Analysis of the kinocilia influence in the cochlea outer hair cells

由于C3 H/HeJ小鼠耳蜗外毛细胞动纤毛中存在瘦素受体，我们分析了瘦素受体敲除的Lepr db/db小鼠，其已知为糖尿病模型。DPOAEs组ABR阈值与对照组相比基本相同，但有早期衰减，其听力损失的责任部位可能是外毛细胞。无静纤毛移位，无毛细胞束转化，但胞质内有PAS染色异常的毛囊，表明DPOAE衰减是由于外毛细胞体的紊乱而非静纤毛功能障碍所致。而瘦素受体完整高血糖状态的C3 H/HeJ小鼠，ABR阈值和DPOAE与对照组相比无明显变化，未见胞浆内PAS染色异常的滤泡。结论：外毛细胞运动纤毛缺失与细胞质异常有关，仅在单纯高血糖状态下无影响。

Because C3H/HeJ mice have leptin receptor in their cochlear outer hair cell kinocilia, we analyze leptin receptor knock out Lepr db/db mice, which were known to model of diabetes mellitus. ABR thresholds were proximately same but accepted early attenuation in DPOAEs compared with control one, the responsible part of their hearing loss was regarded as outer hair cells. There were no stereocilia displacement and no hair cell bundle transformation but abnormal PAS stained follicles in cytoplasm, these meant DPOAEs attenuation were due to outer hair cell body disorder rather than stereocilia disfunction. On the other hand, in leptin receptor intact hyperglycosemia state C3H/HeJ mice, ABR thresholds and DPOAEs were proximately same compared with control one and abnormal PAS stained follicles in cytoplasm were never seen these mice. In conclusion, Absence of outer hair cell kinocilia were related to cytoplasmic abnormality and there ware no affection only in a simple hyperglycosemia state.