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【タイトル】ヒトシナプスの生物学と精神疾患【Title】Thebiology of human synapses and psychiatric disorders 【 講師】林 朗子(理化学研究所 脳神経科学研究センター 多階層精神疾患研究チーム チームディレクター) 【Lecturer】 Akiko Hayashi-Takagi, M.D., Ph.D.（Team Director,Multi-scale Biological Psychiatry, RIKEN Center For Brain Science） 講演60分 + Q&A 30分概要: Can psychiatric disorders bemeaningfully studied in mice? Because psychiatric diagnoses are defined largelyby human subjective experience and complex behaviour, directly reproducing anentire disorder in an animal is neither realistic nor necessarily informative.An alternative is a reverse-translational approach: starting from a clinicallyrecognizable phenotype and asking whether its behavioural features, biologicalbasis and treatment response can be recapitulated in an experimentallytractable model. Using this strategy, we unexpectedly identified abruptbehavioural deterioration during a delayed Go/No-Go task in Chd8+/− andMecp2+/− mice, two genetic models associated with autism. These episodesresembled autistic meltdown, in which sensory or cognitive overloadprecipitates a sudden loss of behavioural control, and exhibited face,construct and predictive validity. We therefore used this phenotype toinvestigate the underlying neural mechanism. Longitudinal two-photon calciumimaging in frontal association cortex revealed a rare population of layer 2/3neurons that remained largely latent before behavioural collapse but abruptlyswitched to burst firing as performance deteriorated. Network topology analysisfurther showed that, immediately before collapse, functional connectionsaccumulated selectively among these neurons, transforming them into a denselyconnected network hub while the surrounding ensemble became disorganised.Importantly, targeted optogenetic inhibition of these meltdown-associated neuronsattenuated the accumulation of erroneous actions, providing causal evidence fortheir contribution to behavioural collapse. These findings illustrate thatmouse models can provide mechanistic insight into psychiatric disorders whenthey are designed through reverse translation around carefully definedphenotypes with face, construct and predictive validity. Rather than askingwhether a mouse can reproduce a psychiatric diagnosis, the critical questionmay be whether an experimentally accessible phenotype faithfully captures aclinically relevant process that can be dissected from network dynamics tocausal circuit mechanisms.日時： 2026年12月8日（木）午後5時00分から午後6時半Date: Dec. 8, 2026 (Thu.) 17:00 – 18:30場所： 基礎研究棟 第2講義室Venue: Lecture Room 2 in the BasicResearch Building 言語： 発表&パワーポイント: 英語Language： Presentation & PowerPoint: English関係専門分野・講座等の連絡担当者：分子細胞学 和氣 弘明（内線 2004）Contact: Molecular Cytology, Division ofHiroaki WAKE (Ext. 2004)＊ 対面講義です。基礎研究棟 第2講義室へお越しください。This is anin-person lecture. Please come to Lecture Room 2 in the Basic ResearchBuilding.＊ 出席は出席カードへの押印をします。特プロ出席カードの該当枠に日付を記入しご持参ください。Attendance will be confirmed by stamping yourattendance card. Please write the date in the appropriate box on your Tokuproattendance card and bring it with you..
📍 基礎研究棟 第2講義室