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神経ペプチド Tac2は,慢性的な社会的孤立ストレスによって引き起こされる分散した脳状態を制御する
Moriel Zelikowsky1, May Hui1, Tomomi Karigo1
1Division of Biology and Biological Engineering 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
Cell
|May 19, 2018
まとめ
慢性的な社会孤立ストレス (SIS) は,タキキニン2 (Tac2) /ニューロキニンB (NkB) を脳全体で向上させることでマウスの行動を変化させます. NkB受容体 (Nk3R) を阻害することで,これらの効果は逆転し,治療の可能性を示唆した.
科学分野:
- 神経科学
- 行動科学
- 分子生物学
背景:
- 慢性的な社会的孤立は人間に重大な心理的苦痛をもたらすが,その根底にある神経機構は完全に理解されていない.
- 社会的孤立の神経生物学を理解することは 効果的な介入の開発に不可欠です
研究 の 目的:
- マウスにおける慢性的な社会的孤立ストレス (SIS) によって引き起こされる行動変化の神経基礎を調査する.
- SISの効果を媒介するタキニン2 (Tac2) /ニューロキニンB (NkB) システムの役割を調査する.
主な方法:
- マウスにおける社会的孤立ストレス (SIS) の誘導は,期間が異なる (24時間対2週間).
- ニューロキニン3受容体 (Nk3R) 抗剤の全身投与
- NkB発現と放出の強化 グループに収容されたマウスで
- 複数の脳領域における Tac2/NkB機能の複合分析
主要な成果:
- 2週間のSISは 24時間ではなく 行動の変化と脳全体の Tac2/NkBの上昇を引き起こしました
- Nk3Rアンタゴニストの投与は,SISによって引き起こされるほとんどの行動変化を予防しました.
- 攻撃性を促進し 防御的行動を変化させた
- Tac2/NkBとNk3Rは,異なるSIS誘発の行動変化を媒介する地域特有の役割を示した.
結論:
- Tac2/NkBシグナリングは慢性的な社会的孤立ストレスに対する行動的および神経的適応の重要な媒介です.
- Tac2/NkBシステムは,SISへの応答を調整するために,複数の脳領域に分散的に作用します.
- Nk3Rアンタゴニストは,社会的孤立に関連した状態に対する有望な治療戦略です.
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