Cellular biological investigation of cochlear function after acoustic trauma in animals models.

• Project/Area Number: 24791814
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Otorhinolaryngology
• Research Institution: Osaka Medical College
• Principal Investigator: Inui Takaki 大阪医科大学, 医学部, 講師 (60465614)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000); Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000); Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: 音響性聴覚障害 / 音響負荷モルモット / 細胞内Ca2+濃度 / 内耳組織障害 / 細胞内Ca2+イオン濃度 / 細胞内カルシウムイオン濃度

Outline of Final Research Achievements

It is known that EP decreases by transient asphyxia, systemic application of high dose furosemide, and acoustic trauma, with simultaneous increase in Ca2+ concentration in endolymph ([Ca]e).
EP was not changed by the endolymphatic perfusion with high Ca2+ artificial endlymph, but decreased by simultaneous injection with ionomycin. These results indicate that the increase in [Ca]e arouse secondary from the decrease in EP, and the cytosolic Ca2+ in the cochlear cells surround endolymph plays an important role in the generation and mediation of EP.