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

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

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Autor: Martínez de Pablos, Rocío
Herrera Carmona, Antonio José
Espinosa Oliva, Ana María
Sarmiento, M.
Muñoz, Mario F.
Machado de la Quintana, Alberto
Venero Recio, José Luis
Departamento: Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular
Fecha: 2014
Publicado en: Journal of Neuroinflammation, 11, 1-18.
Tipo de documento: Artículo
Resumen: 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 proinflamm...
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Cita: Martínez de Pablos, R., Herrera Carmona, A.J., Espinosa Oliva, A.M., Sarmiento, M., Muñoz, M.F., Machado de la Quintana, A. y Venero Recio, J.L. (2014). Chronic stress enhances microglia activation and exacerbates death of nigral dopaminergic neurons under conditions of inflammation. Journal of Neuroinflammation, 11, 1-18.
Tamaño: 2.889Mb
Formato: PDF

URI: http://hdl.handle.net/11441/41594

DOI: http://dx.doi.org/10.1186/1742-2094-11-34

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