PHYSIOLOGICAL BASIS OF OTOTRAUMATIC INSULT

拟议的研究是一项长期计划的延续 研究旨在研究人的生理基础 从暂时性噪声性听力过渡到永久性噪声听力 损失(NIHL)。我们实验室的早期研究表明， 单耳蜗核的电活动测量 神经元是这两种疾病的极其敏感的指标 暂时性和永久性的声源性听力损失。 此外，当在单位内暴露范式中受到挑战时， 神经元发育异常与许多常见的 NIHL的症状。最近，单一神经纤维的研究 显示曝光后的变化显示出减少的 耳蜗核细胞的放电率可以用下列术语来理解 外围的相应变化。此外，中环 与暴露后激发增加到HIGH相关的变化 水平刺激也可以在受体细胞上得到部分解释。 水平。 目前的实验旨在确定声音是否- 耳蜗非线性度的诱导性变化可以解释 观察到单个神经纤维的放电率增加。 在暴露于选定的刺激后，神经纤维的特性将 与相应的声学失真特性有关 产品(DP)，这可能是一种很有前途的新评估方法 NIHL的早期阶段。对于这些研究，相对较短的时间- 持续时间、纯音或八度频段噪声暴露将 被利用了。一旦基本神经纤维的变化被归类为 这些特殊的暴露条件，我们的单元内范例将 叠加以确定不同阶段的损害 影响神经纤维反应性增加的发生率。 其他利用成熟的行为学方法进行的实验 测试技术将评估声音诱导的缺陷 根据频率-位置原则确定阈值，以便 类似地引起的单位和DP活性的改变可以是 适当地解释基础的 组织病理学。这些研究将扩大我们对 NIHL的过渡阶段，并提供了关于如何 在受噪音损伤的耳朵中，感觉编码发生了变化。

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.