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Microglial remodeling of the extracellular matrix promotes synapse plasticity

ABSTRACT: Microglial remodeling of the extracellular matrix promotes synapse plasticity

PROVIDER: PRJNA633361 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11804000.fastq.gz	Fastqsanger.gz
	SRR11803989.fastq.gz	Fastqsanger.gz
	SRR11803990.fastq.gz	Fastqsanger.gz
	SRR11803991.fastq.gz	Fastqsanger.gz
	SRR11803992.fastq.gz	Fastqsanger.gz

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Microglial remodeling of the extracellular matrix promotes synapse plasticity [Microglia]

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Microglial remodeling of the extracellular matrix promotes synapse plasticity [Microglia]

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Microglial Remodeling of the Extracellular Matrix Promotes Synapse Plasticity.

Project description:Synapse remodeling is essential to encode experiences into neuronal circuits. Here, we define a molecular interaction between neurons and microglia that drives experience-dependent synapse remodeling in the hippocampus. We find that the cytokine interleukin-33 (IL-33) is expressed by adult hippocampal neurons in an experience-dependent manner and defines a neuronal subset primed for synaptic plasticity. Loss of neuronal IL-33 or the microglial IL-33 receptor leads to impaired spine plasticity, reduced newborn neuron integration, and diminished precision of remote fear memories. Memory precision and neuronal IL-33 are decreased in aged mice, and IL-33 gain of function mitigates age-related decreases in spine plasticity. We find that neuronal IL-33 instructs microglial engulfment of the extracellular matrix (ECM) and that its loss leads to impaired ECM engulfment and a concomitant accumulation of ECM proteins in contact with synapses. These data define a cellular mechanism through which microglia regulate experience-dependent synapse remodeling and promote memory consolidation.

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Microglial remodeling of the extracellular matrix promotes synapse plasticity

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Microglial Rac1 is essential for experience-dependent brain plasticity and cognitive performance

Project description:Here, we used conditional cell-specific gene targeting in mice with multi-omics approaches, and demonstrated that the RhoGTPase Rac1 was an essential requirement for the microglia to sense and interpret the brain microenvironment, and for crucial microglia-synapse crosstalk driving experience-dependent plasticity. Phosphoproteomics profiling detected a large modulation of RhoGTPase signaling, predominantly of Rac1, in microglia of mice exposed to an environmental enrichment protocol. Ablation of microglial Rac1 affected pathways involved in microglia-synapse communication, disrupted experience-dependent synaptic remodeling, and blocked the gains in learning, memory and sociability induced by environmental enrichment.

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Astrocyte-derived Interleukin-33 promotes microglial synapse engulfment and neural circuit development I

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