Canlon B
Department of Physiology II, Karolinska Institute, Stockholm.
Scand Audiol Suppl. 1988;27:1-45.
The aim of the present investigation was to determine: 1) the relationship between changes in auditory sensitivity and alterations in stereocilia micromechanics and tectorial membrane morphology after acoustic overstimulation; 2) the rate of growth of a threshold shift in stereocilia following in vitro overstimulation; and 3) if the damaging effects of noise trauma can be reduced by pre-exposure to a low level acoustic stimulus. After exposure to a 1.0 kHz pure tone signal at 105 dB SPL for 72 hours, the threshold of the auditory brainstem response was broadly elevated by approximately 40-50 dB; the inner hair cell stereocilia became less stiff; and morphological alterations were observed in the middle zone of the tectorial membrane. The location of both the stereocilia and tectorial membrane alterations corresponded to the region of the cochlea demonstrating a threshold shift. Following a recovery period from overstimulation, the auditory brainstem response showed some improvement yet a 25 dB threshold shift remained. At this time, swelling of the afferent dendrites beneath the inner hair cells was observed together with scattered outer hair cell loss. Also, the inner hair cell stereocilia regained their normal stiffness characteristics. The in vitro experiments demonstrated that overstimulation reduced the stiffness of the inner and outer hair cell stereocilia bundles. A threshold shift increased systematically with exposure duration and intensity. After 6 minutes of overstimulation, the threshold shift exhibited a plateau whose magnitude was dependent upon the exposure intensity. Stereocilia micromechanics were shown to be dependent on the metabolism of the hair cell. The pre-treatment to a low level acoustic stimulus (81 dB SPL) prior to exposure to a stimulus known to yield a permanent threshold shift resulted in a 20 dB reduction in the threshold shift relative to the group not pre-exposed as well as complete recovery from the threshold shift after 2 months.
1）声学过度刺激后听觉敏感度变化与静纤毛微力学及盖膜形态改变之间的关系；2）体外过度刺激后静纤毛阈值偏移的增长速率；3）预先暴露于低强度声刺激是否能降低噪声性创伤的损伤效应。在暴露于105 dB SPL的1.0 kHz纯音信号72小时后，听觉脑干反应阈值大幅升高约40 - 50 dB；内毛细胞静纤毛的硬度降低；盖膜中间区域观察到形态改变。静纤毛和盖膜改变的位置与耳蜗中出现阈值偏移的区域相对应。过度刺激恢复期后，听觉脑干反应有所改善，但仍存在25 dB的阈值偏移。此时，观察到内毛细胞下方传入树突肿胀以及外毛细胞散在性丢失。此外，内毛细胞静纤毛恢复了其正常的硬度特征。体外实验表明，过度刺激降低了内、外毛细胞静纤毛束的硬度。阈值偏移随暴露持续时间和强度系统性增加。过度刺激6分钟后，阈值偏移呈现出一个平台期，其幅度取决于暴露强度。静纤毛微力学被证明依赖于毛细胞的代谢。在暴露于已知会产生永久性阈值偏移的刺激之前，预先给予低强度声刺激（81 dB SPL），相对于未预先暴露的组，阈值偏移降低了20 dB，并且2个月后阈值偏移完全恢复。
