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

By Yang Zhan, R. Paolicelli, F. Sforazzini, L. Weinhard, G. Bolasco, F. Pagani, A. Vyssotski, A. Bifone, A. Gozzi, D. Ragozzino and 1 more. Nature Neuroscience, 2014

1,115 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/4d23899ebe3bd28ecb35caa26fa8829fb372fc6c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. Beth Stevens
2. Jason L. Stein
3. Daniel H. Geschwind

In Developmental Neuroscience

1. Beth Stevens

In Neurology

1. Beth Stevens
2. Liang Liu
3. Qing-Wu Yang
4. Daniel H. Geschwind
5. Xiao-Yi Xiong
6. Jonathan Kipnis

Citations in the corpus

• Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. (2016, background): “However, a lack of neuron-microglia signalling leads to impaired functional brain connectivity and social behaviour (Zhan et al., 2014).”
• Unexpected role of interferon-γ in regulating neuronal connectivity and social behavior (2016, background): “e, Il4−/− mice spend more time than wild-type mice investigating a novel mice; ANOVA for genotype F (1, 32) = 5.”
• Microglia: Dynamic Mediators of Synapse Development and Plasticity (2015, background): “CX3CR1 KO (elevated IL-1b) Reduced LTP (reversed by IL-1b receptor antagonist) [29] Decreased social interaction and increased repetitive behaviors [41]”
• CSF1 receptor signaling is necessary for microglia viability, which unmasks a cell that rapidly repopulates the microglia-depleted adult brain (2014, positive): “Although our results show that microglia are not overtly necessary for these behaviors, previous studies have shown that microglia are crucial during development, with CX3CR1GFP mice showing a transient reduction in microglia during development (Zhan et al., 2014), leading to long-term deficits in b”
• Advancing the understanding of autism disease mechanisms through genetics (2016, positive): “Notably, knockdown of chemokine (C-X3-C motif) receptor 1 ( CX3CR1 ), which is not mutated in individuals with ASD, leads to a reduction in microglia, deficits in synaptic pruning and ASD-like behavioral and functional connectivity defects 224,225 .”
• The Central Nervous System and the Gut Microbiome (2016, background): “In the absence of microglia, for example, the adult brain harbors significantly more synapses, exemplifying that these glial cells are necessary for synaptic pruning (Paolicelli et al., 2011; Zhan et al., 2014).”