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

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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]
Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior.
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  Data: <searchLink fieldCode="AR" term="%22Zhan%2C+Yang%22">Zhan, Yang</searchLink><br /><searchLink fieldCode="AR" term="%22Paolicelli%2C+Rosa+C%22">Paolicelli, Rosa C</searchLink><br /><searchLink fieldCode="AR" term="%22Sforazzini%2C+Francesco%22">Sforazzini, Francesco</searchLink><br /><searchLink fieldCode="AR" term="%22Weinhard%2C+Laetitia%22">Weinhard, Laetitia</searchLink><br /><searchLink fieldCode="AR" term="%22Bolasco%2C+Giulia%22">Bolasco, Giulia</searchLink><br /><searchLink fieldCode="AR" term="%22Pagani%2C+Francesca%22">Pagani, Francesca</searchLink><br /><searchLink fieldCode="AR" term="%22Vyssotski%2C+Alexei+L%22">Vyssotski, Alexei L</searchLink><br /><searchLink fieldCode="AR" term="%22Bifone%2C+Angelo%22">Bifone, Angelo</searchLink><br /><searchLink fieldCode="AR" term="%22Gozzi%2C+Alessandro%22">Gozzi, Alessandro</searchLink><br /><searchLink fieldCode="AR" term="%22Ragozzino%2C+Davide%22">Ragozzino, Davide</searchLink><br /><searchLink fieldCode="AR" term="%22Gross%2C+Cornelius+T%22">Gross, Cornelius T</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Nature+Neuroscience%22">Nature Neuroscience</searchLink>. Mar2014, Vol. 17 Issue 3, p400-406. 7p. 5 Graphs.
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  Data: <searchLink fieldCode="DE" term="%22Microglia%22">Microglia</searchLink><br /><searchLink fieldCode="DE" term="%22Neuroglia%22">Neuroglia</searchLink><br /><searchLink fieldCode="DE" term="%22Phagocytes%22">Phagocytes</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+transmission%22">Neural transmission</searchLink><br /><searchLink fieldCode="DE" term="%22Developmental+disabilities%22">Developmental disabilities</searchLink>
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  Data: 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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  Data: <i>Copyright of Nature Neuroscience is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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              Text: Mar2014
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