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演題詳細

Oral

細胞移動、層・神経核の形成
Cell Migration and Layer/Nuclear Formation

開催日 2014/9/12
時間 16:00 - 17:00
会場 Room J(313+314)
Chairperson(s) 見学 美根子 / Mineko Kengaku (京都大学 物質-細胞統合システム拠点 / Instituete for Integrated Cell-Material Sciences(iCeMS), Kyoto University, Japan)
前田 信明 / Nobuaki Maeda (公益財団法人東京都医学総合研究所神経回路形成プロジェクト / Neural Network Project, Tokyo Metropolitan Institute of Medical Science, Japan)

発生期大脳皮質での新生ニューロン移動制御におけるサブプレート層の役割
The subplate layer plays critical roles in the radial neuronal migration in the developing mouse neocortex

  • O2-J-4-2
  • 丸山 千秋 / Chiaki Maruyama:1 岡本 麻友美 / Mayumi Okamoto:2 岡戸 晴生 / Haruo Okado:3 前田 信明 / Nobuaki Maeda:1 
  • 1:東京都医学総合研・神経回路 / Neural Network, Tokyo Metropol Inst Med Sci, Japan 2:名大院・医・細胞生物 / Dept Anat Cell Biol, Nagoya Univ Grad Sch Med, Aichi, Japan 3:東京都医学総合研・神経細胞分化 / Neuronal Dev, Tokyo Metropol Inst Med Sci, Japan 

During the developmental formation of 6-layered neocortical structure, newborn neurons depart the ventricular zone and migrate toward the pial surface. In this step, there are two different migration modes: multipolar migration, and locomotion. At a middle stage of cortical development, newly differentiated postmitotic neurons show multipolar shape (MP), and move non-radially in the intermediate zone (multipolar migration). When these multipolar neurons pass through the subplate layer (SP), they show dynamic morphological changes and adopt bipolar shape (BP). Then, they migrate toward the pial surface (locomotion). Many KO mice with radial migration defects show abnormal MP-BP conversion at the SP, suggesting that the interaction between migrating neurons and the SP plays critical roles in this change in neuronal polarity.
The SP contains subplate neurons, extracellular matrix components and newly extended axons of premature glutamatergic and GABAergic neurons. Our present working hypothesis is that MP neurons receive certain signals from the SP to change their morphology and migration mode. To test our hypothesis, we are analyzing the interaction between migrating young neurons and SP in many aspects. In this context, we examined neuronal activity of subplate neurons by Ca(2+)-imaging using GCaMP3, and observed that they exhibited calcium oscillations at E15
Moreover, we found that suppression of neuronal activities of subplate neurons by electroporation of inward-rectifier potassium ion channel Kir2.1 led to the impairment of radial migration. This suggests that neuronal activity of SP neurons is critical for this step. We also found that immature leading processes of migrating neurons exhibited spiral shape transiently in the SP just before starting locomotion. We examined this structure using in utero electroporation and immunostaining to explore its biological meaning for the change of migration mode.
Time-lapse imaging of the interaction between RFP-labeled migrating neurons and GFP-labeled SP neurons will also be presented.

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