Yamasoba T, Dolan D F, Miller J M
Kresge Hearing Research Institute, The University of Michigan, Ann Arbor 48109-0506, USA.
Hear Res. 1999 Jan;127(1-2):31-40. doi: 10.1016/s0378-5955(98)00178-6.
Hearing loss caused by intense sound exposure can be significantly reduced by pre-exposing subjects to moderate-level acoustic stimuli. This phenomenon occurs in a variety of mammals. We investigated whether sound conditioning provides acquired resistance to acoustic trauma through local mechanisms selectively in the conditioned ears or if systemic mechanisms are involved that would yield contralateral protection in unconditioned ears. Guinea pigs (group I) in which one external ear canal was occluded were exposed to conditioning sound (2-20 kHz, 85 dB SPL, 5 h/day, 10 days). After removing the occlusion, the animals were then subjected bilaterally to intense noise (2-20 kHz, 110 dB SPL, 5 h) 5 days after the last conditioning exposure. Animals without ear canal occlusion were also exposed to the intense sound without conditioning (group II) or following the same conditioning exposure (group III). Intense sound exposure caused significantly greater permanent ABR threshold shifts at all frequencies tested (4, 8, 12, 16 and 20 kHz) in group II than in group III. In group I, the occluded ears showed significantly greater threshold shifts at all frequencies compared to the unoccluded ears. The threshold shifts in the occluded ears in group I were identical to those observed in group II; and the shifts in unoccluded ears in group I were identical to those in group III. Protective effects provided by sound conditioning were almost the same in group III and in the unoccluded ears in group I. The extent of hair cell damage supported the physiological findings. These results indicate that acquired resistance to acoustic trauma provided by sound conditioning is restricted to the cochlea exposed to conditioning sound, suggesting that conditioning protection is mediated primarily by the changes that occur locally within the conditioned cochlea. This animal model, with unilateral external ear canal occlusion during sound conditioning, is useful for studies of the mechanisms of conditioning protection.
通过让受试者预先暴露于中等强度的声学刺激,可以显著降低因强烈声音暴露导致的听力损失。这种现象在多种哺乳动物中都有发生。我们研究了声音预处理是否通过局部机制在经过预处理的耳朵中选择性地提供对声损伤的后天抗性,或者是否涉及全身机制,从而在未经预处理的耳朵中产生对侧保护作用。将一侧外耳道堵塞的豚鼠(第一组)暴露于预处理声音(2 - 20 kHz,85 dB SPL,每天5小时,共10天)。去除堵塞后,在最后一次预处理暴露5天后,对动物双侧施加强烈噪声(2 - 20 kHz,110 dB SPL,5小时)。未堵塞外耳道的动物也暴露于强烈声音,一组未进行预处理(第二组),另一组进行相同的预处理暴露(第三组)。在所有测试频率(4、8、12、16和20 kHz)下,第二组中强烈声音暴露导致的永久性ABR阈值变化显著大于第三组。在第一组中,堵塞的耳朵在所有频率下的阈值变化均显著大于未堵塞的耳朵。第一组中堵塞耳朵的阈值变化与第二组中观察到的相同;第一组中未堵塞耳朵的变化与第三组中的相同。第三组和第一组中未堵塞耳朵的声音预处理提供的保护作用几乎相同。毛细胞损伤程度支持了生理学研究结果。这些结果表明,声音预处理提供的对声损伤的后天抗性仅限于暴露于预处理声音的耳蜗,这表明预处理保护主要是由预处理耳蜗内局部发生的变化介导的。这种在声音预处理期间单侧外耳道堵塞的动物模型,对于研究预处理保护机制很有用。