Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques

One of the main pathological hallmarks of Alzheimer's disease (AD) is the accumulation of plaques in the cerebral cortex, which may appear either in the neuropil or in direct association with neuronal somata. Since different axonal systems innervate the dendritic (mostly glutamatergic) and peri...

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Autores: Garcia Marin, Virginia, Blazquez Llorca, Lidia, Rodriguez, José Rodrigo, Boluda Casas, Susana, Muntané Medina, Gerard, Ferrer, Isidro (Ferrer Abizanda), DeFelipe, Javier
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2009
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:2445/126816
Acceso en línea:https://hdl.handle.net/2445/126816
Access Level:acceso abierto
Palabra clave:Malaltia d'Alzheimer
Epilèpsia
Alzheimer's disease
Epilepsy
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spelling Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaquesGarcia Marin, VirginiaBlazquez Llorca, LidiaRodriguez, José RodrigoBoluda Casas, SusanaMuntané Medina, GerardFerrer, Isidro (Ferrer Abizanda)DeFelipe, JavierMalaltia d'AlzheimerEpilèpsiaAlzheimer's diseaseEpilepsyOne of the main pathological hallmarks of Alzheimer's disease (AD) is the accumulation of plaques in the cerebral cortex, which may appear either in the neuropil or in direct association with neuronal somata. Since different axonal systems innervate the dendritic (mostly glutamatergic) and perisomatic (mostly GABAergic) regions of neurons, the accumulation of plaques in the neuropil or associated with the soma might produce different alterations to synaptic circuits. We have used a variety of conventional light, confocal and electron microscopy techniques to study their relationship with neuronal somata in the cerebral cortex from AD patients and APP/PS1 transgenic mice. The main finding was that the membrane surfaces of neurons (mainly pyramidal cells) in contact with plaques lack GABAergic perisomatic synapses. Since these perisomatic synapses are thought to exert a strong influence on the output of pyramidal cells, their loss may lead to the hyperactivity of the neurons in contact with plaques. These results suggest that plaques modify circuits in a more selective manner than previously thought.Frontiers Media2018201820092018info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersion18 p.application/pdfapplication/pdfhttps://hdl.handle.net/2445/126816Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésReproducció del document publicat a: https://doi.org/10.3389/neuro.05.028.2009Frontiers in Neuroanatomy, 2009, vol. 3https://doi.org/10.3389/neuro.05.028.2009cc by (c) Garcia Marin et al., 2009http://creativecommons.org/licenses/by/3.0/es/info:eu-repo/semantics/openAccessoai:recercat.cat:2445/1268162026-05-29T05:05:01Z
dc.title.none.fl_str_mv Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
title Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
spellingShingle Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
Garcia Marin, Virginia
Malaltia d'Alzheimer
Epilèpsia
Alzheimer's disease
Epilepsy
title_short Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
title_full Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
title_fullStr Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
title_full_unstemmed Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
title_sort Diminished perisomatic GABAergic terminals on cortical neurons adjacent to amyloid plaques
dc.creator.none.fl_str_mv Garcia Marin, Virginia
Blazquez Llorca, Lidia
Rodriguez, José Rodrigo
Boluda Casas, Susana
Muntané Medina, Gerard
Ferrer, Isidro (Ferrer Abizanda)
DeFelipe, Javier
author Garcia Marin, Virginia
author_facet Garcia Marin, Virginia
Blazquez Llorca, Lidia
Rodriguez, José Rodrigo
Boluda Casas, Susana
Muntané Medina, Gerard
Ferrer, Isidro (Ferrer Abizanda)
DeFelipe, Javier
author_role author
author2 Blazquez Llorca, Lidia
Rodriguez, José Rodrigo
Boluda Casas, Susana
Muntané Medina, Gerard
Ferrer, Isidro (Ferrer Abizanda)
DeFelipe, Javier
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Malaltia d'Alzheimer
Epilèpsia
Alzheimer's disease
Epilepsy
topic Malaltia d'Alzheimer
Epilèpsia
Alzheimer's disease
Epilepsy
description One of the main pathological hallmarks of Alzheimer's disease (AD) is the accumulation of plaques in the cerebral cortex, which may appear either in the neuropil or in direct association with neuronal somata. Since different axonal systems innervate the dendritic (mostly glutamatergic) and perisomatic (mostly GABAergic) regions of neurons, the accumulation of plaques in the neuropil or associated with the soma might produce different alterations to synaptic circuits. We have used a variety of conventional light, confocal and electron microscopy techniques to study their relationship with neuronal somata in the cerebral cortex from AD patients and APP/PS1 transgenic mice. The main finding was that the membrane surfaces of neurons (mainly pyramidal cells) in contact with plaques lack GABAergic perisomatic synapses. Since these perisomatic synapses are thought to exert a strong influence on the output of pyramidal cells, their loss may lead to the hyperactivity of the neurons in contact with plaques. These results suggest that plaques modify circuits in a more selective manner than previously thought.
publishDate 2009
dc.date.none.fl_str_mv 2009
2018
2018
2018
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/126816
url https://hdl.handle.net/2445/126816
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Reproducció del document publicat a: https://doi.org/10.3389/neuro.05.028.2009
Frontiers in Neuroanatomy, 2009, vol. 3
https://doi.org/10.3389/neuro.05.028.2009
dc.rights.none.fl_str_mv cc by (c) Garcia Marin et al., 2009
http://creativecommons.org/licenses/by/3.0/es/
info:eu-repo/semantics/openAccess
rights_invalid_str_mv cc by (c) Garcia Marin et al., 2009
http://creativecommons.org/licenses/by/3.0/es/
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 18 p.
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
dc.source.none.fl_str_mv Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
reponame:Recercat. Dipósit de la Recerca de Catalunya
instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
instname_str Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
reponame_str Recercat. Dipósit de la Recerca de Catalunya
collection Recercat. Dipósit de la Recerca de Catalunya
repository.name.fl_str_mv
repository.mail.fl_str_mv
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