Effects of Sensorineural Hearing Loss on Robust Speech Coding

感音神经性听力损失对鲁棒语音编码的影响

• 批准号: 9178651
• 负责人: Michael G Heinz
• 金额: $ 32.24万
• 依托单位: PURDUE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-09-18 至 2019-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9178651
• 关键词: Acoustic Nerve; Address; Affect; Anatomy; Animals; Audiometry; Auditory; Behavioral; Biological Assay; Brain Stem; Characteristics; Chinchilla (genus); Clinical; Cochlear nucleus; Code; Cues; Data; Detection; Development; Diagnostic; Diagnostic tests; Discrimination; Dissociation; Ear; Electrophysiology (science); Equilibrium; Event; Fiber; Frequencies; Functional disorder; Funding; Grant; Hair Cells; Hearing Aids; Human; Kale - dietary; Link; Location; Measures; Modeling; Music; Nerve Fibers; Neurons; Noise; Noise-Induced Hearing Loss; Pathway interactions; Patients; Pattern; Phase; Physiological; Prevalence; Psychometrics; Pure-Tone Audiometry; Rehabilitation therapy; Role; Sensorineural Hearing Loss; Speech; Speech Perception; Structure; Synapses; Techniques; Temporary Threshold Shift; Training; Translating; Travel; Work; Workplace; base; behavior measurement; clinical diagnostics; clinical practice; design; experience; experimental study; hearing impairment; neurophysiology; programs; public health relevance; relating to nervous system; response; sound; spatiotemporal; translational impact

DESCRIPTION (provided by applicant): Significant perceptual and physiological aspects of sensorineural hearing loss (SNHL) remain "hidden" from standard clinical diagnostics (i.e., pure tone audiometry, which measures the ear's sensitivity in quiet). Suprathreshold deficits in temporal processing occur in many listeners with SNHL, even at frequencies with a normal audiometric threshold. Furthermore, significant permanent cochlear synaptopathy (up to 50% loss) can occur in noise-exposed ears that "only" experience a temporary threshold shift. The current proposal provides a systematic approach to directly link physiological and behavioral effects of noise-induced hearing loss in cases of both temporary and permanent threshold shift. These experiments were designed based on evidence from the auditory nerve that physiological deficits in temporal coding due to SNHL may be hidden in quiet conditions, may be different for narrowband vs. broadband sounds, and may be more prominent in the slowly varying fluctuations in sound ("temporal envelope") than in the rapidly varying "fine-structure." Specific Aim 1 is to quantify the effects of permanent noise-induced hearing loss on temporal coding in the ventral cochlear nucleus, which is the first processing station of the ascending auditory brainstem pathway and an obligatory synapse of all auditory-nerve fibers. The balance of fine-structure/envelope strength and tonotopicity will be measured from responses to broadband noise recorded from single neurons in the ventral cochlear nucleus of anesthetized chinchillas. Neurometric analyses will quantify the effects of hearing loss on envelope modulation detection and discrimination thresholds, vs. modulation depth and background-noise level. Specific Aim 2 is to quantify the effects of synaptopathy following temporary threshold shift on auditory-nerve and ventral-cochlear- nucleus responses. Immunohistochemical techniques will be used to quantify synaptopathy and to evaluate sensitivity of non-invasive physiological assays to cochlear-synapse loss. The same single-neuron measures as in Aim 1 will be made for both synaptopathic and non-synaptopathic noise exposures. Specific Aim 3 is to relate behavioral and physiological consequences of noise exposure. Chinchillas will be trained to perform detection and discrimination tasks in background noise. Tone detection, intensity discrimination, and envelope modulation detection and discrimination will be measured. Psychometric (Aim 3) and neurometric (Aims 1 and 2) thresholds will be compared. We hypothesize that hair-cell dysfunction and cochlear synaptopathy will alter envelope more than fine-structure coding, and that this imbalance in temporal coding will be perceptually relevant at low modulation depths associated with listening in noise. No matter whether this hypothesis is supported or refuted, these fundamental data will be extremely useful for linking physiological and perceptual effects of sensorineural hearing loss. By closely coordinating these behavioral and physiological measures with collaborators studying human perceptual deficits after noise exposure, we maximize the potential for translating our animal results to diagnostic and prevalence measures of hidden hearing loss in humans.

描述（由申请人提供）：感音神经性听力损失（SNHL）的重要感知和生理方面仍然“隐藏”在标准临床诊断中（即纯音测听，测量耳朵在安静状态下的灵敏度）。许多患有 SNHL 的听众都会出现时间处理的阈上缺陷，即使在听力阈值正常的频率下也是如此。此外，暴露于噪声的耳朵“仅”经历暂时的阈值偏移，可能会发生显着的永久性耳蜗突触病变（高达 50% 的损失）。当前的提案提供了一种系统方法，可以在暂时和永久阈值漂移的情况下直接将噪声引起的听力损失的生理和行为影响联系起来。这些实验是基于来自听觉神经的证据而设计的，即由于 SNHL 导致的时间编码的生理缺陷可能隐藏在安静条件下，窄带声音与宽带声音可能不同，并且在声音缓慢变化的波动中可能更为突出。 “时间包络”）比快速变化的“精细结构”。具体目标 1 是量化永久性噪声引起的听力损失对腹侧耳蜗核时间编码的影响，腹侧耳蜗核是上行听觉脑干通路的第一个处理站，也是所有听觉神经纤维的必然突触。精细结构/包络强度和音位性的平衡将通过对麻醉龙猫腹侧耳蜗核中单个神经元记录的宽带噪声的响应来测量。神经测量分析将量化听力损失对包络调制检测和辨别阈值以及调制深度和背景噪声水平的影响。具体目标 2 是量化暂时阈值偏移后突触病对听觉神经和腹侧耳蜗核反应的影响。免疫组织化学技术将用于量化突触病变并评估非侵入性生理测定对耳蜗突触损失的敏感性。对于突触和非突触噪声暴露，将进行与目标 1 中相同的单神经元测量。具体目标 3 是将噪声暴露的行为和生理后果联系起来。龙猫将接受训练，在背景噪音中执行检测和辨别任务。将测量音调检测、强度辨别以及包络调制检测和辨别。将比较心理测量（目标 3）和神经测量（目标 1 和 2）阈值。我们假设毛细胞功能障碍和耳蜗突触病将比精细结构编码改变更多的包络，并且时间编码的这种不平衡在与噪声聆听相关的低调制深度下将在感知上相关。无论这一假设是否得到支持或反驳，这些基本数据对于将感音神经性听力损失的生理和知觉影响联系起来都非常有用。通过与研究噪声暴露后人类感知缺陷的合作者密切协调这些行为和生理测量，我们最大限度地发挥了将动物结果转化为人类隐性听力损失的诊断和患病率测量的潜力。