MECHANISMS OF ACOUSTIC DISTORTION GENERATION

畸变产物耳声发射（DPOAE）在2f 1-f2处表现出很大的 作为临床诊断感音神经性疾病的有力工具 听力损失 以前在兔子和 啮齿类动物，由PI和其他人，强烈支持一个“黑箱”模型， 其中2f 1-f2 DPOAE由两个离散的耳蜗源产生，一个 在高刺激水平（高于60-70 dB SPL）下占主导地位， 在较低的水平上占主导地位。 然而，这两个来源的性质， 他们与听证会的关系是模糊的。 主要目标 的建议项目是调查的位置，和 豚鼠两种DPOAE源的生理机制 猪，以收集开发PI所需的知识 模型，通过结合已知的耳蜗过程。 因此，镇压， 干扰和局部噪声创伤范例将用于测试 两个DPOAE源位于不同地点的假设 沿着耳蜗分区，相对于主音调区域。 此外，还将记录DPOAE和其他耳声发射类型 同时进行耳蜗功能的电生理测量 在被认为是专门损害的作用， 耳蜗放大器 这些实验将增强我们对 DPOAE和其他发射现象的产生，具体地， 将有助于澄清耳声发射与 耳蜗放大器，被认为是基于外毛细胞 电动性 由于耳声发射的性质存在很大差异， 在小型哺乳动物和人类之间，目前尚不清楚 离散的低和高级别DPOE源，根据数据开发 从小型哺乳动物，可以推广到人类。 一个主要目标的 建议的项目是测试假设，有离散低- 和人耳中的高水平DPOAE源， 类似于那些用来确定两个DPOAE源在小 哺乳动物，专门测试PI模型的预测。 这些 技术包括详细测量DPOAE振幅和相位 刺激参数和测量的系统变化的变化 阿司匹林摄入对低剂量和高剂量DPOAE的影响 水平刺激。 此外，还讨论了DPOAEs与其他 耳声发射现象将通过同步测量进行研究 DPOAE和其他发射类型，在豚鼠在各种 耳蜗操作，以及人类服用阿司匹林期间。 这些 实验将提高我们的理解的关系， 各种耳声发射现象相互影响， 过程 这些知识将有助于设计，实验测试， 以及利用耳声的临床测试结果的解释 排放

The distortion-product otacoustic emission (DPOAE) at 2f1-f2 shows great potential as a powerful tool for the clinical diagnosis of sensorineural hearing losses. Previous studies of this emission in rabbits and rodents, by the PI and others, strongly support a "black-box" model in which the 2f1-f2 DPOAE is produced by two discrete cochlear sources, one dominant at high stimulus levels (above 60-70 dB SPL), and the other dominant at lower levels. However, the nature of the two sources, and their relationship to the hearing process, are obscure. A primary aim of the proposed project is to investigate the locations of, and the physiological mechanisms underlying, the two DPOAE sources, in guinea pigs, in order to gather the knowledge required to develop the PI's model, by incorporating known cochlear processes. Thus, suppression, interference, and localized noise-trauma paradigms will be used to test the hypothesis that the two DPOAE sources are located at different sites along the cochlear partition, relative to the primary-tone region. Additionally, DPOAEs and other otacoustic-emission types will be recorded concurrently with electrophysiological measures of cochlear function during manipulations thought to specifically impair the action of the cochlear amplifier. These experiments will enhance our understanding of the generation of DPOAEs and other emission phenomena and, specifically, will help to clarify the relationship[ of otacoustic emissions to the cochlear amplifier, thought to be based in outer hair-cell electromotility. Because of major differences of the properties of otacoustic emissions between small mammals and humans, it is not clear that the model of discrete low- and high-level DPOE sources, developed on the basis of data from small mammals, can be generalized to humans. A primary aim of the proposed project is to test the hypothesis that there are discrete low- and high-level DPOAE sources in human ears, by utilizing techniques, similar to those employed to identify the two DPOAE sources in small mammals, that specifically test predictions of the PI's model. These techniques include detailed measurement of DPOAE-amplitude and phase variations upon systematic changes of stimulus parameters and measurement of the effect of aspirin ingestion on DPOAEs elicited by low- and high- level stimuli. In addition, the relationship of DPOAEs and the other otacoustic-emission phenomena will be studied by concurrent measurement of DPOAEs and the other emission types, in guinea pigs during a variety of cochlear manipulations, and in humans during aspirin ingestion. These experiments will improve our understanding of the relationship of the various otacoustic-emission phenomena to each other, and to the hearing process. This knowledge will aid in the design, experimental testing, and interpretation of results of clinical tests utilizing otacoustic emissions.