期刊
NATURE NEUROSCIENCE
卷 22, 期 11, 页码 1782-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41593-019-0514-0
关键词
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资金
- National Institutes of Health [R01 EY019277, R21 NS099973, R01 AA027111, R01 EY028219, F31 NS105249, T32 NS007489, F31 NS086241, F32 EY028028]
- National Science Foundation [NSF 1557971]
- Schmitt Program on Integrative Brain Research grant
- University of Rochester Bilski-Mayer Fellowship
- University of Rochester Medical Center Summer Scholars Fellowship
Microglia are the brain's resident innate immune cells and also have a role in synaptic plasticity. Microglial processes continuously survey the brain parenchyma, interact with synaptic elements and maintain tissue homeostasis. However, the mechanisms that control surveillance and its role in synaptic plasticity are poorly understood. Microglial dynamics invivo have been primarily studied in anesthetized animals. Here we report that microglial surveillance and injury response are reduced in awake mice as compared to anesthetized mice, suggesting that arousal state modulates microglial function. Pharmacologic stimulation of beta(2)-adrenergic receptors recapitulated these observations and disrupted experience-dependent plasticity, and these effects required the presence of beta(2)-adrenergic receptors in microglia. These results indicate that microglial roles in surveillance and synaptic plasticity in the mouse brain are modulated by noradrenergic tone fluctuations between arousal states and emphasize the need to understand the effect of disruptions of adrenergic signaling in neurodevelopment and neuropathology.
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