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Examining the Role of the Tectorial Membrane in Otoacoustic Emission Generation

机译:检查扭膜膜在耳声发射产生的作用

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A mouse lacking CEACAM16, a member of the carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family of proteins, shows changes in tectorial membrane (TM) structure including loss of a defined striated-sheet matrix, absence of Hensen's stripe and increased porosity. In spite of these changes, thresholds for distortion product emissions (DPOAEs) and auditory brainstem responses (ABR) are near normal for most frequencies in the mouse audiogram [11]. In contrast, stimulus frequency emissions (SFOAE) are larger in knockouts (KO) and the incidence of spontaneous emissions (SOAE) is -70% [5]. This latter statistic is remarkable considering that SOAEs are uncommon in normal wild-type (WT) mice. In order to understand how the TM might influence emissions, SFOAE magnitude and phase were examined and group delays computed. As in humans, an approximately one-cycle phase change is observed in association with SFOAE fine structure. In addition, CEACAM 16 KO mice and their WT controls showed similar group delays/phase slopes indicating no obvious changes in the mechanisms associated with emission generation.
机译:缺乏CEACAM16的小鼠,癌症抗原相关细胞粘附分子(CEACAM)蛋白质的成员,表明扭曲膜(TM)结构的变化,包括损失限定的条纹 - 片状基质,不存在Hensen的条纹和增加的孔隙率。尽管有这些变化,但失真产品排放(DPOA)和听觉脑干响应(ABR)的阈值对于鼠标AudioGram中的大多数频率接近正常情况下[11]。相比之下,刺激频率发射(SFOAE)在敲除(KO)中较大,自发排放(SOAE)的发生率为-70%[5]。考虑到在正常的野生型(WT)小鼠中,后一种统计数据显着是显着的。为了了解TM如何影响排放,检查了SFOAE幅度和相位并计算延迟。与人类一样,与SFOAE精细结构相关联观察到大致单循环的相变。此外,CEACAM 16 KO小鼠及其WT对照显示出类似的组延迟/相位斜率,表明与发射产生相关的机制没有明显变化。

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