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Nat Commun. 2016 Aug 25;7:12540. doi: 10.1038/ncomms12540.

Microglia contact induces synapse formation in developing somatosensory cortex.

Author information

1
Division of Homeostatic Development, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
2
Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development, Tokyo 100-0004, Japan.
3
Department of Physiological Sciences, The Graduate School for Advanced Study, Hayama 240-0193, Japan.
4
Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency, Saitama 102-0076, Japan.
5
Division of Visual Information Processing, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
6
Department of Pharmacology, Graduated School of Medical and Engineering, Yamanashi University, Chuo 409-3898, Japan.
7
Section of Multiphoton Neuroimaging, National Institute for Physiological Sciences, Okazaki 444-8585, Japan.
8
School of Medical Sciences, The University of New South Wales, Sydney, New South Wales 2052, Australia.

Abstract

Microglia are the immune cells of the central nervous system that play important roles in brain pathologies. Microglia also help shape neuronal circuits during development, via phagocytosing weak synapses and regulating neurogenesis. Using in vivo multiphoton imaging of layer 2/3 pyramidal neurons in the developing somatosensory cortex, we demonstrate here that microglial contact with dendrites directly induces filopodia formation. This filopodia formation occurs only around postnatal day 8-10, a period of intense synaptogenesis and when microglia have an activated phenotype. Filopodia formation is preceded by contact-induced Ca(2+) transients and actin accumulation. Inhibition of microglia by genetic ablation decreases subsequent spine density, functional excitatory synapses and reduces the relative connectivity from layer 4 neurons. Our data provide the direct demonstration of microglial-induced spine formation and provide further insights into immune system regulation of neuronal circuit development, with potential implications for developmental disorders of immune and brain dysfunction.

PMID:
27558646
PMCID:
PMC5007295
DOI:
10.1038/ncomms12540
[Indexed for MEDLINE]
Free PMC Article

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