青の心臓のギャングリオンにおけるインパルスブロックは,シナプス組織の変化における部分的デナーベーションと似ていない
Science (New York, N.Y.)
|October 6, 1978
まとめ
の心臓神経の外科的脱皮は,残った神経がシナプス結合を再編成することを引き起こします. この再編成は,神経活動の欠如によるものではなく,むしろ神経が消去された神経の物理的な存在によるものです.
科学分野:
- 神経科学は神経科学である.
- 心血管生理学 心血管の生理学
背景:
- の心臓のパラシンパティック・インナーベーションは,主に迷走神経によって媒介されます.
- 神経の可塑性とシナプス再編成を理解することは,再生医療と神経学的障害を理解するために不可欠です.
研究 の 目的:
- 青の心臓のシナプス再編成の基礎となるメカニズムを調査する. 部分的デナーベーション後の青の心臓.
- 衝動活動や物理的な神経の存在がシナプス可塑性を誘発するかどうかを判断する.
主な方法:
- カエルの迷走神経の1つを手術で切断することによって,部分的脱皮が達成されました.
- 他の迷走神経の衝動活動は,テトロドトキシンに浸透したマシュットを用いて遮断された.
- シナプスの再編成を観察するために,内静化パターンを分析した.
主要な成果:
- 手術による脱皮は,残った迷走神経による機能的なシナプス結合の重要な再編成につながった.
- テトロドトキシンで神経衝動を遮断すると,同様の再編成が誘発されず,これは単に活動不足によるものではないことを示しています.
- テトロドトキシンで処理された管繊維は,発芽し,神経が消去されたニューロンに新しいシナプスを形成する能力を維持しました.
結論:
- 衝動的な活動だけでなく,神経繊維の物理的な存在が,カエルの心臓のパラシンパシー系におけるシナプス再編成に影響を与えます.
- これは,神経の可塑性やシナプス形成において,活動に依存しないメカニズムの役割を示唆している.
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