| Co-Investigator(Kenkyū-buntansha) |
KAWASE Tetsuaki Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (50169728)
KATORI Yukio Tohoku University, Hospital, Instructor, 病院・助手 (20261620)
YOSHIDA Naohiro Tohoku University, Hospital, Instructor, 病院・助手 (90291260)
菊地 俊彦 東北大学, 大学院・医学系研究科, 助教授 (70177799)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Research Abstract |
In the mammalian inner ear, there are two independent gap junction systems, the epithelial cell gap junction system and the connective tissue cell gap junction system. Potassium ions, which play a pivotal role in the mechanoelectrical transduction process in the mammalian cochlea, are recycled via these two gap junction systems. Four different connexins, including connexin 26, 30, 31, and 43, have been reported in the mammalian inner ear. Connexin 26, 30, and 43 are distributed in both epithelial and connective tissue cell gap junction systems. In contrast, connexin 31 is localized to the connective tissue cells gap junction system. In the present investigation, we have shown that intense voltage-gated potassium channel Kv3.1b subunit-like immunoreactivity is found in the type I, type III, and type IV fibrocytes in the spiral ligament. Voltage-gated potassium channel, containing Kv3.1b, in the fibrocytes of the cochlear lateral wall may control the intracellular potential and play an important role in regulating the potassium ion recycling mechanism. Immunohistochemical localizations of inwardly rectifying Kir4.1 potassium channels were also studied in the guinea pig cochlea. Kir4.1 potassium channel in the cochlea may play an important role in the K+ recycling pathway. Further investigations are needed in order to elucidate the detailed potassium ion recycling mechanism in the mammalian inner ear.
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