| Project/Area Number |
17K16912
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Osaka University |
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Principal Investigator |
OHATA KAZUYA 大阪大学, 医学部附属病院, 医員 (10778632)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | セロトニン / 内耳障害 / シスプラチン / 外有毛細胞 / 聴覚 |
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| Outline of Final Research Achievements |
We found that 5-HT3A receptors were expressed in efferent neurons which innervated outer hair cells in coshlear. Moreover, thresholdshift in 5-HT3A receptor defficient mice administered with CDDP in ABR or DPOAE were smaller tha that in wild-type mice.
Meanwhile, 5-HT3A receptor defficient mice showed weaker MOC function and severer cochlear damage than wild-type mice after noise exposure. These results showed that the 5-HT3A receptor is essential for normal MOC function and 5-HT3A receptor deficient leads to weaker MOC function, which results in severer cochlear damage after acoustic trauma.
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| Academic Significance and Societal Importance of the Research Achievements |
内耳障害と5-HT3A受容体の関連については今まででほとんど報告がなく、今回の知見は非常に学術的意義が大きいものと考えられる。さらに、薬理学的検討にて5-HT3A受容体阻害薬の投与により、シスプラチンの内耳障害を軽減可能であったことは学術的および社会的観点からも意義深いものと思われる。なぜならば、通常抗ガン剤としてシスプラチンを用いる際に制吐剤として5-HT3受容体阻害薬が用いられている。我々の知見と併せて考えると、この5-HT3受容体阻害薬が内耳障害も予防できていた可能性がある。
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