Developmental dynamics : an official publication of the American Association of Anatomists · 2024
Developmental cochlear defects are involved in early-onset hearing loss in A/J mice.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kui Lihong, Ma Peng, Zhao Wenben, Yan Bin, Kuang Xiaojing, Li Bo, Geng Ruishuang, Zheng Tihua, Zheng Qingyin
Аннотация
BACKGROUND: A/J mice exhibited a severe hearing loss (HL) at juvenile stage. Up-to-date, studies on HL in A/J mice have mostly focused on the damage or dysfunction of hair cells (HCs), spiral ganglion neurons (SGNs), and stereocilia. We examined A/J mice at the early postnatal stage and found that the damage and the loss of outer hair cells (OHCs) are not severe enough to explain the profound HL observed at this age, which suggests that other cochlear defects may be responsible for HL. To better understand the mechanisms of early-onset HLin A/J mice, we characterized the pathology of the cochlea from postnatal day 3 to day 21.
RESULTS: Our results showed defects in cochlear HC stereocilia and MET channel function as early as 3 days old. We also found abnormal localization and a significant reduction in the number of ribbon synapses in 2-week-old A/J mice. There are also abnormalities in the cochlear nerve innervation and terminal swellings in 3-week-old A/J mice.
CONCLUSION: All of the abnormalities of cochlear existed in the A/J mice were identified in the juvenile stage and occurred before HCs or auditory nerve loss and was the initial pathological change. Our results suggest that developmental defects and subsequent cochlear degeneration are responsible for early-onset hearing loss in A/J mice.
RESULTS: Our results showed defects in cochlear HC stereocilia and MET channel function as early as 3 days old. We also found abnormal localization and a significant reduction in the number of ribbon synapses in 2-week-old A/J mice. There are also abnormalities in the cochlear nerve innervation and terminal swellings in 3-week-old A/J mice.
CONCLUSION: All of the abnormalities of cochlear existed in the A/J mice were identified in the juvenile stage and occurred before HCs or auditory nerve loss and was the initial pathological change. Our results suggest that developmental defects and subsequent cochlear degeneration are responsible for early-onset hearing loss in A/J mice.