The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.
Layer V cortical neurons require microglial support for survival during postnatal development
Abstract
Neurons require trophic support during neural circuit formation; however, how the cellular milieu contributes to neuronal survival remains unclear. We found that layer V cortical neurons require support from microglia for survival during postnatal development. Specifically, we found that microglia accumulated close to the subcerebral and callosal projection axons in the postnatal brain. Inactivation of microglia by minocycline treatment or transient ablation of microglia in CD11b-DTR transgenic mice led to increased apoptosis, specifically in layer V subcerebral and callosal projection neurons. CX3CR1 in microglia was required for the survival of layer V neurons. Microglia consistently promoted the survival of cortical neurons in vitro. In addition, we identified microglia-derived IGF1 as a trophic factor that maintained neuronal survival. Our results highlight a neuron-glia interaction that is indispensable for network formation during a specific period in the developing brain.
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“Another group showed that these microglia were the predominant source of Igf1 in the early postnatal brain, and Igf1 conditional knockout in microglia affected the health of developing cortical neurons at the same age (Ueno et al., 2013).”
From Complex cell-state changes revealed by single cell RNA sequencing of 76,149 microglia throughout the mouse lifespan and in the injured brain (2018) · cites this paper as Ueno et al., 2013
In the citing paper
“Igf1 is abundantly expressed by microglia during postnatal development, aging or following brain injuries and plays a vital role in promoting neuronal survival (59,63–66).”
From Trem2 promotes anti-inflammatory responses in microglia and is suppressed under pro-inflammatory conditions (2020) · cites this paper as [63]
Citations
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Selective depletion of macrophages reveals distinct, opposing roles during liver injury and repair
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Research works printed but not linked: 1
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Metadata
- Authors
- Ueno, M., Fujita, Y., Tanaka, T., Nakamura, Y., Kikuta, J., Ishii, M., & Yamashita, T.
- Affiliations
- Japan Science and Technology Agency (JP)
- Asahikawa Medical University (JP)
- Immunology Frontier Research Center, The University of Osaka (JP)
- Corresponding author
- Ueno, Masaki
- Yamashita, Toshihide
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2013-03-24
- Volume
- 16
- Issue
- 5
- Pages
- 543-551
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2015412022
- Cited by
- 781
- References
- 50
- Citations by year
- 2026: 41 · 2025: 54 · 2024: 67 · 2023: 61 · 2022: 65 · 2021: 81 · 2020: 82 · 2019: 69 · 2018: 64 · 2017: 52 · 2016: 50 · 2015: 43 · 2014: 41 · 2013: 11
- FWCI
- 26.72
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- microglia, neuronal survival, postnatal brain development, insulin-like growth factor I, trophic support, neuron-glia interactions, CX3CR1, apoptosis, minocycline, callosal projection neurons, microglial activation
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Animals, Newborn, Calcium-Binding Proteins, Cell Survival, Cells, Cultured, Diphtheria Toxin, Embryo, Mammalian, Enzyme Inhibitors, Humans, Insulin-Like Growth Factor I, Mice, Inbred C57BL, Mice, Transgenic, Microfilament Proteins, Nerve Tissue Proteins, Neurons, Visual Cortex, Apoptosis, Microglia, Gene Expression Regulation, Developmental, Coculture Techniques, Receptors, Chemokine, CD11b Antigen, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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