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SUMMARY:【特プロ】ニューロサイエンスコース Neuroscience C
 ourse
DTSTART;VALUE=DATE-TIME:20261208T080000Z
DTEND;VALUE=DATE-TIME:20261208T093000Z
UID:132529796916
DESCRIPTION:【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&amp\;A 30分概要: Can psychiatric disorders bemeaningfully studi
 ed in mice? Because psychiatric diagnoses are defined largelyby human subj
 ective experience and complex behaviour\, directly reproducing anentire di
 sorder in an animal is neither realistic nor necessarily informative.An al
 ternative is a reverse-translational approach: starting from a clinicallyr
 ecognizable phenotype and asking whether its behavioural features\, biolog
 icalbasis and treatment response can be recapitulated in an experimentally
 tractable model. Using this strategy\, we unexpectedly identified abruptbe
 havioural deterioration during a delayed Go/No-Go task in Chd8+/− andMec
 p2+/− mice\, two genetic models associated with autism. These episodesre
 sembled autistic meltdown\, in which sensory or cognitive overloadprecipit
 ates a sudden loss of behavioural control\, and exhibited face\,construct 
 and predictive validity. We therefore used this phenotype toinvestigate th
 e underlying neural mechanism. Longitudinal two-photon calciumimaging in f
 rontal association cortex revealed a rare population of layer 2/3neurons t
 hat remained largely latent before behavioural collapse but abruptlyswitch
 ed to burst firing as performance deteriorated. Network topology analysisf
 urther showed that\, immediately before collapse\, functional connectionsa
 ccumulated selectively among these neurons\, transforming them into a dens
 elyconnected network hub while the surrounding ensemble became disorganise
 d.Importantly\, targeted optogenetic inhibition of these meltdown-associat
 ed neuronsattenuated the accumulation of erroneous actions\, providing cau
 sal evidence fortheir contribution to behavioural collapse. These findings
  illustrate thatmouse models can provide mechanistic insight into psychiat
 ric disorders whenthey are designed through reverse translation around car
 efully definedphenotypes with face\, construct and predictive validity. Ra
 ther than askingwhether a mouse can reproduce a psychiatric diagnosis\, th
 e critical questionmay be whether an experimentally accessible phenotype f
 aithfully 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&amp\;パワーポイント: 
 英語Language：     Presentation &amp\; 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\, Divi
 sion 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. Pl
 ease 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 conf
 irmed by stamping yourattendance card. Please write the date in the approp
 riate box on your Tokuproattendance card and bring it with you..
LOCATION:基礎研究棟　第2講義室
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