Microglia complement signaling promotes neuronal elimination and normal brain functional connectivity.
cell death
complement
cortex
microglia
neurodevelopment
Journal
Cerebral cortex (New York, N.Y. : 1991)
ISSN: 1460-2199
Titre abrégé: Cereb Cortex
Pays: United States
ID NLM: 9110718
Informations de publication
Date de publication:
14 10 2023
14 10 2023
Historique:
received:
05
12
2022
revised:
10
08
2023
accepted:
11
08
2023
medline:
9
11
2023
pubmed:
18
9
2023
entrez:
17
9
2023
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 37718159
pii: 7275621
doi: 10.1093/cercor/bhad313
pmc: PMC10629900
doi:
Substances chimiques
Receptors, Complement
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
10750-10760Subventions
Organisme : NIMH NIH HHS
ID : R21 MH116473
Pays : United States
Organisme : NIH HHS
ID : 1R21MH116473-01A1
Pays : United States
Organisme : European Research Council
Pays : International
Informations de copyright
© The Author(s) 2023. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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