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Article: Corticosterone-mediated microglia activation affects dendritic spine plasticity and motor learning functions in minimal hepatic encephalopathy

TitleCorticosterone-mediated microglia activation affects dendritic spine plasticity and motor learning functions in minimal hepatic encephalopathy
Authors
KeywordsMinimal hepatic encephalopathy
Dendritic spine
Motor learning
Microglia
Glucocorticoid hormone
Issue Date2019
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybrbi
Citation
Brain, Behavior, and Immunity, 2019, v. 82, p. 178-187 How to Cite?
AbstractMinimal hepatic encephalopathy (MHE) is characterized as cognitive deficits including memory and learning dysfunctions after liver injuries or hepatic diseases. Our understandings of neurological mechanisms of MHE-associated cognitive syndromes, however, are far from complete. In the current study we generated a mouse MHE model by repetitive administrations of thioacetamide (TAA), which induced hyperammonemia plus elevated proinflammatory cytokines in both the general circulation and motor cortex. MHE mice presented prominent motor learning deficits, which were associated with excess dendritic spine pruning in the motor cortex under 2-photon in vivo microscopy. The pharmaceutical blockade of glucocorticoid receptor or suppression of its biosynthesis further rescued motor learning deficits and synaptic protein loss. Moreover, MHE mice presented microglial activation, which can be alleviated after glucocorticoid pathway inhibition. In sum, our data demonstrates corticosterone-induced microglial activation, synaptic over-pruning and motor learning impairments in MHE, providing new insights for MHE pathogenesis and potential targets of clinical interventions.
Persistent Identifierhttp://hdl.handle.net/10722/288408
ISSN
2019 Impact Factor: 6.633
2015 SCImago Journal Rankings: 2.884

 

DC FieldValueLanguage
dc.contributor.authorSun, X-
dc.contributor.authorHan, R-
dc.contributor.authorCheng, T-
dc.contributor.authorZheng, Y-
dc.contributor.authorXiao, J-
dc.contributor.authorSo, KF-
dc.contributor.authorZhang, L-
dc.date.accessioned2020-10-05T12:12:27Z-
dc.date.available2020-10-05T12:12:27Z-
dc.date.issued2019-
dc.identifier.citationBrain, Behavior, and Immunity, 2019, v. 82, p. 178-187-
dc.identifier.issn0889-1591-
dc.identifier.urihttp://hdl.handle.net/10722/288408-
dc.description.abstractMinimal hepatic encephalopathy (MHE) is characterized as cognitive deficits including memory and learning dysfunctions after liver injuries or hepatic diseases. Our understandings of neurological mechanisms of MHE-associated cognitive syndromes, however, are far from complete. In the current study we generated a mouse MHE model by repetitive administrations of thioacetamide (TAA), which induced hyperammonemia plus elevated proinflammatory cytokines in both the general circulation and motor cortex. MHE mice presented prominent motor learning deficits, which were associated with excess dendritic spine pruning in the motor cortex under 2-photon in vivo microscopy. The pharmaceutical blockade of glucocorticoid receptor or suppression of its biosynthesis further rescued motor learning deficits and synaptic protein loss. Moreover, MHE mice presented microglial activation, which can be alleviated after glucocorticoid pathway inhibition. In sum, our data demonstrates corticosterone-induced microglial activation, synaptic over-pruning and motor learning impairments in MHE, providing new insights for MHE pathogenesis and potential targets of clinical interventions.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybrbi-
dc.relation.ispartofBrain, Behavior, and Immunity-
dc.subjectMinimal hepatic encephalopathy-
dc.subjectDendritic spine-
dc.subjectMotor learning-
dc.subjectMicroglia-
dc.subjectGlucocorticoid hormone-
dc.titleCorticosterone-mediated microglia activation affects dendritic spine plasticity and motor learning functions in minimal hepatic encephalopathy-
dc.typeArticle-
dc.identifier.emailXiao, J: jiaxiao@hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.bbi.2019.08.184-
dc.identifier.pmid31437533-
dc.identifier.scopuseid_2-s2.0-85071083575-
dc.identifier.hkuros315765-
dc.identifier.volume82-
dc.identifier.spage178-
dc.identifier.epage187-
dc.publisher.placeUnited States-

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