American journal of translational research · 2019
Decreased levels of superoxide dismutase in inner pillar cells contribute to ribbon synapse impairment in presbycusis.
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Wang Haolin, Qin Yuhong, Zhang Yue, Cui Wanming, Lei Yu, Ma Xiaorui, Cheng Yu, Shi Lin, Lv Mei
Аннотация
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).
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).