Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation

Background: Parkinson’s disease is an irreversible neurodegenerative disease linked to progressive movement disorders and is accompanied by an inflammatory reaction that is believed to contribute to its pathogenesis. Since sensitivity to inflammation is not the same in all brain structures, the aim...

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Autores: Martínez de Pablos, Rocío, Herrera Carmona, Antonio José, Espinosa Oliva, Ana María, Sarmiento Soto, Manuel, Muñoz Pinto, Mario Faustino, Machado Quintana, Alberto, Venero Recio, José Luis
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2014
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/41594
Acceso en línea:http://hdl.handle.net/11441/41594
https://doi.org/10.1186/1742-2094-11-34
Access Level:acceso abierto
Palabra clave:Glucocorticoids
Lipopolysaccharide
Microglia
Parkinson’s disease
Stress
Substantia nigra
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spelling Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammationMartínez de Pablos, RocíoHerrera Carmona, Antonio JoséEspinosa Oliva, Ana MaríaSarmiento Soto, ManuelMuñoz Pinto, Mario FaustinoMachado Quintana, AlbertoVenero Recio, José LuisGlucocorticoidsLipopolysaccharideMicrogliaParkinson’s diseaseStressSubstantia nigraBackground: Parkinson’s disease is an irreversible neurodegenerative disease linked to progressive movement disorders and is accompanied by an inflammatory reaction that is believed to contribute to its pathogenesis. Since sensitivity to inflammation is not the same in all brain structures, the aim of this work was to test whether physiological conditions as stress could enhance susceptibility to inflammation in the substantia nigra, where death of dopaminergic neurons takes place in Parkinson’s disease. Methods: To achieve our aim, we induced an inflammatory process in nonstressed and stressed rats (subject to a chronic variate stress) by a single intranigral injection of lipopolysaccharide, a potent proinflammogen. The effect of this treatment was evaluated on inflammatory markers as well as on neuronal and glial populations. Results: Data showed a synergistic effect between inflammation and stress, thus resulting in higher microglial activation and expression of proinflammatory markers. More important, the higher inflammatory response seen in stressed animals was associated with a higher rate of death of dopaminergic neurons in the substantia nigra, the most characteristic feature seen in Parkinson’s disease. This effect was dependent on glucocorticoids. Conclusions: Our data demonstrate that stress sensitises midbrain microglia to further inflammatory stimulus. This suggests that stress may be an important risk factor in the degenerative processes and symptoms of Parkinson’s diseaseBioMed CentralBioquímica y Biología Molecular2014info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/11441/41594https://doi.org/10.1186/1742-2094-11-34reponame:idUS. Depósito de Investigación de la Universidad de Sevillainstname:Universidad de Sevilla (US)InglésJournal of Neuroinflammation, 11, 1-18.10.1186/1742-2094-11-34info:eu-repo/semantics/openAccessoai:idus.us.es:11441/415942026-06-17T12:51:07Z
dc.title.none.fl_str_mv Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
title Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
spellingShingle Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
Martínez de Pablos, Rocío
Glucocorticoids
Lipopolysaccharide
Microglia
Parkinson’s disease
Stress
Substantia nigra
title_short Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
title_full Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
title_fullStr Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
title_full_unstemmed Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
title_sort Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation
dc.creator.none.fl_str_mv Martínez de Pablos, Rocío
Herrera Carmona, Antonio José
Espinosa Oliva, Ana María
Sarmiento Soto, Manuel
Muñoz Pinto, Mario Faustino
Machado Quintana, Alberto
Venero Recio, José Luis
author Martínez de Pablos, Rocío
author_facet Martínez de Pablos, Rocío
Herrera Carmona, Antonio José
Espinosa Oliva, Ana María
Sarmiento Soto, Manuel
Muñoz Pinto, Mario Faustino
Machado Quintana, Alberto
Venero Recio, José Luis
author_role author
author2 Herrera Carmona, Antonio José
Espinosa Oliva, Ana María
Sarmiento Soto, Manuel
Muñoz Pinto, Mario Faustino
Machado Quintana, Alberto
Venero Recio, José Luis
author2_role author
author
author
author
author
author
dc.contributor.none.fl_str_mv Bioquímica y Biología Molecular
dc.subject.none.fl_str_mv Glucocorticoids
Lipopolysaccharide
Microglia
Parkinson’s disease
Stress
Substantia nigra
topic Glucocorticoids
Lipopolysaccharide
Microglia
Parkinson’s disease
Stress
Substantia nigra
description Background: Parkinson’s disease is an irreversible neurodegenerative disease linked to progressive movement disorders and is accompanied by an inflammatory reaction that is believed to contribute to its pathogenesis. Since sensitivity to inflammation is not the same in all brain structures, the aim of this work was to test whether physiological conditions as stress could enhance susceptibility to inflammation in the substantia nigra, where death of dopaminergic neurons takes place in Parkinson’s disease. Methods: To achieve our aim, we induced an inflammatory process in nonstressed and stressed rats (subject to a chronic variate stress) by a single intranigral injection of lipopolysaccharide, a potent proinflammogen. The effect of this treatment was evaluated on inflammatory markers as well as on neuronal and glial populations. Results: Data showed a synergistic effect between inflammation and stress, thus resulting in higher microglial activation and expression of proinflammatory markers. More important, the higher inflammatory response seen in stressed animals was associated with a higher rate of death of dopaminergic neurons in the substantia nigra, the most characteristic feature seen in Parkinson’s disease. This effect was dependent on glucocorticoids. Conclusions: Our data demonstrate that stress sensitises midbrain microglia to further inflammatory stimulus. This suggests that stress may be an important risk factor in the degenerative processes and symptoms of Parkinson’s disease
publishDate 2014
dc.date.none.fl_str_mv 2014
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 http://hdl.handle.net/11441/41594
https://doi.org/10.1186/1742-2094-11-34
url http://hdl.handle.net/11441/41594
https://doi.org/10.1186/1742-2094-11-34
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Journal of Neuroinflammation, 11, 1-18.
10.1186/1742-2094-11-34
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv BioMed Central
publisher.none.fl_str_mv BioMed Central
dc.source.none.fl_str_mv reponame:idUS. Depósito de Investigación de la Universidad de Sevilla
instname:Universidad de Sevilla (US)
instname_str Universidad de Sevilla (US)
reponame_str idUS. Depósito de Investigación de la Universidad de Sevilla
collection idUS. Depósito de Investigación de la Universidad de Sevilla
repository.name.fl_str_mv
repository.mail.fl_str_mv
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