| Project/Area Number |
26861376
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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 |
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| Co-Investigator(Renkei-kenkyūsha) |
Kamakura Takefumi 大阪大学大学院医学系研究科, 神経細胞生物学, 特任研究員 (30600564)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | TRPV4受容体 / 前庭機能 / 低浸透圧刺激 / 前庭神経節 / TRPV4 / 浸透圧 / メイロン |
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| Outline of Final Research Achievements |
We investigated the expression of transient receptor potential vanilloid (TRPV) 4, a non-selective cation channel, in rat vestibular ganglia (VG) neurons TRPV4 RT-PCR product was amplified from the mRNA of VG neurons. In situ hybridization confirmed that the neurons expressed TRPV4 mRNA. Immunoreactivity for TRPV4 was localized in VG neurons. In Ca2+ imaging experiments in primary cultures of rat VG neurons, 4α-PDD caused an increase in intracellular calcium ion concentration ([Ca2+]i); this increase was almost completely inhibited by ruthenium red, a selective antagonist of TRPV channels. Similarly, hypotonic stimulation induced a significant increase in [Ca2+]i that was blocked by ruthenium red. Our histological and physiological studies reveal that TRPV4 is functionally expressed in VG neurons as an ion channel. TRPV4 in VG neurons might participate in vestibular neurotransmission as an osmoreceptor and/or mechanoreceptor.
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