| Project/Area Number |
07671888
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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 | Kansai Medical University |
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Principal Investigator |
KITAJIRI Masanori Kansai Medical University Faculty of Medicine, Assistant Professor, 医学部, 講師 (60161478)
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| Co-Investigator(Kenkyū-buntansha) |
KURIYAMA Hiromichi Kansai Medical University Faculty of Medicine, Research Associate, 医学部, 助手 (90268350)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | gene knockout mice / NMDA receptor / immunohistochemistry / auditory function / 蝸牛 / グルタメイトレセプター / ミュータントマウス |
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| Research Abstract |
There is considerable evidence that the NMDA receptor is a component of excitatory amino acid synapses in the ascending auditory pathway. With the availability of mutant mice defective in NMDAR epsilon1 (epsilon1 mutant mice) and NMDAR epsilon4 (epsilon4 mutant mice), it becomes important to know expression of NMDA receptor in the parent C57/6J wild strain. The distribution of NMDA receptor subunits in the cochlear nucleus (CN) and superior olivary complex (SOC) of the wild mice was therefore examined with nonradioactive in situ hybridization methods. Also, to further investigate the function of the NMDA receptor in the auditory pathway, thresholds before and after noise exposure were examined for wild mice and mutant mice using evoked auditory brainstem response (eABR).
In situ hybridization results showed expression of NMDAR epsilon1 and NMDAR epsilon4 mRNA in major neuronal types of the CN and SOC of the wild mice. Threshold of eABR in the epsilon1 mutant mice was similar to wild mice, and the threshold in epsilon4 mutant mice was elevated signiflcantly. Following exposure to intense sound the thresholds of eABR in epsilon1 mutant mice showed a significant rise and in epsilon4 mutant mice showed no shift.
Results of in situ hybridization suggest that NMDAR epsilon1 and NMDAR epsilon4 are a component of exitatory amino acid synapses in the ascending auditory pathways. Results of eABR support NMDAR epsilon1 is related to synaptic plasticity in the ascending auditory pathways and NMDAR epsilon4 may play a role in development of hearing ability.
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