ArticleMolecular psychiatry2021
Inhibition of colony stimulating factor 1 receptor corrects maternal inflammation-induced microglial and synaptic dysfunction and behavioral abnormalities.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed.
- Article
- Prenatal and postnatal effects of gestational immune activation on synaptic and neurodevelopmental pathways via epigenetic mechanisms.Translational psychiatry · 2026Article
- Microglial activity during postnatal development is required for infantile amnesia in mice.PLoS biology · 2026Article
- Persistent priming of hypothalamic microglia is associated with sensitization of the hypothalamic-pituitary-adrenal axis to acute stress, hyperactivity and behavioral response disruption in male rats.Frontiers in immunology · 2026Article
- Microglia as critical mediators linking perinatal immune stress to mental health trajectories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Microglial plasticity across development mediates infantile amnesia.bioRxiv : the preprint server for biology · 2025Article
- Article
- The "don't eat me" signal CD47 is associated with microglial phagocytosis defects and autism-like behaviors in 16p11.2 deletion mice.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Development and characterization of in vitro inducible immortalization of a murine microglia cell line for high throughput studies.Scientific reports · 2025Article
- Physiological roles of embryonic microglia and their perturbation by maternal inflammation.Frontiers in cellular neuroscience · 2025Review
- Influenza A virus during pregnancy disrupts maternal intestinal immunity and fetal cortical development in a dose- and time-dependent manner.Molecular psychiatry · 2025Article
- Modified neuroimmune processes and emotional behaviour in weaned and late adolescent male and female mice born via caesarean section.Scientific reports · 2024Article
- The Importance of Including Maternal Immune Activation in Animal Models of Hypoxic-Ischemic Encephalopathy.Biomedicines · 2024Article
- Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism.Journal of neuroinflammation · 2024Article
- The role of microglia in early neurodevelopment and the effects of maternal immune activation.Seminars in immunopathology · 2024Review
- P2RX7 plays a critical role in extracellular vesicle-mediated secretion of pathogenic molecules from microglia and astrocytes.Journal of extracellular biology · 2024Article
- The molecular determinants of microglial developmental dynamics.Nature reviews. Neuroscience · 2024Review
- PolyI:C Maternal Immune Activation on E9.5 Causes the Deregulation of Microglia and the Complement System in Mice, Leading to Decreased Synaptic Spine Density.International journal of molecular sciences · 2024Article
- Increased NLRP1 mRNA and Protein Expression Suggests Inflammasome Activation in the Dorsolateral Prefrontal and Medial Orbitofrontal Cortex in Schizophrenia.Biomolecules · 2024Article
- Developmental programming of tissue-resident macrophages.Frontiers in immunology · 2024Review
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Authors and funding
22 authors.
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Abstract
Maternal immune activation (MIA) disrupts the central innate immune system during a critical neurodevelopmental period. Microglia are primary innate immune cells in the brain although their direct influence on the MIA phenotype is largely unknown. Here we show that MIA alters microglial gene expression with upregulation of cellular protrusion/neuritogenic pathways, concurrently causing repetitive behavior, social deficits, and synaptic dysfunction to layer V intrinsically bursting pyramidal neurons in the prefrontal cortex of mice. MIA increases plastic dendritic spines of the intrinsically bursting neurons and their interaction with hyper-ramified microglia. Treating MIA offspring by colony stimulating factor 1 receptor inhibitors induces depletion and repopulation of microglia, and corrects protein expression of the newly identified MIA-associated neuritogenic molecules in microglia, which coalesces with correction of MIA-associated synaptic, neurophysiological, and behavioral abnormalities. Our study demonstrates that maternal immune insults perturb microglial phenotypes and influence neuronal functions throughout adulthood, and reveals a potent effect of colony stimulating factor 1 receptor inhibitors on the correction of MIA-associated microglial, synaptic, and neurobehavioral dysfunctions.
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