低ミエリン化脳におけるナトリウムチャネル密度は,ミエリン塩基タンパク質の遺伝子消去によって増加する
J L Noebels1, P K Marcom, M H Jalilian-Tehrani
1Department of Neurology, Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030.
Nature
|August 1, 1991
まとめ
シャイバーマウスのミエリン塩基タンパク質の欠如は,軸索の過剰なナトリウムチャネルにつながります. この軸索の可塑性は,ミエリン化が損なわれているにもかかわらず,ニューロンの興奮性と機能を維持するのに役立ちます.
科学分野:
- 神経科学は神経科学である.
- 細胞生物学 細胞生物学
- 分子生物学は分子生物学である.
背景:
- トロフィック要因は,興奮性細胞の成熟過程でイオンチャネル発現を調節する.
- 骨髄膜は軸索のイオンチャネル分布に影響するが,分子信号は不明である.
- シャイバー (shi) ミュータントマウスは,遺伝子の削除により,ミエリン基本タンパク質 (MBP) が欠けています.
研究 の 目的:
- 軸索におけるナトリウムチャネル密度の調節におけるミエリン基本タンパク質 (MBP) の役割を調査する.
- オリゴデンドロサイト-アクソレマの相互作用を媒介する分子信号を決定する.
- ディスミエリン状態における補償メカニズムとしての軸索の可塑性を探求する.
主な方法:
- 骨髄蛋白基本タンパク質遺伝子に欠損したシベラー変異マウスモデルを利用した.
- ミュータントの脳の大口径の繊維経路におけるイオンチャネルトポグラフィーを調べました.
- 中枢神経系の投影ニューロンの機能的興奮性を評価した.
主要な成果:
- Shivererミュータントの脳は,大口径の非ミエリン化アクソンでナトリウムチャネルの有意な過剰を示しています.
- MBPの欠如は,グリアル-アクソン接触だけでなく,アクソナルナトリウムチャネルのダウンレギュレーションに不可欠であるようです.
- 非ミエリン化繊維を持つ成熟ニューロンは,興奮性を維持するためにナトリウムチャネル密度を増加させます.
結論:
- ミエリン基質タンパク質または関連する膠質信号は,軸索のナトリウムチャネル密度を調節するために重要です.
- 軸索の可塑性,特にナトリウムチャネル密度の増加は,ミエリン化の欠如を補償する.
- この可塑性は,シャイバーマウスの軽度の神経学的欠陥を説明し,筋縮性疾患からの回復に関する洞察を提供します.
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