| Project/Area Number |
09557113
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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 | 展開研究 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | HIROSAKI UNIVERSITY |
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Principal Investigator |
SEKIYA Tetsuji Hirosaki University, School of Medicine, Department of Neurosurgery, associate professor, 医学部, 助教授 (70154656)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Shigeharu Hirosaki University, School of Medicine, Department of Neurosurgery, professor, 医学部, 教授 (30004708)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1999: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | animal model / cochlear nerve / nerve degeneration / COCHLEAR NERVE / NERVE DEGENERATION / Experimental model / NERVE COMPRESSION / NERVE REGENERATION / COMPUTER SYSTEM |
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| Research Abstract |
In the available in vivo experimental models for cochlear neuronal degeneration, the peripheral (hair-cell side) process of the cochlear nerve has been injured in order to induce neuronal degeneration. However, there has been no dependable experimental model in which cochlear neuronal degeneration begins from the central (brainstem side) process. This lack of a central process injury model has probably been due to the experimental difficulties that had to be overcome in order to reproducibly and selectively injure the central process of the cochlear neurons while maintaining the patency of the internal auditory artery in small experimental animals such as rats. Using rats, we first developed a central process injury model in which the reduction of the spiral ganglion cells due to retrograde degeneration of cochlear neurons can be quantitativery evaluated. In our experimental model, the cochlear nerve was compressed and injured by a compression-recording (CR) electrode placed at the internal auditory meatus. First, the cochlear nerve was compressed until the compound action potentials of the cochlear nerve became flat, and then the CR electrode was advanced by various compression speeds (5, 10, or 200 μ m/sec) to reach the same depth (400μm). In our model, therefore, the reduction of the spiral ganglion cells was caused compression-speed-dependently. This method made it possible to produce compression injury to the cochlear nerve without evidence of damage to the blood supply to the cochlea via the internal auditory artery. This model gives us the means to obtain knowledge that was previously impossible to derive from the peripheral process injury models.
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