Nature reviews. Neuroscience, Journal Year: 2021, Volume and Issue: 22(11), P. 657 - 673
Published: Sept. 20, 2021
Language: Английский
Nature reviews. Neuroscience, Journal Year: 2021, Volume and Issue: 22(11), P. 657 - 673
Published: Sept. 20, 2021
Language: Английский
Nature reviews. Immunology, Journal Year: 2017, Volume and Issue: 18(4), P. 225 - 242
Published: Nov. 20, 2017
Language: Английский
Citations
1628Nature Medicine, Journal Year: 2017, Volume and Issue: 23(9), P. 1018 - 1027
Published: Sept. 1, 2017
Language: Английский
Citations
1465Cell, Journal Year: 2019, Volume and Issue: 179(2), P. 292 - 311
Published: Oct. 1, 2019
Language: Английский
Citations
1065Neuron, Journal Year: 2022, Volume and Issue: 110(21), P. 3458 - 3483
Published: Nov. 1, 2022
Language: Английский
Citations
1065Nature, Journal Year: 2020, Volume and Issue: 586(7829), P. 417 - 423
Published: Sept. 30, 2020
Language: Английский
Citations
738Nature Communications, Journal Year: 2018, Volume and Issue: 9(1)
Published: March 26, 2018
Abstract Microglia are highly motile glial cells that proposed to mediate synaptic pruning during neuronal circuit formation. Disruption of signaling between microglia and neurons leads an excess immature connections, thought be the result impaired phagocytosis synapses by microglia. However, until now direct has not been reported fundamental questions remain about precise structures phagocytic mechanisms involved. Here we used light sheet fluorescence microscopy follow microglia–synapse interactions in developing organotypic hippocampal cultures, complemented a 3D ultrastructural characterization using correlative electron (CLEM). Our findings define set dynamic interactions, including selective partial phagocytosis, or trogocytosis ( trogo -: nibble), presynaptic induction postsynaptic spine head filopodia These allow us propose mechanism for facilitatory role remodeling maturation.
Language: Английский
Citations
691Cell, Journal Year: 2020, Volume and Issue: 182(2), P. 388 - 403.e15
Published: July 1, 2020
Language: Английский
Citations
482Journal of Neuroinflammation, Journal Year: 2021, Volume and Issue: 18(1)
Published: Nov. 6, 2021
Microglia are emerging as critical regulators of neuronal function and behavior in nearly every area neuroscience. Initial reports focused on classical immune functions microglia pathological contexts, however, immunological concepts from these studies have been applied to describe neuro-immune interactions the absence disease, injury, or infection. Indeed, terms such 'microglia activation' 'neuroinflammation' used ubiquitously changes disparate contexts; particularly stress research, where prompt undue comparisons conditions. This creates a barrier for investigators new neuro-immunology ultimately hinders our understanding effects microglia. As more seek understand role neurobiology behavior, it is increasingly important develop standard methods study define microglial phenotype function. In this review, we summarize primary research physiological contexts. Further, propose framework better microglia1 chronic stress. approach will enable precise characterization different which should facilitate development microglia-directed therapeutics psychiatric neurological disease.
Language: Английский
Citations
446Neuron, Journal Year: 2017, Volume and Issue: 97(2), P. 299 - 312.e6
Published: Dec. 28, 2017
Microglia exhibit two modes of motility: they constantly extend and retract their processes to survey the brain, but also send out targeted envelop sites tissue damage. We now show that these motility differ mechanistically. identify two-pore domain channel THIK-1 as main K+ expressed in microglia situ. is tonically active, its activity potentiated by P2Y12 receptors. Inhibiting function pharmacologically or gene knockout depolarizes microglia, which decreases microglial ramification thus reduces surveillance, whereas blocking receptors does not affect membrane potential, ramification, surveillance. In contrast, process outgrowth damaged requires receptor activation unaffected THIK-1. Block inhibits release pro-inflammatory cytokine interleukin-1β from activated consistent with loss being needed for inflammasome assembly. Thus, immune surveillance require activity.
Language: Английский
Citations
394Neuron, Journal Year: 2017, Volume and Issue: 95(2), P. 341 - 356.e6
Published: July 1, 2017
Language: Английский
Citations
374