Functional analysis of arcuate nucleus astrocytes with feeding disorders

2020 Fiscal Year Final Research Report

• Project/Area Number: 17K00918
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Eating habits
• Research Institution: Hamamatsu University School of Medicine
• Principal Investigator: Mutoh Hiroki 浜松医科大学, 医学部, 助教 (60443040)
• Project Period (FY): 2017-04-01 – 2021-03-31
• Keywords: 摂食障害 / 発育不良 / 神経細胞 / アストロサイト / CaMK2

Outline of Final Research Achievements

CNPY3 and CaMK2β were identified through genetic analysis of patients with neurological diseases and growth failure, and then their functional analysis was performed by generating the mouse models as a feeding disorder.
CNPY3 KO mice have been found to be a mouse model of disease with growth failure and neurological disorders such as schizophrenia and autism. CNPY3 is further investigated as a novel molecule involved in feeding behaviour, because its expression or function in the brain is completely unknown.
CaMK2β mutation mice are also found to be growth failure. As CaMK2β is specifically expressed in neurons, we are conducting electrophysiological studies to understand how patient mutations in CaMK2β alter the activity of AgRP and POMC neurons that control feeding behaviour.

Free Research Field

神経科学

Academic Significance and Societal Importance of the Research Achievements

摂食障害はメタボリックシンドロームを引き起こすだけでなく、様々な精神疾患を誘発する大きな健康問題である。これまでの研究により、神経細胞やグリア細胞、さらにホルモンなど摂食行動に関わるメカニズムは少しずつ解明されているが、摂食障害・発育不良などを引き起こす詳細な研究、または障害により神経疾患が誘発されるメカニズムは明らかにされていない。
本研究課題において、摂食行動に関与する新規の分子を詳しく機能解析することにより、摂食障害を治療する新たな薬剤開発や治療法につながることが期待される。