Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-03

AUTHORS

Yang Zhan, Rosa C Paolicelli, Francesco Sforazzini, Laetitia Weinhard, Giulia Bolasco, Francesca Pagani, Alexei L Vyssotski, Angelo Bifone, Alessandro Gozzi, Davide Ragozzino, Cornelius T Gross

ABSTRACT

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. More... »

PAGES

400-406

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nn.3641

DOI

http://dx.doi.org/10.1038/nn.3641

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036382166

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24487234


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