ネズミの自閉症モデルの社会的欠陥を救出する
Jessica J Walsh1, Daniel J Christoffel1, Boris D Heifets2
1Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford, CA, USA.
Nature
|August 10, 2018
まとめ
ネズミの特定の脳細胞からのセロトニン放出が 双方向的に社会的行動に影響します この発見は,自閉症スペクトル障害に対する新しい治療目標を提供します.
科学分野:
- 神経科学
- 遺伝学
- 行動科学
背景:
- 自閉症スペクトル障害 (ASD) は,社会的相互作用の欠陥によって特徴付けられます.
- 社交性の基礎となる神経メカニズムは ほとんど不明であり,効果的な治療の開発を阻害しています.
研究 の 目的:
- 社会的行動の調節におけるセロトニン (5-HT) 信号伝達の役割を調査する.
- 5HT経路と社交性に対するASDに関連する遺伝子変異の影響を調査する.
主な方法:
- ASDの遺伝的原因である染色体16p11.2の 合成領域に欠陥があるマウスモデルを使用した.
- 背中の5HTニューロンの活動を調節するために光遺伝学を使用した.
- 社会的行動を評価し 5HTニューロンの活動を測定しました
主要な成果:
- 5-HTニューロンの遺伝的消去は 社会的行動に障害をもたらし ニューロンの活動を低下させた.
- 脊髄の5HTニューロンの光遺伝的活性化が これらの社会的欠陥を救った.
- レスキュー効果は,核アクンベンスの5-HT1b受容体の活性化に依存し,それを模倣した.
結論:
- 背面ラフェニューロンからのセロトニンの放出は,アクンベンズ核に作用し,社会的行動の調節に重要な役割を果たします.
- この5HT経路をアキュンベンスの中核に標的にすることは,ASDにおける社会的欠陥に対する新しい治療戦略を提供することができる.
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