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演題詳細

Oral

幹細胞、ニューロンとグリアの分化 2
Stem Cells, Neuronal and Glial Production/Differentiation 2

開催日 2014/9/12
時間 15:00 - 16:00
会場 Room J(313+314)
Chairperson(s) 榎本 秀樹 / Hideki Enomoto (神戸大学大学院医学研究科 生理学・細胞生物学講座 神経分化・再生分野 / Department of Physiology and Cell Biology, Graduate School of Medicine, Kobe University, Japan)
小曽戸 陽一 / Yoichi Kosodo (川崎医科大学 解剖学 / Department of Anatomy, Kawasaki Medical School, Japan)

生後初期 SVZ にニューロン新生とオリゴデンドロサイト新生を促進する活性化ミクログリア集団が存在する
Discovery of the population of activated microglia which enhance neurogenesis and oligodendrogenesis in the early posnatal subventricuar zone

  • O2-J-3-2
  • 佐藤 薫 / Kaoru Sato:1 重本-最上 由香里 / Yukari Shigemoto-Mogami:1 干川 和枝 / Kazue Hoshikawa:1 Goldman James E / James E Goldman:2 関野 祐子 / Yuko Sekino:1 
  • 1:国立医薬品食品衛生研究所 / NIHS, Japan 2:Columbia Univ.. USA / Dept Pathol, Cell Biol, Columbia Univ, USA 

CNS microglia have long been considered as resident immune cells, which are activated in response to pathological events. However, increasing evidence suggests that they also have physiological roles in the development of the normal central nervous system (CNS). In this study, we found large numbers of activated microglia in the forebrain subventricular zone (SVZ) of the rat from P1 to P10. Pharmacological suppression of the activation by minocycline, which produces a decrease in levels of a number of proinflammatory cytokines, i.e., IL-1β, IL-6, TNF-α, and IFNγ, significantly inhibited neurogenesis and oligodendrogenesis in the SVZ. In vitro neurosphere assays reproduced the enhancement of neurogenesis and oligodendrogenesis by activated microglia. Interestingly, any single function-blocking antibody to IL-1β, IL-6, TNF-α, or IFN-γ, did not change the effects of activated microglia on neurogenesis and oligodendrogenesis, however, the effects were significantly suppressed by a mixture of all of these function-blocking antibodies. These results suggest that activated microglia accumulate in the early postnatal SVZ and that they enhance neurogenesis and oligodendrogenesis via complementary effects of released cytokines.

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