Gliogenic LTPはノシセプティブ経路で広く拡散する

M T Kronschläger¹, R Drdla-Schutting¹, M Gassner¹

¹Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Spitalgasse 4, 1090 Vienna, Austria.

Science (New York, N.Y.)

|December 10, 2016

まとめ

科学者たちは脊髄内の新しい形態の長期増強 (LTP) を発見しました脊髄細胞によって誘発され脳脊髄液に広がります痛みの経路に広がった痛みと記憶の痕跡を説明するかもしれません.

科学分野:

神経科学
細胞生物学
痛みに関する研究

背景:

長期増強 (LTP) は学習と記憶に不可欠であり,通常,シナプスの特異性のために同時に前と後シナプスの活動が必要です.
このホモシナプス型LTPメカニズムは脳内で確立されていますが,特定の神経学的現象を完全に説明することはできません.
痛覚経路における説明できない記憶の痕跡と広範な痛みの過敏性は代替的な可塑性メカニズムが存在することを示唆している.

研究の目的:

脊髄における新種のLTPを調査する
この脊髄LTPの誘導体と媒介体を特定する.
痛みの過敏症と記憶におけるこの新しいLTP形態の潜在的役割を調査する.

主な方法:

脊髄の膠質細胞活性化によるLTP誘導
d-セリンと腫瘍死滅因子 (TNF) を含む,拡散可能な細胞外伝達物質の分析.
脳脊髄液 (CSF) 経由の長距離移動を追跡する.

主要な成果:

脊髄で特定された独特の形態のLTPは,gliogenic LTPと呼ばれています.
このLTPを誘発するのは,グリアル細胞の活性化であることが判明した.
D-セリンやTNFのような拡散媒体は,CSFを通って移動し,リモートシナプスに影響を及ぼす,グリオゲン的なLTPを媒介する.

結論:

脊髄のGliogenic LTPは,脳のLTPとは異なる働きをしており,Glial細胞と長距離シグナル伝達を利用しています.
このメカニズムは痛みの経路で観察された記憶の痕跡の潜在的な説明を提供する.
この発見は,グリオゲン性LTPが,広範な痛みの過敏症の根底にある可能性があることを示唆している.

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