| Literature DB >> 31831638 |
Csaba Cserép1, Balázs Pósfai1,2, Nikolett Lénárt1, Rebeka Fekete1,2, Zsófia I László2,3, Zsolt Lele3, Barbara Orsolits1, Gábor Molnár4, Steffanie Heindl5, Anett D Schwarcz1, Katinka Ujvári1, Zsuzsanna Környei1, Krisztina Tóth1,2, Eszter Szabadits1, Beáta Sperlágh6, Mária Baranyi6, László Csiba7, Tibor Hortobágyi8,9,10, Zsófia Maglóczky11, Bernadett Martinecz1, Gábor Szabó12, Ferenc Erdélyi12, Róbert Szipőcs13, Michael M Tamkun14, Benno Gesierich5, Marco Duering5,15, István Katona3, Arthur Liesz5,15, Gábor Tamás4, Ádám Dénes16.
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.Entities:
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Year: 2019 PMID： 31831638 DOI： 10.1126/science.aax6752
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728