The brain's resident macrophages have many roles beyond synaptic pruning.
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Defining microglial-synapse interactions.
Science
September 2023
Department of Psychiatry and Behavioral Sciences and Weill Institute for Neurosciences, Kavli Institute for Fundamental Neurosciences, University of California San Francisco, San Francisco, CA, USA.
The brain's resident macrophages have many roles beyond synaptic pruning.
View Article and Find Full Text PDFTime-dependent and selective microglia-mediated removal of spinal synapses in neuropathic pain.
Cell Rep
January 2023
Department of Pharmacology and Therapeutics, McGill University, Montréal, QC H3G 1Y6, Canada; Department of Anatomy and Cell Biology, McGill University, Montréal, QC H3A 0C7, Canada; Alan Edwards Centre for Research on Pain, McGill University, Montréal, QC H3A 2B4, Canada. Electronic address:
Neuropathic pain is a debilitating condition resulting from damage to the nervous system. Imbalance of spinal excitation and inhibition has been proposed to contribute to neuropathic pain. However, the structural basis of this imbalance remains unknown.
View Article and Find Full Text PDFMicroglial pattern recognition via IL-33 promotes synaptic refinement in developing corticothalamic circuits in mice.
J Exp Med
February 2023
Departments of Psychiatry and Behavioral Sciences/Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
Microglia are critical regulators of brain development that engulf synaptic proteins during postnatal synapse remodeling. However, the mechanisms through which microglia sense the brain environment are not well defined. Here, we characterized the regulatory program downstream of interleukin-33 (IL-33), a cytokine that promotes microglial synapse remodeling.
View Article and Find Full Text PDFSARS-CoV-2 promotes microglial synapse elimination in human brain organoids.
Mol Psychiatry
October 2022
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Neuropsychiatric manifestations are common in both the acute and post-acute phase of SARS-CoV-2 infection, but the mechanisms of these effects are unknown. In a newly established brain organoid model with innately developing microglia, we demonstrate that SARS-CoV-2 infection initiate neuronal cell death and cause a loss of post-synaptic termini. Despite limited neurotropism and a decelerating viral replication, we observe a threefold increase in microglial engulfment of postsynaptic termini after SARS-CoV-2 exposure.
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