Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior.

Détails

ID Serval
serval:BIB_560F71FF6DC5
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior.
Périodique
Nature neuroscience
Auteur⸱e⸱s
Zhan Y., Paolicelli R.C., Sforazzini F., Weinhard L., Bolasco G., Pagani F., Vyssotski A.L., Bifone A., Gozzi A., Ragozzino D., Gross C.T.
ISSN
1546-1726 (Electronic)
ISSN-L
1097-6256
Statut éditorial
Publié
Date de publication
03/2014
Peer-reviewed
Oui
Volume
17
Numéro
3
Pages
400-406
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Microglia are phagocytic cells that infiltrate the brain during development and have a role in the elimination of synapses during brain maturation. Changes in microglial morphology and gene expression have been associated with neurodevelopmental disorders. However, it remains unknown whether these changes are a primary cause or a secondary consequence of neuronal deficits. Here we tested whether a primary deficit in microglia was sufficient to induce some autism-related behavioral and functional connectivity deficits. Mice lacking the chemokine receptor Cx3cr1 exhibit a transient reduction of microglia during the early postnatal period and a consequent deficit in synaptic pruning. We show that deficient synaptic pruning is associated with weak synaptic transmission, decreased functional brain connectivity, deficits in social interaction and increased repetitive-behavior phenotypes that have been previously associated with autism and other neurodevelopmental and neuropsychiatric disorders. These findings open the possibility that disruptions in microglia-mediated synaptic pruning could contribute to neurodevelopmental and neuropsychiatric disorders.
Mots-clé
Animals, Behavior, Animal/physiology, Brain/metabolism, Brain/pathology, CX3C Chemokine Receptor 1, Connectome/instrumentation, Connectome/methods, Female, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Microglia/metabolism, Microglia/pathology, Neurons/metabolism, Neurons/pathology, Receptors, Chemokine/physiology, Signal Transduction/physiology, Social Behavior, Synapses/metabolism, Synaptic Transmission/physiology
Pubmed
Web of science
Création de la notice
18/12/2018 11:35
Dernière modification de la notice
20/08/2019 15:10
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