Effect of Sensorineural Hearing Loss on the Neural Coding of Spatial Hearing

项目总结 感音神经性听力损失(SNHL)是最常见的永久性听力损失形式，通常由 累积暴露在响亮的声音中。众所周知，SNHL患者对声音的敏感度降低，但 鲜为人知的是，定位声源和使用双耳提示辅助声音的能力存在缺陷 噪声环境中的信号源可探测性和可理解性。大多数哺乳动物，包括人类，都将 通过识别声音强度和到达时间的差异来确定声源的方位(水平位置) 两只耳朵的电波，分别称为耳间电平和时差(ILD和ITD)。神经 对ITD和ILD的敏感性首先出现在投射到下部中央核的听性脑干核团 丘脑(IC)。该项目的目的是确定SNHL对神经表征的影响。 IC中央核的声源方位角。将在荷兰腰带开发SNHL模型 兔子，一种听力图与人类相当的物种。麻醉状态下兔SNHL模型的建立 通过过度暴露在巨大的噪音中。耳蜗功能的变化将通过测量暴露后的 诱发听性脑干反应(ABR)所必需的阈值声级的变化，其最早的 成分来自听神经，或失真产物耳声发射(DPOAE)，它们是 与耳蜗外毛细胞功能有关。ABR和DPOAE的阈值漂移将与 免疫荧光法测定暴露对耳蜗内、外毛细胞数量的影响 在共聚焦显微镜下进行标记。丘脑中央核内单个神经元的声诱发反应 将在有或没有噪声诱导的SNHL的清醒兔身上测量IC并进行比较。敏感度 将测量每个神经元的声源频率、电平、方位角(ITD和ILD共同变化) 而且只有ITD一个人。关于IC神经元传输的声源方位角的信息将使用 信息论和种群解码分析。SNHL兔的IC神经元被预测为 与听力正常的兔子相比，传递有关声源方位的信息更少。机制： 将使用IC的信号处理模型来研究IC中双耳编码的潜在中断 基于已知的SNHL对听神经纤维反应的影响。

PROJECT SUMMARY Sensorineural hearing loss (SNHL) is the most common form of permanent hearing loss, often caused by cumulative exposure to loud sounds. Individuals with SNHL have a well-known reduced sensitivity to sound, but lesser-known are the deficits in the abilities to both localize sound sources and use binaural cues to aid sound source detectability and intelligibility in noisy environments. Most mammals, including humans, localize the azimuth (horizontal position) of sound sources by identifying differences in the intensity and arrival time of sound waves at the two ears, known as interaural level and time differences (ILD and ITD), respectively. Neural sensitivity to ITD and ILD first arises in auditory brainstem nuclei that project to the central nucleus of the inferior colliculus (IC). The purpose of the project is to determine the effect of SNHL on the neural representation of sound source azimuth in the central nucleus of the IC. A model of SNHL will be developed in Dutch-belted rabbits, a species with a comparable audiogram to humans. SNHL will be induced in rabbits under anesthesia via overexposure to loud noise. Changes in cochlear function will be quantified by measuring the post-exposure shift in threshold sound level necessary to evoke either the auditory brainstem response (ABR), whose earliest component arises from the auditory nerve, or distortion product otoacoustic emissions (DPOAE), which are related to cochlear outer hair cell function. Threshold shifts in ABRs and DPOAEs will be compared to post- exposure changes in the number of inner and outer hair cells in the cochlea, measured with immunofluorescent labeling under a confocal microscope. Sound-evoked responses of single neurons in the central nucleus of the IC will be measured in and compared between awake rabbits with or without noise-induced SNHL. The sensitivity of each neuron will be measured to sound source frequency, level, azimuth (ITD and ILD co-varying together) and ITD alone. The information about sound source azimuth transmitted by IC neurons will be computed using information-theoretic and population decoding analyses. IC neurons from rabbits with SNHL are predicted to transmit less information about sound source azimuth than those of normal-hearing rabbits. Mechanisms of potential disruption of binaural coding in the IC will be investigated using signal processing models of the IC based on known effects of SNHL on auditory nerve fiber responses.