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

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Bibliographic Details
Title:	Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior.
Authors:	Zhan, Yang, Paolicelli, Rosa C, Sforazzini, Francesco, Weinhard, Laetitia, Bolasco, Giulia, Pagani, Francesca, Vyssotski, Alexei L, Bifone, Angelo, Gozzi, Alessandro, Ragozzino, Davide, Gross, Cornelius T
Source:	Nature Neuroscience. Mar2014, Vol. 17 Issue 3, p400-406. 7p. 5 Graphs.
Subjects:	Microglia, Neuroglia, Phagocytes, Neural transmission, Developmental disabilities
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. [ABSTRACT FROM AUTHOR]
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Database:	Psychology and Behavioral Sciences Collection

Description
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. [ABSTRACT FROM AUTHOR]
ISSN:	10976256
DOI:	10.1038/nn.3641