| Project/Area Number |
08457356
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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 |
Cerebral neurosurgery
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| Research Institution | Hirosaki University |
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Principal Investigator |
SEKIYA Tetsuji Hirosaki University Scool 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 Scool of Medicine, Department of Neurosurgery, professor, 医学部, 教授 (30004708)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1997: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1996: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | cochlear nerve / nerve compression / nerve degeneration / NERVE REGENERATION / NERVE CEGENERATION |
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| Research Abstract |
Although loss of hearing due to cochlear nerve degeneration has long been regarded as a sort of irreversible process to which no feasible measures have been available, recent molecular experimental studies such as the trials of neurotrophins gene therapy gradually make such view obsolete. In in vivo models used for such investigations, the peripheral (hair-cell side) process of the cochlear nerve is injured to induce cochlear nerve degeneration, but there has been no dependable experimental model in which cochlear nerve degeneration begins from the central (brainstem side) process. We first developed a central process injured model in which cochlear nerve degeneration resulted can be quantitatively evaluated. Using this model, we investigated the efficacy of various neurothophins, such as brain derived neurotrophic factor (BDNF) and neurotrophin 3 (NT3) on injured cochlear nerve. So far we have not detected any effects of these factors to prevent cochlear nerve degeneration. These results are different from those from in vitro experiments. Such difference may be derived at least partly from the difference of injury sites, namely peripheral process or central process. Having a central process injured model, the tools to investigate cochlear nerve degeneration are first completed because cochlear nerve degeneration could be thoroughly investigated not only from the peripheral but also from the central side. Our experimental model may give us the knowledge that could not obtain only by the peripheral process injured models. This may become a basic and useful technique for well-controlled scientific research on cochlear nerve pathologies in the future.
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