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: 8825285
• 负责人: Michael G Heinz
• 金额: $ 32.25万
• 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/8825285
• 关键词: Acoustic Nerve; Address; Affect; 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; Equilibrium; Event; Fiber; Frequencies; Functional disorder; Funding; Grant; Hair Cells; Hearing Aids; Human; Life; Link; Location; Measures; Modeling; Music; Nerve Fibers; Neurons; Noise; Noise-Induced Hearing Loss; Pathway interactions; Patients; Pattern; Phase; Physiological; Prevalence; Process; Psychometrics; Pure-Tone Audiometry; Rehabilitation therapy; Relative (related person); Role; Sensorineural Hearing Loss; Speech; Speech Perception; Structure; Synapses; Techniques; Training; Translating; Travel; Work; Workplace; base; behavior measurement; clinical practice; design; experience; hearing impairment; neurophysiology; programs; public health relevance; relating to nervous system; research study; response; sound; spatiotemporal

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”于标准临床诊断（即，纯音测听，测量耳朵在安静时的敏感度）。在时间处理的阈上缺陷发生在许多听众与SNHL，甚至在频率与正常的听力阈值。此外，显著的永久性耳蜗突触病（高达50%的损失）可能发生在暴露于噪声的耳朵中，“仅”经历暂时的阈值偏移。目前的建议提供了一个系统的方法，直接联系的生理和行为的影响，噪声引起的听力损失的情况下，暂时和永久的阈值偏移。这些实验是基于来自听觉神经的证据设计的，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，可能对于窄带声音与宽带声音不同，并且可能在声音的缓慢变化波动（“时间包络”）中比在快速变化的“精细结构”中更突出。“具体目标1是量化永久性噪声引起的听力损失对耳蜗腹侧核中时间编码的影响，耳蜗腹侧核是听觉脑干上行通路的第一个处理站，也是所有听觉神经纤维的强制性突触。精细结构/信封强度和tonotopicity的平衡将被测量的宽带噪声记录从单个神经元在麻醉的龙猫腹侧耳蜗核的反应。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的影响，以及调制深度和背景噪声水平。具体目标2是量化暂时性阈值漂移后突触病对听神经和腹侧耳蜗核反应的影响。免疫组织化学技术将被用来量化突触病，并评估敏感性的非侵入性生理测定耳蜗突触损失。将对突触病变和非突触病变噪声暴露进行与目标1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。龙猫将被训练在背景噪音中执行检测和辨别任务。将测量音调检测、强度鉴别和包络调制检测和鉴别。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改变信封比精细结构编码，这种不平衡的时间编码将感知相关的低调制深度与噪声中的听力。无论这一假设是否得到支持或反驳，这些基础数据都将非常有用，有助于将感音神经性听力损失的生理和感知影响联系起来。通过与研究噪音暴露后人类知觉缺陷的合作者密切协调这些行为和生理措施，我们最大限度地将动物结果转化为人类隐性听力损失的诊断和患病率措施的潜力。