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Microglia permit climbing fiber elimination by promoting GABAergic inhibition in the developing cerebellum

Author

Listed:
  • Hisako Nakayama

    (Hiroshima University
    Tokyo Women’s Medical University)

  • Manabu Abe

    (Niigata University
    Niigata University)

  • Chie Morimoto

    (Hiroshima University
    Hiroshima University)

  • Tadatsune Iida

    (University of Tokyo)

  • Shigeo Okabe

    (University of Tokyo)

  • Kenji Sakimura

    (Niigata University
    Niigata University)

  • Kouichi Hashimoto

    (Hiroshima University)

Abstract

Circuit refinement during postnatal development is finely regulated by neuron–neuron interactions. Recent studies suggest participation of microglia in this process but it is unclear how microglia cooperatively act with neuronal mechanisms. To examine roles of microglia, we ablate microglia by microglia-selective deletion of colony-stimulating factor 1 receptor (Csf1r) by crossing floxed-Csf1r and Iba1-iCre mice (Csf1r-cKO). In Csf1r-cKO mice, refinement of climbing fiber (CF) to Purkinje cell (PC) innervation after postnatal day 10 (P10)–P12 is severely impaired. However, there is no clear morphological evidence suggesting massive engulfment of CFs by microglia. In Csf1r-cKO mice, inhibitory synaptic transmission is impaired and CF elimination is restored by diazepam, which suggests that impairment of CF elimination is caused by a defect of GABAergic inhibition on PCs, a prerequisite for CF elimination. These results indicate that microglia primarily promote GABAergic inhibition and secondarily facilitate the mechanism for CF elimination inherent in PCs.

Suggested Citation

  • Hisako Nakayama & Manabu Abe & Chie Morimoto & Tadatsune Iida & Shigeo Okabe & Kenji Sakimura & Kouichi Hashimoto, 2018. "Microglia permit climbing fiber elimination by promoting GABAergic inhibition in the developing cerebellum," Nature Communications, Nature, vol. 9(1), pages 1-15, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05100-z
    DOI: 10.1038/s41467-018-05100-z
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