海马体
内分泌学
内科学
小胶质细胞
突触素
海马结构
促炎细胞因子
脂多糖
NMDA受体
一氧化氮合酶
糖皮质激素受体
化学
受体
生物
一氧化氮
糖皮质激素
医学
炎症
免疫组织化学
作者
Lanfen Lin,Xuan Chen,Qiuping Zhang,Peixian Huang,Shuqi Jiang,Hui‐Fang Wang,Yiyu Deng
标识
DOI:10.1016/j.neulet.2019.134364
摘要
Synaptic structure integrity plays a key role in learning and memory. Previous studies have shown that there is cognitive dysfunction in septic neonates in later life. In this study, intraperitoneal injection of lipopolysaccharide (LPS) in the developing rats was used as a sepsis model to determine whether hippocampal synapses would be affected. Expression of synaptophysin (Syn), synaptosomal associated protein of 25 kD (SNAP-25), and N-methyl d-aspartate receptor (NMDAR) in the hippocampus in septic brain were significantly reduced. Consistent with this, the number of dendritic spines associated with the pyramidal neurons in the CA1 region of hippocampus at 28d after LPS administration was decreased. Additionally, the number of synapse and synaptic vesicles were reduced and appeared swollen. The number of neurons in the CA1 and CA3 of hippocampus at 14, and 28d after LPS injection remained unchanged. Coupled with the above was upregulated expression of interleukin-1β (IL-1β), IL-1 receptor 1 (IL-R1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) at 1-3d after LPS injection. IL-1β expression was specifically detected in activated microglia. The plasma corticosterone (CORT) concentration in the LPS treatment rats was increased; but the glucocorticoid receptor (GR) expression in the hippocampus was decreased. We conclude that LPS injection in neonatal rats can cause synaptic disruption in the hippocampus which may be attributed to inflammatory response due to excess production of proinflammatory cytokines e.g., IL-1β derived from activated microglia. The significance of increased plasma CORT concentration and decreased GR expression in the hippocampus is discussed.
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