A study on ASD-related model animals

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K07362
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 49010:Pathological biochemistry-related
• Research Institution: Gunma University (2021-2022); Tokyo Women's Medical University (2020)
• Principal Investigator: Miyoshi Goichi 群馬大学, 大学院医学系研究科, 教授 (20519326)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 自閉スペクトラム症 / 抑制回路発達 / 神経発達障害 / 生後発達

Outline of Final Research Achievements

We found that increased or decreased FoxG1 expression in both excitatory and inhibitory neurons results in ASD-related circuit and social behavior deficits in our mouse models. The second postnatal week is the critical period when regulation of FoxG1 expression is required to prevent subsequent ASD-like social impairments. Transplantation of GABAergic precursor cells prior to this critical period and reduction in GABAergic tone via Gad2 mutation ameliorates and exacerbates circuit functionality and social behavioral defects, respectively.

Free Research Field

抑制回路発達と発達障害

Academic Significance and Societal Importance of the Research Achievements

自閉症モデル動物において、発達期脳内回路にどのような変化が生じることが要因となり発症や治療が進むのかを解明することは、自閉スペクトラム症研究のブレイクスルーになると考えられる。