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2017 Fiscal Year Final Research Report

Analysis of mTOR signaling in central nervous systems

Research Project

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Project/Area Number 15K06701
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurophysiology / General neuroscience
Research InstitutionThe University of Tokyo

Principal Investigator

Kassai Hidetoshi  東京大学, 大学院医学系研究科(医学部), 准教授 (40403232)

Project Period (FY) 2015-04-01 – 2018-03-31
KeywordsmTOR / トランスジェニックマウス / 小脳
Outline of Final Research Achievements

We aimed to examine mTOR functions in cerebellar Purkinje cells (PCs) by establishing a mouse model of chronically activated mTOR pathway in PCs. Using constitutively active mTOR, we established double transgenic mice line, in which active mTOR mutant is expressed specifically in PCs (L7-mTOR Tg mice). Immunohistochemical analysis showed that PCs of L7-mTOR Tg mice were remarkably hypertrophied and significantly decreased in their number at 4 weeks of age. Molecularly, L7-mTOR Tg PCs were immunopositive for cleaved caspase 3 and HIF-1alpha, suggesting that PC loss by mTORC1 activation may be caused by apoptotic cell death via hypoxic stress signaling. Behavioral analyses revealed that L7-mTOR Tg mice displayed impaired motor coordination, but normal social behavior. Together, these results indicate that mTORC1 signaling is essential for PC survival and cerebellar functions.

Free Research Field

分子遺伝学

URL: 

Published: 2019-03-29  

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