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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.

2020-07-01 | GSE150713 | GEO

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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Microglial remodeling of the extracellular matrix promotes synapse plasticity

Project description: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.

| S-EPMC7497728 | biostudies-literature

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

Project description: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.

2023-10-23 | PXD045719 | Pride

Neuronal TIMP2 regulates hippocampus-dependent plasticity and extracellular matrix complexity

Project description:The functional output of the hippocampus, a brain region subserving memory processes, depends on highly orchestrated cellular and molecular processes that regulate synaptic plasticity throughout life. The structural requirements of such plasticity and molecular processes involved in this regulation are poorly understood. Specific molecules, including tissue inhibitor of metalloproteinases-2 (TIMP2) have been implicated in serving a pro-plasticity role in the hippocampus, a role that decreases with brain aging. Here, we report that TIMP2 is highly expressed by neurons within the hippocampus and its loss drives changes in cellular programs related to adult neurogenesis and dendritic spine turnover with corresponding impairments in hippocampus-dependent memory. We find that TIMP2 regulates accumulation of extracellular matrix (ECM) around synapses in the hippocampus with concomitant hindrance in migration of newborn neurons through a denser ECM network. A conditional TIMP2 KO mouse reveals that neuronal TIMP2 regulates adult neurogenesis, accumulation of ECM, and ultimately hippocampus-dependent memory. Our results define a mechanism whereby hippocampus-dependent function is regulated by TIMP2 and its interactions with the ECM to regulate diverse processes associated with synaptic plasticity.

2023-11-02 | GSE223188 | GEO

Elimination of the four extracellular matrix molecules tenascin-C, tenascin-R, brevican and neurocan modifies the expression of key molecules of synapse formation and transmission

Project description:The extracellular matrix (ECM) molecules tenascin-C (Tnc), tenascin-R (Tnr), brevican (Bcan) and neurocan (Ncan) are completely knocked out in the quadruple knockout mouse. This removal of these central ECM molecules lead to an altered gene expression in the hippocampus of postnatal day (P) 21 old quadruple knockout mice. Among others, the expression of genes involved in the process of synapse formation associated with synaptic transmission were significantly changed in the quadruple knockout hippocampus compared to the wildtype hippocampus. We found e.g. an upregulated expression of Gamma-aminobutyric acid receptor subunit theta (Gabrq), Glutamate decarboxylase (Gad2) and semaphorin 4c (Sema4c), which are known contributors at synapses. Interestingly, some extracellular molecules e.g. like glypican 3 (Gpc3), calreticulin (Calr) and three different types of collagens (Col1a2, Col4a3 and Col27a1) showed also a modified expression. These data indicate the importance of the four ECM molecules for an intact gene expression in the murine hippocampus.

2019-10-08 | GSE127216 | GEO

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

Project description:Microglia, the largest population of brain immune cells, continuously interact with synapses to maintain brain homeostasis. We aimed at understanding the role of Rac1 on microglia functions. 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, a fundamental brain property impaired in several neuropsychiatric disorders.

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