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http://purl.uniprot.org/citations/35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35513229http://www.w3.org/2000/01/rdf-schema#comment"Neonatal inflammation can increase the risk of anxiety disorder in adulthood. The balance between glutamatergic excitatory and GABAergic inhibitory transmissions in the basolateral amygdala (BLA) plays a vital role in controlling anxiety state. Based on the reports that early-life inflammation had adverse effects on GABAergic system, the aim of this study was to investigate whether and how neonatal inflammation affects excitatory-inhibitory circuits in the BLA resulting in anxiety disorder. Neonatal mice received a daily subcutaneous injection of lipopolysaccharide (LPS, 50 μg/kg) or saline on postnatal days 3-5. LPS-treated mice developed anxiety behaviors accompanied by the hyperactivity of adrenal axis in adulthood. Electrophysiological study revealed the increase of postsynaptic neuronal excitability in the cortical-BLA excitatory synapses of LPS mice which could be recovered by bath-application of GABAAR agonist suggesting the impairment of GABAergic system in LPS mice. Compared with controls, GABAARα2 subunit expression and density of GABA-evoked current in BLA principal neurons were reduced in LPS mice. Additionally, neonatal LPS treatment resulted in the down-regulation of transforming growth factor-beta 1 (TGF-β1) expression and PKC signaling pathway in the adult BLA. The local TGF-β1 overexpression in the BLA improved GABAARα2 expression via up-regulating the activity of PKC signaling, which corrected GABAAR-mediated inhibition leading to the abolishment of anxiety-like change in adrenal axis regulation and behaviors in LPS mice. These data suggest the persistent TGF-β1deficit induces the down-regulation of GABAARα2 expression and subsequent disruption of the excitation-inhibition balance in the BLA circuits, which is the important mechanisms of neonatal inflammation-induced anxiety disorder."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.org/dc/terms/identifier"doi:10.1016/j.nbd.2022.105745"xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Yang Y."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Zhong H."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Zhou R."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Liang M."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/author"Rong J."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/name"Neurobiol Dis"xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/pages"105745"xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/title"Neonatal inflammation via persistent TGF-beta1 downregulation decreases GABApisub>Api/sub>R expression in basolateral amygdala leading to the imbalance of the local excitation-inhibition circuits and anxiety-like phenotype in adult mice."xsd:string
http://purl.uniprot.org/citations/35513229http://purl.uniprot.org/core/volume"169"xsd:string
http://purl.uniprot.org/citations/35513229http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/35513229
http://purl.uniprot.org/citations/35513229http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/35513229
http://purl.uniprot.org/uniprot/#_P04202-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/#_P22723-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/#_Q3UNK5-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/#_Q3UVW2-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/#_Q8C7N0-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/#_Q8C8H5-mappedCitation-35513229http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/P22723http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/Q8C7N0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35513229
http://purl.uniprot.org/uniprot/Q8C8H5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/35513229