小膠質細胞通過專門的體嘌呤能神經連接監測和保護神經元功能
作者:
小柯機器人發布時間:2020/2/10 11:38:33
匈牙利實驗醫學研究所Ádám Dénes研究組在研究中取得進展。他們的最新工作發現,小膠質細胞通過專門的體嘌呤能神經連接監測和保護神經元功能。 相關論文於2020年1月31日發表在《科學》雜誌上。
研究人員確定了小鼠和人腦中神經元細胞體與小膠質細胞過程之間的相互作用位點。體細胞小膠質細胞與神經元的連接具有專門針對嘌呤能信號傳導而優化的納米結構。神經元線粒體的活性與小膠質細胞連接形成有關,其能夠迅速響應神經元活化從而被誘導並能夠被P2Y12受體的抑制所阻斷。由腦損傷引起的體細胞連接變化能夠觸發P2Y12受體依賴性小膠質細胞神經保護作用,調節神經元鈣負荷和功能連接性。因此,在這些連接處的小膠質細胞突起可能監視和保護神經元功能。
據悉,小膠質細胞是大腦中的主要免疫細胞,在腦穩態和神經系統疾病中起作用。小膠質細胞與神經元通訊的基礎機制仍然難以捉摸。
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
Science:《科學》,創刊於1880年。隸屬於美國科學促進會,最新IF:41.037