Zheng X Y, Ding D L, McFadden S L, Henderson D
Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 14214, USA.
Hear Res. 1997 Nov;113(1-2):76-88. doi: 10.1016/s0378-5955(97)00127-5.
The role of the inner hair cells (IHCs) in generating the cochlear summating potentials (SP) was assessed by measuring SP, cochlear nerve action potentials (CAP), cochlear microphonics (CM) and 2f1-f2 distortion product otoacoustic emissions (DPOAEs) in 15 chinchillas with either acute chemical de-afferentation, accomplished by applying kainic acid to the round window, or surgical de-afferentation and basal IHC loss, which developed within two months after sectioning the auditory nerve. In the auditory nerve sectioned ears, type I ganglion cells disappeared whereas most, if not all, type II ganglion cells were still present. Histological analysis of surface preparations and sections through the modiolus verified the de-afferentation in both models and showed a large IHC loss at the base of the cochlea in the ears with the auditory nerve sectioned while other structures of the cochlea remained intact. Unoperated (left) ears of 9 animals served as controls. CM and DPOAEs were normal in all ears whereas the CAP was substantially depressed in de-afferented ears. Comparisons among the SP input-output functions suggest that (1) the IHCs are the major generator of SP recorded from the round window in chinchilla, in particular at low to moderate stimulus levels, (2) the SP recorded from the round window largely reflects the responses from hair cells at the base of the cochlea, and (3) kainic acid results in an increase of SP amplitude to high-level stimuli whereas the SP to low- to moderate-level stimuli remains in the normal range.
通过测量15只龙猫的耳蜗总和电位(SP)、耳蜗神经动作电位(CAP)、耳蜗微音电位(CM)和2f1-f2畸变产物耳声发射(DPOAE),评估了内毛细胞(IHC)在产生耳蜗总和电位中的作用。这些龙猫分别经历了两种处理:一种是通过向圆窗施加 kainic 酸实现急性化学去传入,另一种是在切断听神经后两个月内出现的手术去传入和基底 IHC 损失。在切断听神经的耳朵中,I 型神经节细胞消失,而大多数(如果不是全部)II 型神经节细胞仍然存在。通过对蜗轴表面标本和切片的组织学分析,证实了两种模型中的去传入情况,并显示在切断听神经的耳朵中,耳蜗底部有大量 IHC 损失,而耳蜗的其他结构保持完整。9只动物未手术的(左)耳作为对照。所有耳朵的CM和DPOAE均正常,而去传入耳朵中的CAP则显著降低。对SP输入-输出函数的比较表明:(1)在龙猫中,IHC是从圆窗记录到的SP的主要产生者,特别是在低至中等刺激水平时;(2)从圆窗记录到的SP在很大程度上反映了耳蜗底部毛细胞的反应;(3)kainic 酸导致对高电平刺激的SP幅度增加,而对低至中等电平刺激的SP仍保持在正常范围内。