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セロトニン は 拡張 さ れ た 桃体 の 中 で,不安 と 恐れ を 引き起こす 循環 を 引き起こす
Catherine A Marcinkiewcz1, Christopher M Mazzone1,2, Giuseppe D'Agostino3
1Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Nature
|August 25, 2016
まとめ
背面ラフェ核 (5-HT DRN) のセロトニンは,マウスの恐怖と不安の回路を活性化します. この経路は,選択的セロトニン再吸収阻害剤 (SSRI) の早期の有害作用を説明する.
科学分野:
- 神経科学
- 神経生物学
- 行動科学
背景:
- セロトニン (5-ヒドロキシトリプトミン,5-HT) は感情の調節に不可欠です.
- 5-HT媒介による嫌悪状態の根底にある特定の神経回路は不明である.
研究 の 目的:
- 脊髄核セロトニン (5-HT DRN) が恐怖と不安に影響を与える神経回路を解明する.
- セロトニン再吸収阻害剤 (SSRI) の初期有害作用におけるこの回路の役割を調査する.
主な方法:
- マウスモデルを用いて,5-HT DRNがストリア・ターミナリス (BNST) のベッド・ニュークレウスに投射される役割を調査した.
- BNSTにおける5-HT2C受容体 (5-HT2CRs) とコルチコトロピン放出因子 (CRF) の関与を調べた.
- 1型CRF受容体 (CRF1R) 反抗性のSSRI誘発行動への影響を評価した.
主要な成果:
- 5-HT DRNは,BNST (CRFBNST) のCRFニューロンを5-HT2CRsを通じて活性化させます.
- この活性化により BNSTから発する 抗不安物質は抑制され 恐怖や不安を助長します
- CRF1Rアンタゴニズムは,SSRI誘発の嫌悪的な学習を防止し,早期のSSRI副作用におけるその役割を示した.
結論:
- 恐怖と不安を制御する 重要な5HTDRN → CRFBNST回路を特定しました
- この回路は,不安障害に対するSSRI治療中にいくつかの患者で観察された初期の有害事象のメカニズム的説明を提供します.
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