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活動に依存する転写因子NPAS4は,ドメイン特異的阻害を調節する

Brenda L Bloodgood¹, Nikhil Sharma, Heidi Adlman Browne

¹1] Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA [2] Division of Biological Sciences, University of California San Diego, La Jolla, California 92093, USA [3].

|November 9, 2013

まとめ

ネズミの行動誘発によるNPAS4発現は,CA1ピラミッド神経細胞の抑制シナプスを再配置する. この調節は体内阻害を増加させ, dendritic阻害を減少させ,ニューロンの出力と可塑性に影響を与えます.

科学分野:

神経科学は神経科学である.
分子生物学は分子生物学である.
計算神経科学とは

背景:

阻害性ニューロンは,ピラミッド型ニューロンのシナプス経由でニューラル回路の情報流れを調節する.
ソマティックおよびデンドリティック阻害は,神経の興奮性と可塑性を差異的に制御します.
NPAS4 (NPAS4) は,抑制シナプスの数と機能を調節する活動に依存した転写因子です.

研究の目的:

異なる神経領域における阻害シナプス分布の調整におけるNPAS4のインビボの役割を調査する.
ヒポキャンパスのCA1ピラミッドニューロンにおける体対 dendritic阻害にNPAS4がどのように影響するか解明する.

主な方法:

ネズミのモデルを使って,海馬におけるNPAS4の機能を研究した.
行動主導のNPAS4発現とその抑制シナプス分布への影響を分析した.
これらの効果を媒介する脳由来神経栄養因子 (BDNF) などのNPAS4標的遺伝子の役割を調査した.

主要な成果:

行動主導のNPAS4発現は,CA1ピラミッドニューロンにおける抑制シナプスの再分布を誘発した.
NPAS4は細胞体 (soma) の抑制シナプス数を増加させ,アピカルデンドライトの抑制シナプス数を減少させた.
NPAS4標的遺伝子であるBDNFは媒介者として特定され,特に体内抑制を調節する.

結論:

感覚刺激は,NPAS4誘導を介して,神経抑制の空間的特徴を差異的に制御します.
この空間的再編成は,体内抑制を強化することによって,ニューロンの出力を制限する.
この発見は,NPAS4が阻害を調節することによって,可塑性を許容するデンドリート環境を作り出すことを示唆している.

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