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2014 Fiscal Year Final Research Report

Functional characterization of putative mechanoelectrical transducer channel proteins using knockout mice.

Research Project

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Project/Area Number 23390399
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurophysiology / General neuroscience
Research InstitutionNagoya City University

Principal Investigator

UGAWA SHINYA  名古屋市立大学, 医学(系)研究科(研究院), 教授 (20326135)

Co-Investigator(Kenkyū-buntansha) KITAMURA Ken  東京医科歯科大学, その他部局等, 教授 (90010470)
NOGUCHI Yoshihiro  信州大学, 医学部, 教授 (50282752)
MURAKAMI Shingo  名古屋市立大学, 大学院医学研究科, 教授 (80157750)
UEDA Takashi  名古屋市立大学, 大学院医学研究科, 准教授 (90244540)
KAJITA Kenji  名古屋市立大学, 大学院医学研究科, 研究員 (80381820)
SAKUMA Eisuke  名古屋市立大学, 大学院医学研究科, 講師 (90295585)
Research Collaborator KROS Corne  University of Sussex, UK, Dr.
Project Period (FY) 2011-04-01 – 2015-03-31
Keywords酸感受性イオンチャネル / メカノセンサー / 有毛細胞 / 難聴 / ノックアウトマウス / ABR / DPOAE / ASIC1b
Outline of Final Research Achievements

We investigated whether ASIC1b located at the ankle regions of stereocilia in mouse auditory hair cells contributes to normal auditory function, using ASIC1b knockout (KO) mice. Transmission electron microscopy demonstrated that the morphology of inner and outer hair cells of adult KO mice were normal. Patch-clamp experiments showed that immature inner and outer hair cells of wild-type mice generated large inward currents in response to acidic stimuli, and those currents were abolished in the presence of amiloride, an inhibitor of ASIC1b. Proton-induced ASIC-like currents were still detected in inner and outer hair cells of age-matched KO mice, suggesting that other ASIC subtypes also exist in mouse auditory hair cells. We are currently conducting ABR (auditory brainstem response) and DPOAE (distortion product otoacoustic emission) tests to evaluate peripheral auditory function in KO mice. Further experiments are needed to elucidate functional roles of ASIC1b in the stereocilia.

Free Research Field

耳科学

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Published: 2016-06-03  

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