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Isolation of Cortical Microglia with Preserved Immunophenotype and Functionality From Murine Neonates
Published on: January 30, 2014
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Transient microglial absence assists postmigratory cortical neurons in proper differentiation
Yuki Hattori1,2, Yu Naito3, Yoji Tsugawa4,5,6
1Department of Anatomy and Cell Biology, Graduate School of Medicine, Nagoya University, Nagoya, Japan. ha-yuki@med.nagoya-u.ac.jp.
Nature Communications
|April 4, 2020
Summary
Microglia temporarily leave the developing cortical plate, attracted by CXCL12. Their absence is crucial for proper neuron differentiation and functional circuit formation, as their presence disrupts neuronal maturation.
Area of Science:
- Neuroscience
- Developmental Biology
- Immunology
Background:
- Postmigratory neurons in the developing cortex differentiate within the cortical plate (CP).
- Microglia, immune cells, transiently disappear from the midembryonic CP, but the reasons and consequences are unclear.
Purpose of the Study:
- To investigate the mechanism behind microglial absence from the midembryonic CP.
- To determine the significance of this microglial absence for neuronal development and cortical circuit formation.
Main Methods:
- Utilized in vivo and in vitro models to study microglial migration and neuronal differentiation.
- Analyzed the role of CXCL12 in microglial migration.
- Assessed the impact of microglia-derived factors (IL-6, type I interferon) on neuronal differentiation.
Main Results:
- Microglia migrate out of the midembryonic CP, attracted by CXCL12 from the meninges and subventricular zone.
- Excessive microglial presence in the CP leads to abnormal neuronal differentiation and disturbed gene expression.
- Interleukin 6 and type I interferon secreted by microglia are key mediators of this abnormal differentiation.
Conclusions:
- Microglial "sanctuarization" in the midembryonic CP is essential for precise neuronal differentiation.
- This absence allows neurons to fine-tune molecular expression for proper maturation.
- Ensures the establishment of functional cortical circuits by preventing microglial interference.
