Immunohistochemical study on the vestibular nervous system in senescence accelerated mouse

加速衰老小鼠前庭神经系统的免疫组织化学研究

• 批准号: 03670804
• 负责人: SHINKAWA Hideichi
• 金额: $ 1.28万
• 依托单位: Hirosaki University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1993
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670804/
• 关键词: 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

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.

用免疫细胞化学方法观察了加速衰老小鼠（SAM）前庭神经节内钙结合蛋白（calbindin）阳性和阴性细胞的变化。钙结合蛋白的免疫反应在larfe神经节细胞，而大多数小神经节细胞显示没有免疫反应。钙结合蛋白阴性神经节细胞，这是相对较小的尺寸，在SAMP/1（加速衰老pron）的数量减少。这些结果与显示较高钙结合蛋白的神经元可能对变性更具抵抗力的事实一致。钙结合蛋白阴性细胞数量的减少可能是由于衰老过程中钙介导的细胞毒性事件，并且可能是年龄相关的失衡的原因之一。