| Project/Area Number |
03670804
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Hirosaki University |
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Principal Investigator |
SHINKAWA Hideichi Hirosaki University School of Medicine Department of Otolaryngology Professor, 医学部, 教授 (90125584)
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| Co-Investigator(Kenkyū-buntansha) |
USAMI Shin-ichi Hirosaki University School of Medicine Department of Otolaryngology Associate Pr, 医学部, 助教授 (10184996)
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| Project Period (FY) |
1991 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1992: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1991: ¥800,000 (Direct Cost: ¥800,000)
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| Keywords | Vestibule / Vestibular Ganglion / Immunohistochemistry / Senescence Accelerated Mouse / Calcium Binding Protein / calbindin / 前庭神経節 / 細胞骨格蛋白 / 神経伝達物質 / 加齢動物 / シナプトフィジン |
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| Research Abstract |
Changes in calbindin-positive/negative cells in the vestibular ganglion of senescence accelerated mouse (SAM) were examined by means of an immunocytochemical method. Calbindin immunoreactivity was found in the larfe ganglion cells, whereas most small ganglion cells showed no immunoreactivity. Calbindin-negative ganglion cells, which are relatively small in size, were decreased in number in SAMP/1 (accelerated senescence pron). These results are in line with the fact that neurons showing higher calbindin may be more resistant to degeneration. The decrease in number of calbindin-negative cells may be due to calcium-mediated cytotoxic events during aging, and may be one of the causes of age-related dysequilibrium.
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