| Project/Area Number |
10671581
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Nagasaki University (1999)
Tohoku University (1998) |
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Principal Investigator |
KIKUCHI Toshihiko Department of Otolaryngology, Nagasaki University Hospital, Assistant Professor, 医学部・附属病院, 講師 (70177799)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Fujinobu Department of Otolaryngology, Nagasaki University School of Medicine, Instructor, 医学部, 助手 (00284688)
KOBAYASHI Toshimitsu Department of Otolaryngology, Nagasaki University School of Medicine, Professor, 医学部, 教授 (80133958)
大島 猛史 東北大学, 医学部, 助手 (40241608)
池田 勝久 東北大学, 医学部, 講師 (70159614)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | gap junction / connexin 26 / connexin 31 / Na,K-ATPase / Na-K-Cl cotransporter / endolymphatic potential / Brain-4 / connexin26 |
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| Research Abstract |
1. Immunohistochemical localization of Na,K-ATPase, Na-K-Cl cotransporter, connexin 26 and connexin 31 in the mouse cochlea was studied in the present investigation. Intense Na,K-ATPase-like immunoreactivity was observed in the type II fibrocyte in the spiral ligament, suprastrial fibrocytes and marginal cells in the stria vascularis. The distribution pattern of Na-K-Cl cotransporter was comparable to that of Na,K-ATPase. Connexin 26 was densely distributed among the fibrocytes in the spiral ligament and along the basal cells of the stria vascularis. Connexin 31 was also widely distributed among the fibrocytes in the spiral ligament.
2. The expression of Na,K-ATPase and connexin 26 was studied in the postnatal developmental process of the mouse cochlea. The expression patterns of Na,K-ATPase and connexin 26 in the fibrocytes in the spiral ligament coincided with the rapid growth and maturation of the endolymphatic potential.
3. The endolymphatic potential was significantly decreased in the mutant mouse lacking Brain-4. It is suggested that a dysfunction of fibrocytes and an interruption of the transcellular route via gap junctions can cause a depression of endolymphatic potential in the cochlea of this mutant mouse.
4. The perilymphatic perfusion of long-chain alcohol resulted in the depression of endolymphatic potential.
These results obtained in the present study strongly suggest that the transcellular pathway via gap junctions plays a very important role in the generation of endolymphatic potential in the cochlea.
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