Journal
CELL REPORTS
Volume 27, Issue 10, Pages 2895-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.05.010
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Funding
- Fondation Leducq
- Canadian Institute for Health Research [FDN-148397]
- CIHR Banting Fellowship
- Heart and Stroke Foundation
- Michael Smith Foundation for Health Research
- Fonds de Recherche Sante Quebec
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Microglia, the brain's immune cells, maintain homeostasis and sense pathological changes by continuously surveying the parenchyma with highly motile large processes. Here, we demonstrate that microglia also use thin actin-dependent filopodia that allow fast nanoscale sensing within discrete regions. Filopodia are distinct from large processes by their size, speed, and regulation mechanism. Increasing cyclic AMP (cAMP) by activating norepinephrine G(s)-coupled receptors, applying nitric oxide, or inhibiting phosphodiesterases rapidly increases filopodia but collapses large processes. Alternatively, G(i)-coupled P2Y12 receptor activation collapses filopodia but triggers large processes extension with bulbous tips. Similar control of cytoskeletal dynamics and microglial morphology by cAMP is observed in ramified primary microglia, suggesting that filopodia are intrinsically generated sensing structures. Therefore, nanoscale surveillance of brain parenchyma by microglia requires localized cAMP increases that drive filopodia formation. Shifting intracellular cAMP levels controls the polarity of microglial responses to changes in brain homeostasis and alters the scale of immunosurveillance.
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