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Published on: April 13, 2017
Microglia complement signaling promotes neuronal elimination and normal brain functional connectivity
Senthilkumar Deivasigamani1, Mariya T Miteva1,2, Silvia Natale1,3
1Epigenetics & Neurobiology Unit, EMBL Rome, European Molecular Biology Laboratory, Via Ramarini 32, 00015 Monterotondo, Italy.
Abstract:
Complement signaling is thought to serve as an opsonization signal to promote the phagocytosis of synapses by microglia. However, while its role in synaptic remodeling has been demonstrated in the retino-thalamic system, it remains unclear whether complement signaling mediates synaptic pruning in the brain more generally. Here we found that mice lacking the Complement receptor 3, the major microglia complement receptor, failed to show a deficit in either synaptic pruning or axon elimination in the developing mouse cortex. Instead, mice lacking Complement receptor 3 exhibited a deficit in the perinatal elimination of neurons in the cortex, a deficit that is associated with increased cortical thickness and enhanced functional connectivity in these regions in adulthood. These data demonstrate a role for complement in promoting neuronal elimination in the developing cortex.
Insights
Complement signaling promotes neuronal elimination in the developing brain, not synaptic pruning. Mice lacking Complement receptor 3 showed deficits in neuron removal, impacting cortical development and adult connectivity.
Area of Science:
- Neuroscience
- Immunology
- Developmental Biology
Background:
- Complement signaling is implicated in synaptic pruning by microglia.
- Its broader role in brain development, beyond the retino-thalamic system, is not fully understood.
Purpose of the Study:
- To investigate the role of complement signaling in general synaptic pruning and neuronal elimination in the developing mouse cortex.
- To determine the function of Complement receptor 3 (CR3) in microglia-mediated developmental processes.
Main Methods:
- Utilized knockout mice lacking Complement receptor 3 (CR3).
- Assessed synaptic pruning, axon elimination, and neuronal elimination in the developing mouse cortex.
- Analyzed cortical thickness and functional connectivity in adult mice.
Main Results:
- Mice lacking CR3 did not exhibit deficits in synaptic pruning or axon elimination.
- CR3 deficiency led to impaired perinatal neuronal elimination in the cortex.
- These mice showed increased cortical thickness and enhanced adult functional connectivity.
Conclusions:
- Complement signaling, via CR3, promotes neuronal elimination during cortical development.
- CR3 is crucial for eliminating excess neurons, influencing cortical structure and function.
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