Kirk D L, Patuzzi R B
Physiology Department, University of Western Australia, Nedlands.
Hear Res. 1997 Oct;112(1-2):49-68. doi: 10.1016/s0378-5955(97)00105-6.
After exposure to a loud, non-traumatic low-frequency tone, auditory thresholds are elevated. Thresholds recover to normal in a non-monotonic manner, decreasing rapidly at first before increasing again, until they finally decrease monotonically towards normal. Although the transient elevation of thresholds after the initial improvement was originally called a 'bounce' by Hirsh and Ward (1952), Kemp (1986) suggests that the initial rapid recovery is the oddity: under some conditions a low-frequency tone can produce hypersensitivity in otoacoustic emissions, psychophysical thresholds, and perceived loudness (Kemp's 'bounce') without a later elevation of threshold (Hirsh and Ward's 'bounce'). Kemp also suggested that the transient hypersensitivity was caused by changes in the sensitivity of the active process within the cochlea. We have investigated the origin of this transient hypersensitivity (Kemp's bounce) in guinea pigs, recording cochlear potentials (CM, CAP, SP and EP) and otoacoustic emissions (DPOAEs at f2-f1, 2f1-f2, 2f2-2f1 and 3f1-2f2). Our results indicate that the bounce does not require neural activity, but is probably produced by non-neural cochlear mechanisms, possibly a transient decrease in the permeability of the organ of Corti which produces a small but significant change in standing current through outer hair cells. At least part of these changes, which are reduced as the stimulation frequency increases, and absent above 2 kHz, seem due to a small and transient movement of the cochlear partition towards scala tympani, probably due to a transient osmotic imbalance.
暴露于响亮的、非创伤性的低频音调后，听觉阈值会升高。阈值以非单调的方式恢复到正常水平，起初迅速下降，然后再次上升，直到最终单调下降至正常水平。尽管最初改善后阈值的短暂升高最初被赫什和沃德（1952年）称为“反弹”，但肯普（1986年）认为最初的快速恢复才是异常现象：在某些情况下，低频音调可在耳声发射、心理物理阈值和感知响度方面产生超敏反应（肯普的“反弹”），而随后阈值不会升高（赫什和沃德的“反弹”）。肯普还提出，这种短暂的超敏反应是由耳蜗内主动过程的敏感性变化引起的。我们研究了豚鼠中这种短暂超敏反应（肯普的反弹）的起源，记录了耳蜗电位（CM、CAP、SP和EP）和耳声发射（f2 - f1、2f1 - f2、2f2 - 2f1和3f1 - 2f2频率处的DPOAE）。我们的结果表明，这种反弹不需要神经活动，而可能是由非神经耳蜗机制产生的，可能是柯蒂氏器通透性的短暂降低，这会导致通过外毛细胞的静息电流产生微小但显著的变化。随着刺激频率增加，这些变化至少部分会减小，在2 kHz以上则不存在，这似乎是由于耳蜗隔板向鼓阶的微小且短暂的移动，可能是由于短暂的渗透失衡所致。
