Impact of TLR4 on behavioral and cognitive dysfunctions associated with alcohol-induced neuroinflammatory damage
Impacto
Scholar |
Otros documentos de la autoría: Pascual, María; Baliño, Pablo; Alfonso Loeches, Silvia; González Aragón, Carlos Manuel; Guerri, Consuelo
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Mostrar el registro completo del ítemcomunitat-uji-handle:10234/9
comunitat-uji-handle2:10234/8033
comunitat-uji-handle3:10234/8636
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http://dx.doi.org/10.1016/j.bbi.2011.02.012 |
Metadatos
Título
Impact of TLR4 on behavioral and cognitive dysfunctions associated with alcohol-induced neuroinflammatory damageAutoría
Fecha de publicación
2011-06-01Editor
ElsevierISSN
0889-1591; 1090-2139Cita bibliográfica
Brain, Behavior and Immunity (1 June 2011), vol. 25, suppl. 1, S80-S91Tipo de documento
info:eu-repo/semantics/articleVersión de la editorial
http://www.sciencedirect.com/science/article/pii/S0889159111000626Versión
info:eu-repo/semantics/publishedVersionPalabras clave / Materias
Resumen
Toll-like receptors (TLRs) play an important role in the innate immune response, and emerging evidence indicates their role in brain injury and neurodegeneration. Our recent results have demonstrated that ethanol is ... [+]
Toll-like receptors (TLRs) play an important role in the innate immune response, and emerging evidence indicates their role in brain injury and neurodegeneration. Our recent results have demonstrated that ethanol is capable of activating glial TLR4 receptors and that the elimination of these receptors in mice protects against ethanol-induced glial activation, induction of inflammatory mediators and apoptosis. This study was designed to assess whether ethanol-induced inflammatory damage causes behavioral and cognitiveconsequences, and if behavioral alterations are dependent of TLR4 functions. Here we show in mice drinking alcohol for 5 months, followed by a 15-day withdrawal period, that activation of the astroglial and microglial cells in frontal cortex and striatum is maintained and that these events are associated withcognitive and anxiety-related behavioral impairments in wild-type (WT) mice, as demonstrated by testing the animals with object memory recognition, conditioned taste aversion and dark and light box anxiety tasks. Mice lacking TLR4 receptors are protected against ethanol-induced inflammatory damage, andbehavioralassociated effects. We further assess the possibility of the epigenetic modifications participating in short- or long-term behavioral effects associated with neuroinflammatorydamage. We show that chronicalcohol treatment decreases H4 histone acetylation and histone acetyltransferases activity in frontal cortex, striatum and hippocampus of WT mice. Alterations in chromatin structure were not observed in TLR4−/−mice. These results provide the first evidence of the role that TLR4 functions play in the behavioralconsequences of alcohol-induced inflammatory damage and suggest that the epigenetic modifications mediated by TLR4 could contribute to short- or long-term alcohol-inducedbehavioral orcognitivedysfunctions [-]
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© 2011 Elsevier Inc. All rights reserved
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