Department of Otolaryngology-Head & Neck Surgery, The Catholic University of Korea, College of Medicine, St. Mary's Hospital, 505 Banpodong, Seochogu, Seoul 137-701, Republic of Korea.
Neurosci Res. 2011 Nov;71(3):303-10. doi: 10.1016/j.neures.2011.07.1835. Epub 2011 Aug 5.
OBJECTIVES/HYPOTHESIS: Efferent nerves under the outer hair cells (OHCs) play a role in the protection of these cells from loud stimuli. Previously, we showed that cochlear α-synuclein expression is localized to efferent auditory synapses at the base of the OHCs. To prove our hypothesis that α-synuclein deficiency and efferent auditory deficit might be a cause of hearing loss, we compared the morphology of efferent nerve endings and α-synuclein expression within the cochleae of two mouse models of presbycusis.
Comparative animal study of presbycusis.
The C57BL/6J(C57) mouse strain, a well-known model of early-onset hearing loss, and the CBA mouse strain, a model of relatively late-onset hearing loss, were examined. Auditory brainstem responses and distortion product otoacoustic emissions were recorded, and cochlear morphology with efferent nerve ending was compared. Western blotting was used to examine α-synuclein expression in the cochlea.
Compared with CBA mice, C57 mice showed earlier onset high-frequency hearing loss and decreased function in OHCs, especially within high-frequency regions. C57 mice demonstrated more severe pathologic changes within the cochlea, particularly within the basal turn, than CBA mice of the same age. Weaker α-synuclein and synaptophysin expression in the efferent nerve endings and cochlear homogenates in C57 mice was observed.
Our results support the hypothesis that efferent nerve degeneration, possibly due to differential α-synuclein expression, is a potential cause of early-onset presbycusis. Further studies at the cellular level are necessary to verify our results.
目的/假说：毛细胞下传出神经在保护这些细胞免受大声刺激方面发挥作用。先前，我们发现耳蜗α-突触核蛋白表达定位于毛细胞底部的传出听觉突触。为了证明我们的假说，即α-突触核蛋白缺乏和传出听觉缺陷可能是听力损失的原因，我们比较了两种衰老性听力损失小鼠模型耳蜗传出神经末梢的形态和α-突触核蛋白的表达。
衰老性听力损失的动物比较研究。
使用 C57BL/6J（C57）小鼠品系，这是一种众所周知的早期听力损失模型，以及 CBA 小鼠品系，这是一种相对较晚出现听力损失的模型，进行了研究。记录了听觉脑干反应和畸变产物耳声发射，并比较了传出神经末梢的耳蜗形态。使用 Western blot 检测了耳蜗中α-突触核蛋白的表达。
与 CBA 小鼠相比，C57 小鼠表现出高频听力损失更早出现，毛细胞功能下降，尤其是高频区域。C57 小鼠的耳蜗比同年龄的 CBA 小鼠表现出更严重的病理变化，尤其是基底回。在 C57 小鼠的传出神经末梢和耳蜗匀浆中观察到较弱的α-突触核蛋白和突触小泡蛋白表达。
我们的结果支持传出神经退化，可能是由于α-突触核蛋白表达的差异，是早期衰老性听力损失的潜在原因。有必要在细胞水平进一步研究来验证我们的结果。
