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首页> 外文期刊>Brain, Behavior, and Immunity >Hippocampal interleukin-1 mediates stress-enhanced fear learning: A potential role for astrocyte-derived interleukin-1β
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Hippocampal interleukin-1 mediates stress-enhanced fear learning: A potential role for astrocyte-derived interleukin-1β

机译：海马白细胞介素-1介导应力增强的恐惧学习：星形胶质细胞衍生的白细胞介素-1β的潜在作用

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Highlights ? Blocking DH stress-induced IL-1 signaling prevents stress-enhanced fear learning. ? Hippocampal Iba-1, but not GFAP, is attenuated 48h after stress exposure. ? Stress-induced hippocampal IL-1β is colocalized primarily with GFAP. Abstract Post-traumatic stress disorder (PTSD) is associated with immune dysregulation. We have previously shown that severe stress exposure in a preclinical animal model of the disorder, stress-enhanced fear learning (SEFL), is associated with an increase in hippocampal interleukin-1β (IL-1β) and that blocking central IL-1 after the severe stress prevents the development of SEFL. Here, we tested whether blocking hippocampal IL-1 signaling is sufficient to prevent enhanced fear learning and identified the cellular source of stress-induced IL-1β in this region. Experiment 1 tested whether intra-dorsal hippocampal (DH) infusions of interleukin-1 receptor antagonist (IL-1RA, 1.25μg per hemisphere) 24 and 48h after stress exposure prevents the development of enhanced fear learning. Experiment 2 used triple fluorescence immunohistochemistry to examine hippocampal alterations in IL-1β, glial fibrillary acidic protein (GFAP), an astrocyte-specific marker, and ionized calcium binding adaptor molecule -1 (Iba-1), a microglial-specific marker, 48h after exposure to the severe stressor of the SEFL paradigm. Intra-DH IL-1RA prevented SEFL and stress-induced IL-1β was primarily colocalized with astrocytes in the hippocampus. Further, hippocampal GFAP immunoreactivity was not altered, whereas hippocampal Iba-1 immunoreactivity was significantly attenuated following severe stress. These data suggest that hippocampal IL-1 signaling is critical to the development of SEFL and that astrocytes are a predominant source of stress-induced IL-1β.
机译：强调 ？阻断DH应激诱导的IL-1信号阻止压力增强的恐惧学习。还在压力暴露后，海马IBA-1，但不是GFAP，在48h衰减48小时。还应激诱导的海马IL-1β主要与GFAP共定位。摘要创伤后应激障碍（PTSD）与免疫失调相关。我们之前已经表明，在临床前的动物模型中严重的压力暴露，应激增强的恐惧学习（SEFL），与海马白细胞介素-1β（IL-1β）的增加有关，并且在其中阻断了中央IL-1。严重的压力阻止了SEFL的发展。在这里，我们测试了阻断海马IL-1信号传导是否足以防止增强的恐惧学习并鉴定该区域中应激诱导的IL-1β的细胞源。实验1测试了在压力暴露后的白细胞介素-1受体拮抗剂（IL-1RA，每半球，1.25μg）24和48H的内部蛋白-1受体拮抗剂（IL-1RA，1.25μg）的输注阻止了增强恐惧学习的发展。实验2使用三重荧光免疫组织化学来检查IL-1β，胶质纤维酸性蛋白质（GFAP），星形胶质细胞特异性标记和电离钙结合衔接子分子-1（IBA-1）的海马改变，小特异性标记，48h暴露于SEFL范例的严重压力后。 DH IN-1RA的INTRA-1ra预防SEFL和应激诱导的IL-1β主要用海马的星形胶质细胞分开。此外，未改变海马GFAP免疫反应性，而在严重应激后，海马IBA-1免疫反应性显着减弱。这些数据表明海马IL-1信号传导对SEFL的发育至关重要，并且该星形胶质细胞是应激诱导的IL-1β的主要来源。

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