Microglia contact induces synapse formation in developing somatosensory cortex

Akiko Miyamoto, Hiroaki Wake, Ayako Wendy Ishikawa, Kei Eto, Keisuke Shibata, Hideji Murakoshi, Schuichi Koizumi, Andrew J. Moorhouse, Yumiko Yoshimura and Junichi Nabekura ()
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Akiko Miyamoto: National Institute for Physiological Sciences
Hiroaki Wake: National Institute for Physiological Sciences
Ayako Wendy Ishikawa: The Graduate School for Advanced Study
Kei Eto: National Institute for Physiological Sciences
Keisuke Shibata: Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development
Hideji Murakoshi: Precursory Research for Embryonic Science and Technology, Japan Science and Technology Agency
Schuichi Koizumi: Core Research for Evolutional Science and Technology, Japan Agency for Medical Research and Development
Andrew J. Moorhouse: School of Medical Sciences, The University of New South Wales
Yumiko Yoshimura: The Graduate School for Advanced Study
Junichi Nabekura: National Institute for Physiological Sciences

Nature Communications, 2016, vol. 7, issue 1, 1-12

Abstract: 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 Ca2+ 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.

Date: 2016
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DOI: 10.1038/ncomms12540

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