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発達中の神経筋肉の結界点におけるシュワンン細胞アポトシスは,膠質成長因子によって調節されます
J T Trachtenberg1, W J Thompson
1Department of Zoology, University of Texas, Austin 78712, USA.
Nature
|January 11, 1996
まとめ
新生児の脱神経化は,神経筋の結界点におけるシュワンン細胞死を引き起こし,神経再生を妨げます. 膠質成長因子は,このアポトーシスを防止し,神経系の発達にとって重要なアクソン-シュワーン細胞相互作用を強調します.
科学分野:
- 神経科学は神経科学である.
- 発達生物学 発達生物学について
- 細胞生物学 細胞生物学
背景:
- シュヴァン細胞 (SCs) は,成人哺乳類の神経再生に不可欠であり,軸索の再生を導く.
- デナーバ化された新生児の筋肉の再内接が損なわれ,大人の場合と異なり,軸索の芽生えが欠けています.
研究 の 目的:
- 新生児のシュヴァンン細胞 (SCs) が,成人SCsと比較して,脱皮化に異なった反応をするかどうかを調査する.
- 新生児の神経筋肉の発達におけるアクソン-シュワーン細胞相互作用の役割を調査する.
主な方法:
- 新生ラットの神経筋結節におけるデナーベーションに対するシュヴァン細胞 (SC) 反応を調べた.
- SCアポトーシスに対する膠質成長因子 (GGF) の効果を in vivo で調査した.
主要な成果:
- 新生児のデナーベーションは,ネズミの神経筋肉の交差点におけるシュワン細胞 (SCs) の急速なアポプトシス死を引き起こした.
- 膠質成長因子 (GGF) のインビボ注射は,SCアポトーシスを予防しました.
結論:
- シュヴァン細胞 (SCs) は,発達中の神経の成長を調節する上で重要な役割を果たします.
- アクソン=シュワンの細胞のトロフィック相互作用は,正常な神経筋肉系の発達に不可欠である.
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