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首页> 外文期刊>The European Journal of Neuroscience >Serotonin of mast cell origin contributes to hippocampal function
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Serotonin of mast cell origin contributes to hippocampal function

机译:肥大细胞起源的血清素有助于海马功能

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In the central nervous system, serotonin, an important neurotransmitter and trophic factor, is synthesized by both mast cells and neurons. Mast cells, like other immune cells, are born in the bone marrow and migrate to many tissues. We show that they are resident in the mouse brain throughout development and adulthood. Measurements based on capillary electrophoresis with native fluorescence detection indicate that a significant contribution of serotonin to the hippocampal milieu is associated with mast cell activation. Compared with their littermates, mast cell-deficient C57BL/6 Kit W-sh/W-sh mice have profound deficits in hippocampus-dependent spatial learning and memory and in hippocampal neurogenesis. These deficits are associated with a reduction in cell proliferation and in immature neurons in the dentate gyrus, but not in the subventricular zone - a neurogenic niche lacking mast cells. Chronic treatment with fluoxetine, a selective serotonin reuptake inhibitor, reverses the deficit in hippocampal neurogenesis in mast cell-deficient mice. In summary, the present study demonstrates that mast cells are a source of serotonin, that mast cell-deficient C57BL/6 Kit W-sh/W-sh mice have disrupted hippocampus-dependent behavior and neurogenesis, and that elevating serotonin in these mice, by treatment with fluoxetine, reverses these deficits. We conclude that mast cells contribute to behavioral and physiological functions of the hippocampus and note that they play a physiological role in neuroimmune interactions, even in the absence of inflammatory responses. Mast cells are immune cells that are resident in the mouse brain within and near the hippocampus throughout development and adulthood. Their activation contributes serotonin to the hippocampus. A lack of mast cells is associated with deficits in spatial learning and memory and decreased hippocampal neurogenesis which can be restored through administration of the selective serotonin reuptake inhibitor fluoxetine.
机译:在中枢神经系统中,肥大细胞和神经元都合成了5-羟色胺(一种重要的神经递质和营养因子)。肥大细胞与其他免疫细胞一样,都出生于骨髓中并迁移到许多组织。我们显示它们在整个发育和成年期都驻留在小鼠大脑中。基于具有天然荧光检测的毛细管电泳的测量结果表明,血清素对海马环境的重要贡献与肥大细胞活化有关。与它们的同窝仔相比,缺乏肥大细胞的C57BL / 6 Kit W-sh / W-sh小鼠在依赖海马的空间学习和记忆以及海马神经发生中具有严重的缺陷。这些缺陷与齿状回中细胞增殖和未成熟神经元减少有关,但与脑室下区域(缺乏肥大细胞的神经源性利基)无关。氟西汀(一种选择性的5-羟色胺再摄取抑制剂)的长期治疗可逆转肥大细胞缺陷小鼠海马神经发生的缺陷。总而言之,本研究表明肥大细胞是血清素的来源,肥大细胞缺陷型C57BL / 6 Kit W-sh / W-sh小鼠破坏了海马依赖性行为和神经发生,并且升高了这些小鼠中的血清素,通过用氟西汀治疗,可以逆转这些缺陷。我们得出的结论是,肥大细胞有助于海马的行为和生理功能,并指出,即使在没有炎症反应的情况下,它们也会在神经免疫相互作用中发挥生理作用。肥大细胞是免疫细胞,在整个发育和成年期都位于海马内和附近的小鼠大脑中。它们的活化为海马体提供了5-羟色胺。肥大细胞的缺乏与空间学习和记忆的缺乏以及海马神经发生的减少有关,这可以通过施用选择性5-羟色胺再摄取抑制剂氟西汀来恢复。

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