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

ABSTRACT: This study defines a molecular interaction between neurons and microglia that drives experience-dependent synapse remodeling in the hippocampus.

ORGANISM(S): Mus musculus

PROVIDER: GSE150712 | GEO | 2020/07/01

REPOSITORIES: GEO

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Microglial remodeling of the extracellular matrix promotes synapse plasticity [Neuronal nuclei]

Project description:This study defines a molecular interaction between neurons and microglia that drives experience-dependent synapse remodeling in the hippocampus.

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

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

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Extracellular matrix proteolysis maintains synapse plasticity during brain development

Project description:Maintaining a dynamic neuronal synapse pool is critical to brain development. The extracellular matrix (ECM) regulates synaptic plasticity via mechanisms that are still being defined and are studied predominantly in adulthood. Using live imaging of excitatory synapses in zebrafish hindbrain we observed a bimodal distribution of short-lived (dynamic) and longer-lived (stable) synapses. Disruption of ECM via digestion or brevican deletion destabilized dynamic synapses and led to decreased synapse density. Conversely, loss of matrix metalloproteinase 14 (MMP14) led to accumulation of brevican and increased the lifetime of the dynamic synapse pool without affecting stable synapse pool, resulting in increased synapse density. Microglial MMP14 was essential to these effects in both fish and human iPSC-derived cultures. Both MMP14 and brevican were required for experience-dependent synapse plasticity in a motor learning assay. These data, complemented by mathematical modeling, define an essential role of ECM remodeling in maintaining a dynamic subset of synapses during brain development.

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Microglial remodeling of the extracellular matrix promotes synapse plasticity

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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 [Neuronal nuclei]

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Microglial remodeling of the extracellular matrix promotes synapse plasticity

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-07-01 | GSE150714 | GEO

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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