Auditory processing deficits in early-onset conductive hearing loss

描述（由申请人提供）：这项工作的长期目标是确定由于发育性听力损失而限制感知能力的神经机制。在听觉系统中，儿童的慢性中耳感染（中耳炎）导致发育期间的波动性传导性听力损失（HLC）。听力损失的持续时间与持续的感知问题相关，包括语音处理缺陷。时变听觉信号的处理特别容易受到早期听力损失的影响。最近在动物身上的工作 传导性听力损失模型显示，早期听力损伤改变了听觉皮层中的突触特性和对声音的反应。然而，目前尚不清楚改变的突触元件如何形成皮层调谐，或者改变的皮层调谐如何有助于受损的感知。为了解决这些问题，该项目研究了听力损失引发的事件链，以建立听觉皮层神经元突触变化之间的联系，它们对这些神经元的声音诱发反应的影响，以及感知受损。目标1将确定易受早期听力损失影响的响应特性。目的二是探讨听觉皮层神经元反应特性改变的突触机制。目标3将确定皮层对听觉刺激的反应， 听力损失引起的变化与知觉障碍有关。早期听力损失在多大程度上导致单纯的发育迟缓或新的病理学尚不清楚。由于早期听力损失引起的几种神经变化表明突触成分和听觉反应的成熟延迟。然而，听力受损动物的时间响应特性并不都是不成熟的，目标1将确定那些易受听觉剥夺影响的时变刺激的元素。特别是，早期听力损失损害缓慢但不是快速幅度调制（AM）的处理。然而，初步的数据表明，它可能是在AM信号的幅度上升的速率，而不是调制的频率，elevated异常的神经反应。这个区别很重要：语音是由周期性的幅度和频率调制组成的，具有各种各样的慢和快的上升时间。对阅读障碍和特定语言障碍的研究表明，这些语言成分的一个子集的神经处理受损，这导致了定向治疗干预。该建议将确定哪些刺激参数引起的反应会因早期听力损失而改变。了解慢性传导性听力损失导致的损伤的神经基础是提供干预和补救目标的必要步骤。

DESCRIPTION (provided by applicant): The long-term goal of this work is to identify neural mechanisms that limit perceptual abilities as a result of developmental hearing loss. In the auditory system, chronic middle ear infections (otitis media) in children result in fluctuating conductive hearing loss (HLC) during development. The duration of hearing loss is correlated with persistent perceptual problems including speech processing deficits. Processing of time-varying auditory signals is particularly vulnerable to early hearing loss. Recent work in an animal model of conductive hearing loss shows that early hearing impairment shifts both synaptic properties and responses to sound in auditory cortex. However, it is unknown how altered synaptic elements shape cortical tuning, or how altered cortical tuning contributes to impaired perception. To address these issues, this project examines the chain of events initiated by hearing loss in order to establish the links between synaptic changes in auditory cortical neurons, their effects on the sound-evoked responses of these neurons, and impaired perception. Aim 1 will determine response properties that are vulnerable to early hearing loss. Aim 2 will determine the synaptic mechanisms that shape altered response properties of neurons in auditory cortex. Aim 3 will identify how cortical responses to auditory stimuli that are altered by hearing loss relate to perceptual impairments. The degree to which early hearing loss causes a simple maturational delay or novel pathology is unknown. Several neural changes due to early hearing loss indicate a delayed maturation of synaptic components and auditory responses. However, temporal response properties in hearing-impaired animals are not uniformly immature, and Aim 1 will identify those elements of time-varying stimuli that are susceptible to the effects of auditory deprivation. In particular, early hearing loss impairs processing of slow but not fast amplitude modulations (AM). However, preliminary data indicate that it may be the rate of the amplitude rise in AM signals, rather than the frequency of the modulations, that elicits abnormal neural responses. This distinction is important: speech is composed of periodic amplitude and frequency modulations with a variety of slow and fast rise times. Studies of dyslexia and specific language impairment indicate that the neural processing of a subset of these speech components is impaired, which has led to directed therapeutic interventions. This proposal will identify which stimulus parameters elicit responses that are altered by early hearing loss. Understanding the neural basis of impairments resulting from chronic conductive hearing loss is a necessary step toward providing targets for intervention and remediation.