| Project/Area Number |
14370546
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Tohoku University |
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Principal Investigator |
KIKUCHI Toshihiko Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (70177799)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIDA Naohiro Tohoku University, Hospital, Research Associate, 医学部附属病院, 助手 (90291260)
KAWASE Tetsuaki Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (50169728)
KOBAYASHI Toshimitsu Tohoku University, Graduate School of Medicine, Professor, 大学院・医学系研究科, 教授 (80133958)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥14,100,000 (Direct Cost: ¥14,100,000)
Fiscal Year 2003: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥11,300,000 (Direct Cost: ¥11,300,000)
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| Keywords | inner ear / herediatary deafness / endocochlear / voltage-gated potassium channel / Kir4.1 / connexin 26 / GLAST / glutamine synthetase / gap junction / pottassium ion / cochlea / sodium channel / Navl.6 / potassium ion / spiral ganglion cell |
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| Research Abstract |
1.Inwardly rectifying potassium channel Kir4.1 was expressed in the stria vascularis, cochlear supporting cell and satellite cells surround spiral ganglion cells. Kir4.1 was also found in the outer sulcus cells. These results suggest that inwardly rectifying Kir4.1 potassium channel in the outer sulcus cells may play a important role in the potassium ion recycling mechanism via gap junctions.
2.In the Brn-4-deficient, Na, K-ATPase-like immunoreactivity in the type II fibrocytes of the cochlear lateral wall was remarkably decreased. Connexin 26 was sparsely distributed among the fibrocytes in the mutant cochlear lateral wall. In contrast, Na, K-ATPase and voltage-gated potassium channel KCNQ1 were abundantly expressed in the marginal cells of the stria vascularis in this mutant. These findings suggest that a dysfunction of fibrocytes in the cochlear lateral wall and an interruption of the K+ ion recycling pathway via gap junctions may result in the depression of endocochlear potential and profound hearing loss in human DFN3 non-syndromic deafness.
3.Intense GLAST-like immunoreactivity was found in the type I fibocytes, type II fibrocytes and the suprastrial fibrocytes in the spiral ligament. Glutamine synthetase was abundantly expressed in the type I fibrocytes, the type II fibrocytes, the type III fibrocytes and the suprastrial fibrocytes in the spiral ligament, the basal cells of the stria vascularis. These results suggest that abundant GLAST and glutamine synthetase in the connective tissue cells in the cochlea may function to maintain the perilymphatic glutamate concentration at a low (nontoxic) level.
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