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Heterogeneous complement and microglia activation mediates stress-induced synapse loss.

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    Summary
    This summary is machine-generated.

    Stress causes specific synapse loss in the brain via complement and microglia. Blocking complement component C3 protects against this loss and associated behavioral deficits.

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    Area of Science:

    • Neuroscience
    • Immunology
    • Molecular Biology

    Background:

    • Spatially heterogeneous synapse loss is a hallmark of neurological and psychiatric disorders, yet its mechanisms remain elusive.
    • Understanding the cellular and molecular drivers of this localized neuronal damage is crucial for developing targeted therapies.

    Approach:

    • Investigated the role of complement activation in stress-induced synapse loss in the mouse medial prefrontal cortex (mPFC).
    • Utilized single-cell RNA sequencing to identify stress-associated microglia states.
    • Employed C3 knockout mice to assess the necessity of complement component 3 in mediating these effects.

    Key Points:

    • Spatially restricted complement activation drives heterogeneous microglia activation and synapse loss in the upper layers of the mPFC following stress.
    • A stress-associated microglia state characterized by high apolipoprotein E (ApoE) expression was identified in the upper mPFC.
    • Mice lacking complement component C3 were protected from stress-induced layer-specific synapse loss and ApoE-high microglia accumulation.
    • C3 knockout mice exhibited resilience to stress-induced anhedonia and working memory deficits.

    Conclusions:

    • Complement component 3 and microglia activation are key mediators of stress-induced, layer-specific synapse loss in the mPFC.
    • These findings highlight the role of region-specific complement and microglia activity in the spatially restricted patterns of synapse loss observed in brain diseases.
    • Targeting complement pathways may offer a therapeutic strategy for psychiatric and neurological disorders characterized by synapse loss.