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首页> 外文期刊>American Journal of Translational Research >Decreased levels of superoxide dismutase in inner pillar cells contribute to ribbon synapse impairment in presbycusis
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Decreased levels of superoxide dismutase in inner pillar cells contribute to ribbon synapse impairment in presbycusis

机译：内柱细胞中超氧化物歧化酶水平的降低导致老年性耳聋丝带突触受损

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Objective: To determine if decreased Cu/Zn superoxide dismutase (SOD1) levels in inner pillar cells is associated and diminished inner hair cell ribbon synapse plasticity in presbycusis. Methods: We evaluated the auditory brainstem responses (ABRs) of 2-, 5-, 6-, and 7-month-old C57BL/6J mice. ABRs were obtained using clicks and 4-, 12-, and 32-kHz tone bursts. Cochleae were collected immediately after audiometric assessment for Western blot analysis. The inner and outer hair cells and the inner hair cell ribbon synapses were separately counted. Frozen tissue sections were exposed to immunofluorescent staining for examine of SOD1 expression in the cochlea. Results: ABR thresholds were elevated in the 6- and 7-month groups. The maximal elevation was detected at 32 kHz. Distortion product otoacoustic emission amplitudes decreased in the mice at 5 months. SOD1 levels in the cochlea decreased as the mice aged. A reduction of SOD1 in the inner pillar cells was detected. Hair cell counting showed an apparent decrease in OHCs from 6 months onwards. The mean number of ribbon synapses was 17.2 ± 1.4, 17.7 ± 2.74, 12.8 ± 0.95, and 9.7 ± 3.08 in the 2-, 5-, 6-, and 7-month groups, respectively. This number significantly decreased with increasing age (P < 0.05). Conclusion: Our study revealed that age-related hearing loss (ARHL) of C57BL/6J mice was caused by multi-site degeneration in the cochlea. Decreased expression of SOD1 in the cochlea is consistent with changes in the hearing threshold. Decreased SOD1 levels in the inner pillar cells may lead to diminished basilar membrane vibration and a reduction in the number of ribbon synapses, which plays an essential role in age-related hearing loss (ARHL).
机译：目的：确定老年柱状细胞内柱状细胞中铜/锌超氧化物歧化酶（SOD1）含量降低是否与内毛细胞带状突触可塑性降低相关联，以及是否减弱。方法：我们评估了2、5、6和7个月大的C57BL / 6J小鼠的听性脑干反应（ABR）。使用咔嗒声和4、12和32 kHz音调突发获得ABR。听力测定后立即收集耳蜗用于蛋白质印迹分析。内部和外部毛细胞和内部毛细胞带状突触分别计数。将冷冻的组织切片暴露于免疫荧光染色以检查耳蜗中SOD1的表达。结果：6个月和7个月组的ABR阈值升高。在32 kHz处检测到最大仰角。在5个月时，小鼠的畸变产物耳声发射幅度降低。随年龄增长，耳蜗中的SOD1水平下降。检测到内部柱状细胞中SOD1的减少。从6个月起，毛细胞计数显示OHC明显减少。在2个月，5个月，6个月和7个月组中，带状突触的平均数分别为17.2±1.4、17.7±2.74、12.8±0.95和9.7±3.08。随着年龄的增长，这个数字显着下降（P <0.05）。结论：我们的研究表明C57BL / 6J小鼠的年龄相关性听力损失（ARHL）是由耳蜗的多部位变性引起的。耳蜗中SOD1的表达减少与听力阈值的变化一致。内部柱状细胞中SOD1水平的降低可能会导致基底膜振动的减少和色带突触数量的减少，这在与年龄有关的听力损失（ARHL）中起着至关重要的作用。

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