Objective To establish the mice model of AHL, to investigate the relationship between AHL and the cytoactive factors of the cochlear hair cells in C57BL/6J mice, and to classify the presbycusis models of the C57BL/6J mice. Methods C57BL/6J mice were divided into 6 experimental groups by age (A: 3 months old(m), B: 8 m, C: 9 m, D: 10 m, F: 17 m, G: 18 m) . The auditory functions mice were measured by auditory brainstem response (ABR) with the stimulus click and toneburst at 6 kHz and 8 kHz. 3 months later, Groups C , G, E and H were tested again for ABR. After ABR testing, the cytoactive of the hair cells was detected by succinate dehydrogenase staining and surface preparation technique(two mice from each group except groups C and G). Results The ABR thresholds elevated with age, and the marked change of the cochlea was the degeneration of the cytoactive of the cochlear hair cells, especially those of the outer hair cells. In the beginning, the basement of the basal membrane suffered from the mitochondrion degeneration in the outer hair cells, then it spread to the top region. Subsequently, the inner hair cells were involved. Conclusion C57BL/6J mouse was a typical animal model for the AHL,and the main change of the cochlea was the degeneration of the hair cells, especially the outer hair cells. Thus, C57BL/6J mice can be used as a suitable animal model for the study of presbycusis.%目的 建立年龄相关性听力损失(age-related hearing loss,AHL)的小鼠动物模型,探讨C57BL/6J小鼠发生AHL与毛细胞活性变化的关系,并初步对C57BL/6J小鼠AHL模型进行AHL的病理分类.方法 按3、8、9、10、17、18月龄段分6组培育C57BL/6J小鼠,各组分别进行听性脑干反应(ABR)测试,对耳蜗毛细胞行琥珀酸脱氢酶染色并作基底膜硬铺片,观察各年龄段小鼠内外毛细胞线粒体琥珀酸脱氢酶的活性.结果 C57BL/6J小鼠随年龄增大,ABR阈值明显增高,在3月龄到9月龄期间ABR平均反应阈值增大比较缓慢,差异无统计学意义;在10月龄时,出现明显的听力下降,平均阈值比3月龄时约高18～23 dB,差异有统计学意义(click:t=5.78,P＜0.01;6 kHz:t =3.93,P＜0.01;8 kHz:t=3.01,P＜0.05).10月龄后小鼠听力继续下降,21月龄时平均阈值比3月龄时增高约60～68 dB,差异有显著统计学意义(click:t=31.23,P＜0.01;6 kHz:t=30.44,P＜0.01;8 kHz:t=33.83,P＜0.01).琥珀酸脱氰酶染色显示,随年龄增大,毛细胞线粒体活性丧失逐渐加重:先是底回外毛细胞活性下降,接着发生活性消失,并逐渐向顶回发展,最后累及内毛细胞.结论 C57BL/6J小鼠具有典型的年龄相关性听力损失特点,其听力下降的原因早期可能主要足外毛细胞及内毛细胞活性的丧失,晚期可能是由于基底膜结构混乱,导致电生理屏障消失,致耳蜗内电位(EP)不能维持而引起.C57BL/6J小鼠可作为感音型老年性听力损失动物模型.
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