Stress induced morphological microglial activation in the rodent brain: Involvement of interleukin-18
Stress induced morphological microglial activation in the rodent brain: Involvement of interleukin-18
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DOI：
10.1016/j.neuroscience.2007.02.043
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发表时间：
2007-05-25
期刊：
影响因子：
3.3
通讯作者：
Conti, B.
中科院分区：
文献类型：
--
作者：
Sugama, S.;Fujita, M.;Conti, B.
本研究探讨了急性应激可能激活小胶质细胞的可能性。Wistar大鼠暴露于2小时的约束期结合水浸应激之前，通过免疫组织化学与OX-42，补体受体CR 3的标志物的脑分析。一个单一的会议的压力引起强大的形态小胶质细胞激活丘脑，下丘脑，海马，黑质和中央灰质。这些影响早在暴露1 h时就出现，并在2 h时进一步加强。形态学激活不伴随功能激活或炎症标志物的变化，包括白细胞介素-1 β（IL-1 β）、白细胞介素-6（IL-6）和诱导型一氧化氮合酶（iNOS）。用小鼠获得了类似的结果，其中在白细胞介素-18（IL-18 KO）无效的动物中比较了应激的影响，白细胞介素-18 KO是一种先前被证明受应激调节并有助于小胶质细胞活化的细胞因子。结果表明，IL-18 KO小鼠中应激诱导的小胶质细胞活化显著减少。本研究报告的证据表明，身体/情绪压力可能会导致形态小胶质细胞激活的大脑，这种激活是部分介导的白细胞介素-18。(c)2007年IBRO。由爱思唯尔有限公司出版。保留所有权利。
The present study investigated the possibility that acute stress might activate microglial cells. Wistar rats were exposed to 2 h period of restraint combined with water immersion stress prior to brain analysis by immunohistochemistry with OX-42, a marker of complement receptor CR3. A single session of stress provoked robust morphological microglial activation in the thalamus, hypothalamus, hippocampus, substantia nigra and central gray. These effects appeared as early as at I h of exposure and were further intensified at 2 h. Morphological activation was not accompanied with changes in markers of functional activation or of inflammation including interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS). Similar results were obtained with mice where the effects of stress were compared in animals null for interleukin-18 (IL-18 KO), a cytokine previously demonstrated to be modulated by stress and to contribute to microglia activation. The results demonstrated significant reduction of stress-induced microglial activation in IL-18 KO mice. The present study reports evidence that physical/emotional stress may induce morphological microglial activation in the brain and this activation is in part mediated by interleukin-18. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.