Comparing spontaneous and stimulus frequency otoacoustic emissions in mice with tectorial membrane defects.

Comparing spontaneous and stimulus frequency otoacoustic emissions in mice with tectorial membrane defects.
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比较自发性和刺激频率耳声发射在小鼠与覆膜缺损。

DOI:
10.1016/j.heares.2020.108143
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发表时间:
2021-03
期刊:
影响因子:
2.8
通讯作者:
Cheatham MA
Cheatham MA
中科院分区:
医学1区
文献类型:
--
作者:
Cheatham MA

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产生自发耳声发射(SOAE)的全局驻波模型表明,它们是振幅稳定的驻波,并且SOAE之间的间隔对应于由刺激频率耳声发射(SFOAE)的相位梯度延迟确定的相位变化一个周期的间隔。由于非人类哺乳动物的自发和诱发发射之间的关系的数据是有限的,我们研究SOAE和SFOAE在覆膜(TM)突变体和它们的控制。计算表明,相邻的SOAE之间的间距是预测的SFOAE相位梯度延迟TM突变体缺乏Ceacam 16,SOAE频率大于~20 kHz和突变体保持接近正常的听力时,年轻。还检查了在Tecta中具有错义突变的小鼠(TectaY 1870 C/+)以及缺乏耳安可蛋白的小鼠(Otoa−/−)。虽然这些突变体表现出听力损失,但它们产生的SOAE在TectaY 1870 C/+中的平均频率为11 kHz,在Otoa−/−中的平均频率为6 kHz。在这些动物中,相邻SOAE之间的间隔大于SFOAE相位延迟预测的。它也表明,小鼠不表现出强烈的频率依赖性的信号编码,具有良好的低频听力的物种的特点。事实上,过渡发生在小鼠耳蜗的顶端附近,而不是在沿耳蜗分区的中点沿着。因此,与驻波模型的不一致不容易通过耳蜗顶部和底部区域之间的调谐比的过渡来解释,特别是对于TectaY 1870 C/+小鼠中产生的SOAE。
The global standing-wave model for generation of spontaneous otoacoustic emissions (SOAEs) suggests that they are amplitude-stabilized standing waves and that the spacing between SOAEs corresponds to the interval over which the phase changes by one cycle as determined from the phase-gradient delays of stimulus frequency otoacoustic emissions (SFOAEs). Because data characterizing the relationship between spontaneous and evoked emissions in nonhuman mammals are limited, we examined SOAEs and SFOAEs in tectorial membrane (TM) mutants and their controls. Computations indicate that the spacing between adjacent SOAEs is predicted by the SFOAE phase-gradient delays for TM mutants lacking Ceacam16, where SOAE frequencies are greater than ~20 kHz and the mutants retain near-normal hearing when young. Mice with a missense mutation in Tecta (TectaY1870C/+), as well as mice lacking Otoancorin (Otoa−/−), were also examined. Although these mutants exhibit hearing loss, they generate SOAEs with average frequencies of 11 kHz in TectaY1870C/+ and 6 kHz in Otoa−/−. In these animals, the spacing between adjacent SOAEs is larger than predicted by the SFOAE phase delays. It is also demonstrated that mice do not exhibit the strong frequency-dependence in signal coding that characterizes species with good low-frequency hearing. In fact, a transition occurs near the apical end of the mouse cochlea rather than at the mid-point along the cochlear partition. Hence, disagreements with the standing-wave model are not easily explained by a transition in tuning ratios between apical and basal regions of the cochlea, especially for SOAEs generated in TectaY1870C/+ mice.
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