THE PHYSIOLOGICAL BASES OF OTOTRAUMATIC INSULT

拟议的实验是早期和正在进行的研究的继续 噪音导致听力损失的生理基础是什么？ 觉醒和耳蜗核水平的单细胞模型 敏锐的灵长类动物。基本的实验策略继续使用 神经元内设计以研究Brief的相对长期效应 传统上被称为临时性临界点的事件 生理活动的移位(TTS)。到目前为止，其中一位校长 研究结果表明，重大而持久的变化可能会 记录了单个电池的放电响应，而不是 反映在同时测量但敏感度较低的纯音中 测听功能。此外，已经证明，该标准 类似TTS的暴露刺激(100分贝SPL，3分钟)能够影响 应用时对耳蜗管元件的永久性组织学改变 在许多蛾的一段时间内有规律的间隔，从而证明 单单位分析与理解生物学的相关性 现代社会最常见的听力障碍之一的基础，即， 因经常接触中等剂量的空气而导致的慢性听力损失 声音的级别。 在接触到标准方案后，中枢听觉系统 耳蜗核所有分区的神经元都显示出许多 明显的变化，表明外围设备和 引发复杂效应的中心机制。现在 实验旨在区分外周和中枢 听觉神经系统对中等强度的反应的组成部分 利用单根八分之一神经纤维和耳蜗核细胞发出的声音 记录技术，以更集中地识别更改的输入 找到了神经元。这样的研究将确定早期的生理学 TTS潜在的改变，并提供对改变的感觉的有用洞察 编码过程可能伴随着 噪音=耳朵受损。

The proposed experiments are a continuation of earlier and ongoing studies of the physiological bases of noise-induced hearing loss carried out in a single-cell model at the level of the cochlear nucleus in both awake and acute primates. The basic experimental strategy continues to make use of a within-neuron design to study the relatively long-lasting effects of brief episodes of what has traditionally been referred to as temporary threshold shift (TTS) on physiological activity. To date, one of the principal findings has revealed that significant and long-lasting alterations can be documented for the discharge responses of the single cell which are not reflected in simultaneously measured, but less sensitive, pure-tone audiometric functions. Further, it has been demonstrated that the standard TTS-like exposure stimuli (100 dB SPL, 3 min) are capable of effecting permanent histological alterations to cochlear duct elements when applied at regular intervals over a period of many moths thus demonstrating the relevance of single-unit analyses towards understanding the biological bases of one of the most common hearing disorders in modern society, i.e., slowly developing hearing loss caused by regular exposure to moderate levels of sound. Following exposure to the standard protocol, central auditory system neurons of all divisions of the cochlear nucleus demonstrate a number of distinct changes that suggest the contribution of both peripheral and central mechanisms towards eliciting the complex effects. The present experiments are designed to distinguish the peripheral from central components of the auditory nervous system's response to moderately intense sound by employing both single eighth nerve fiber and cochlear nucleus cell recording techniques to identify altered inputs to the more centrally located neurons. Such studies will determine the early physiological changes underlying TTS and provide useful insight into the altered sensory encoding processes that probably accompany perceptual changes in the noise=damaged ear.