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小胶质细胞通过专门的体嘌呤能神经连接监测和保护神经元功能
作者:小柯机器人 发布时间:2020/2/10 11:38:33

匈牙利实验医学研究所Ádám Dénes研究组在研究中取得进展。他们的最新工作发现,小胶质细胞通过专门的体嘌呤能神经连接监测和保护神经元功能。 相关论文于2020年1月31日发表在《科学》杂志上。

研究人员确定了小鼠和人脑中神经元细胞体与小胶质细胞过程之间的相互作用位点。体细胞小胶质细胞与神经元的连接具有专门针对嘌呤能信号传导而优化的纳米结构。神经元线粒体的活性与小胶质细胞连接形成有关,其能够迅速响应神经元活化从而被诱导并能够被P2Y12受体的抑制所阻断。由脑损伤引起的体细胞连接变化能够触发P2Y12受体依赖性小胶质细胞神经保护作用,调节神经元钙负荷和功能连接性。因此,在这些连接处的小胶质细胞突起可能监视和保护神经元功能。
 
据悉,小胶质细胞是大脑中的主要免疫细胞,在脑稳态和神经系统疾病中起作用。小胶质细胞与神经元通讯的基础机制仍然难以捉摸。 
 
附:英文原文

Title: Microglia monitor and protect neuronal function through specialized somatic purinergic junctions

Author: Csaba Cserép, Balázs Pósfai, Nikolett Lénárt, Rebeka Fekete, Zsófia I. László, Zsolt Lele, Barbara Orsolits, Gábor Molnár, Steffanie Heindl, Anett D. Schwarcz, Katinka Ujvári, Zsuzsanna Krnyei, Krisztina Tóth, Eszter Szabadits, Beáta Sperlágh, Mária Baranyi, László Csiba, Tibor Hortobágyi, Zsófia Maglóczky, Bernadett Martinecz, Gábor Szabó, Ferenc Erdélyi, Róbert Szipcs, Michael M. Tamkun, Benno Gesierich, Marco Duering, István Katona, Arthur Liesz, Gábor Tamás, ádám Dénes

Issue&Volume: 2020/01/31

Abstract: Microglia are the main immune cells in the brain and have roles in brain homeostasis and neurological diseases. Mechanisms underlying microglia–neuron communication remain elusive. Here, we identified an interaction site between neuronal cell bodies and microglial processes in mouse and human brain. Somatic microglia–neuron junctions have a specialized nanoarchitecture optimized for purinergic signaling. Activity of neuronal mitochondria was linked with microglial junction formation, which was induced rapidly in response to neuronal activation and blocked by inhibition of P2Y12 receptors. Brain injury–induced changes at somatic junctions triggered P2Y12 receptor–dependent microglial neuroprotection, regulating neuronal calcium load and functional connectivity. Thus, microglial processes at these junctions could potentially monitor and protect neuronal functions.

DOI: 10.1126/science.aax6752

Source: https://science.sciencemag.org/content/367/6477/528

期刊信息
Science:《科学》,创刊于1880年。隶属于美国科学促进会,最新IF:41.037
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