PHYSIOLOGICAL BASIS OF OTOTRAUMATIC INSULT

拟议的研究是一项长期计划的延续 研究的生理基础， 从暂时性噪声听力到永久性噪声听力的转变 损失（NIHL）。 我们实验室的早期研究表明， 单个耳蜗核电活动的测量 神经元是这两个神经元的 暂时性和永久性听力损失。 此外，当在单元内暴露范例中受到挑战时， 神经元出现异常， NIHL的症状 最近，单神经纤维研究 显示出，表现出递减的实验后变化， 耳蜗核细胞的放电率可以理解为 在外围的相应变化。 此外，中央 与刺激后放电增加相关的变化 水平刺激也可以部分解释在受体细胞 水平 本实验旨在确定是否声音- 耳蜗非线性的诱导变化可以解释 观察到单个神经纤维的放电速率增加。 在暴露于选定的刺激后，神经纤维的特性将 与声失真的相应特性有关 产品（DP）在什么可能是一个有前途的新手段评估 NIHL的早期阶段。 对于这些研究，相对较短- 持续时间，纯音或倍频程噪声暴露将 利用。 一旦基本的神经纤维变化被归类为 在这些特定的暴露条件下，我们的单元内范式将 以确定不同阶段的损伤 影响神经纤维反应性增加的发生率。 其他实验利用成熟的行为 测试技术将评估声音引起的缺陷， 根据频域原理进行阈值检测， 类似地诱导的单位和DP活性的改变可 适当地解释与基础 组织病理学 这些研究将扩展我们对 NIHL的过渡阶段，并提供有用的见解如何 感觉编码在噪声损伤的耳朵中改变。

The Proposed studies are a continuation of a long-term program of research designed to study the physiological bases of the transition from temporary to permanent noise-induced hearing loss (NIHL). Earlier studies in our laboratory demonstrated that measures of electrical activity from single cochlear nucleus neurons were extremely sensitive indicators of both the temporary and permanent aspect of sound-inducing hearing loss. Additionally, when challenged in a intraunit-exposure paradigm, neurons developed abnormalities related to a number of common symptoms of NIHL. Most recently, single nerve fiber studies showed that postexposure alterations displaying decrements in firing rates for cochlear nucleus cells can be understood in terms of corresponding changes at the periphery. Moreover, central changes associated with increased postexposure firing to high level stimuli may also be partially explained at the receptor-cell level. The present experiments are designed to determine if sound- induced changes in cochlear nonlinearity can account for augmentations in discharge rate observed for single nerve fibers. Following exposure to selected stimuli, nerve-fiber properties will be related to corresponding characteristics of acoustic distortion products (DPs) in what may be a promising new means of assessing the early stages of NIHL. For these studies, relatively short- duration, pure-tone or octave-band noise exposures will be utilized. Once basic nerve-fiber changes are categorized under these particular exposure conditions, our intraunit paradigm will be superimposed to determine if various stages of damage influence the incidence of increased nerve-fiber responsiveness. Other experiments making use of well-established behavioral testing techniques will assess the sound-induced deficits in threshold-dection according to frequency-place principles so that similarly induced alterations in unit and DP activity can be appropriately interpreted with respect to the underlying histopathology. These studies will extend our knowledge of the transitional stages of NIHL and provide useful insights into how sensory encoding is altered in the noise-damaged ear.