin, Farah D.
Pozzo-Miller, Lucas
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv BDNF
DENDRITIC SPINES
EPIGENETICS
HIPPOCAMPAL SLICE CULTURES
HISTONE DEACETYLASE
QUANTAL RELEASE
SAHA
TSA
topic BDNF
DENDRITIC SPINES
EPIGENETICS
HIPPOCAMPAL SLICE CULTURES
HISTONE DEACETYLASE
QUANTAL RELEASE
SAHA
TSA
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Molecular mechanisms involved in the strengthening and formation of synapses include the activation and repression of specific genes or subsets of genes by epigenetic modifications that do not alter the genetic code itself. Chromatin modifications mediated by histone acetylation have been shown to be critical for synaptic plasticity at hippocampal excitatory synapses and hippocampal-dependent memory formation. Considering that brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity and behavioral adaptations, it is not surprising that regulation of this gene is subject to histone acetylation changes during synaptic plasticity and hippocampal-dependent memory formation. Whether the effects of BDNF on dendritic spines and quantal transmitter release require histone modifications remains less known. By using two different inhibitors of histone deacetylases (HDACs), we describe here that their activity is required for BDNF to increase dendritic spine density and excitatory quantal transmitter release onto CA1 pyramidal neurons in hippocampal slice cultures. These results suggest that histone acetylation/deacetylation is a critical step in the modulation of hippocampal synapses by BDNF. Thus, mechanisms ofepigenetic modulation of synapse formation and function are novel targets to consider for the amelioration of symptoms of intellectual disabilities and neurodegenerative disorders associated with cognitive and memory deficits. © 2011 Wiley Periodicals, Inc.
Fil: Calfa, Gaston Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Farmacología Experimental de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Instituto de Farmacología Experimental de Córdoba; Argentina. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Chapleau, Christopher A.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Campbell, Susan. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
Fil: Inoue, Takafumi. Waseda University. Faculty of Science and Engineering. Department of Life Science and Medical Bioscience; Japón
Fil: Morse, Sarah J.. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
Fil: Lubin, Farah D.. University of Alabama at Birmingahm; Estados Unidos. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos
Fil: Pozzo-Miller, Lucas. The University of Alabama at Birmingham. Civitan International Research Center. Department of Neurobiology; Estados Unidos. University of Alabama at Birmingahm; Estados Unidos
description Molecular mechanisms involved in the strengthening and formation of synapses include the activation and repression of specific genes or subsets of genes by epigenetic modifications that do not alter the genetic code itself. Chromatin modifications mediated by histone acetylation have been shown to be critical for synaptic plasticity at hippocampal excitatory synapses and hippocampal-dependent memory formation. Considering that brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity and behavioral adaptations, it is not surprising that regulation of this gene is subject to histone acetylation changes during synaptic plasticity and hippocampal-dependent memory formation. Whether the effects of BDNF on dendritic spines and quantal transmitter release require histone modifications remains less known. By using two different inhibitors of histone deacetylases (HDACs), we describe here that their activity is required for BDNF to increase dendritic spine density and excitatory quantal transmitter release onto CA1 pyramidal neurons in hippocampal slice cultures. These results suggest that histone acetylation/deacetylation is a critical step in the modulation of hippocampal synapses by BDNF. Thus, mechanisms ofepigenetic modulation of synapse formation and function are novel targets to consider for the amelioration of symptoms of intellectual disabilities and neurodegenerative disorders associated with cognitive and memory deficits. © 2011 Wiley Periodicals, Inc.
publishDate 2012
dc.date.none.fl_str_mv 2012-07
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/11336/198382
Calfa, Gaston Diego; Chapleau, Christopher A.; Campbell, Susan; Inoue, Takafumi; Morse, Sarah J.; et al.; HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons; Wiley-liss, div John Wiley & Sons Inc.; Hippocampus; 22; 7; 7-2012; 1493-1500
1050-9631
1098-1063
CONICET Digital
CONICET
url http://hdl.handle.net/11336/198382
identifier_str_mv Calfa, Gaston Diego; Chapleau, Christopher A.; Campbell, Susan; Inoue, Takafumi; Morse, Sarah J.; et al.; HDAC activity is required for BDNF to increase quantal neurotransmitter release and dendritic spine density in CA1 pyramidal neurons; Wiley-liss, div John Wiley & Sons Inc.; Hippocampus; 22; 7; 7-2012; 1493-1500
1050-9631
1098-1063
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1002/hipo.20990
info:eu-repo/semantics/altIdentifier/url/https://pubmed.ncbi.nlm.nih.gov/22161912/
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
dc.publisher.none.fl_str_mv Wiley-liss, div John Wiley & Sons Inc.
publisher.none.fl_str_mv Wiley-liss, div John Wiley & Sons Inc.
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
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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score 13.001348

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