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2022 Fiscal Year Final Research Report

Elucidation of the function of BRINP protein that regulates neuronal excitation and inhibition

Research Project

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Project/Area Number 20K07748
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 51030:Pathophysiologic neuroscience-related
Research InstitutionMatsuyama University

Principal Investigator

Kobayashi Miwako  松山大学, 薬学部, 准教授 (30396329)

Co-Investigator(Kenkyū-buntansha) 松岡 一郎  松山大学, 薬学部, 客員教員 (40157269)
Project Period (FY) 2020-04-01 – 2023-03-31
KeywordsBRINP / 精神疾患 / 欠損マウス / 大脳皮質
Outline of Final Research Achievements

Neural-specific family gene, BRINP, exhibits abnormal behaviors analogous to symptoms of human psychiatric disorders due to its deficiency. The BRINP genes were expressed in both excitatory and most inhibitory neurons in the adult mouse cortex. In the brain of BRINP1 or BRINP3-deficient mice, mRNA and protein expressions of neurotransmitter receptors, synapse-associated proteins, protein-associated axonal outgrowth were altered, which may lead to the behavioral abnormalities exhibited by deficient mice. We also found that all BRINPs interact with Rab3 and Rab11, its binding preference differ by combination of BRINP member and G protein activation state of Rab.

Free Research Field

分子神経生物学

Academic Significance and Societal Importance of the Research Achievements

脳の機能性障害である精神疾患は,変性疾患を含む器質性精神障害とは異なり,治療法がある程度確立されているものの,発症の原因についてはよくわかっていない。神経特異的に発現するBRINPファミリー遺伝子を欠損させたマウスはヒト精神疾患の症状と似た行動異常を示し,神経細胞および神経細胞がつくる神経回路の正常な機能に必要な遺伝子やタンパク質の発現が変化していた。今回得られた知見をもとにBRINPタンパク質の分子機能を明らかにすることにより,精神疾患の発症メカニズムの解明,新たな治療法の開発につなげることが期待される。

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Published: 2024-01-30  

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