http://purl.uniprot.org/citations/35513229 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/35513229 | http://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/35513229 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.nbd.2022.105745"xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Li Y."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Yang Y."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Zhong H."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Zhou R."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Liang M."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/author | "Rong J."xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/name | "Neurobiol Dis"xsd:string |
http://purl.uniprot.org/citations/35513229 | http://purl.uniprot.org/core/pages | "105745"xsd:string |
http://purl.uniprot.org/citations/35513229 | http://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/35513229 | http://purl.uniprot.org/core/volume | "169"xsd:string |
http://purl.uniprot.org/citations/35513229 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/35513229 |
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