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。在听力系统中，儿童慢性中耳感染(中耳炎)会导致发育过程中的波动性传导性听力损失(HLC)。听力损失的持续时间与包括语音处理缺陷在内的持续性知觉问题有关。对时变听觉信号的处理特别容易受到早期听力损失的影响。一种动物的最新研究成果 传导性听力损失模型表明，早期听力障碍改变了听觉皮质的突触特性和对声音的反应。然而，尚不清楚突触元素改变如何影响大脑皮层调谐，或大脑皮层调谐改变如何导致知觉受损。为了解决这些问题，该项目研究了听力损失引发的一连串事件，以建立听觉皮质神经元的突触变化、它们对这些神经元的声音诱发反应的影响以及感知受损之间的联系。目标1将确定易受早期听力损失影响的反应特性。目的2将确定形成听觉皮质神经元反应特性改变的突触机制。目标3将确定大脑皮层对听觉刺激的反应 听力损失引起的改变与知觉障碍有关。早期听力损失在多大程度上导致简单的成熟延迟或新的病理尚不清楚。由于早期听力丧失而引起的一些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反应特性并不都是不成熟的，目标1将确定那些时变刺激中容易受到听觉剥夺影响的元素。特别是，早期听力损失会损害对慢而不是快的幅度调制(AM)的处理。然而，初步数据表明，引起异常神经反应的可能是AM信号的幅度上升速度，而不是调制的频率。这一区别很重要：语音是由周期性的幅度和频率调制组成的，具有各种缓慢和快速的上升时间。对阅读障碍和特定语言障碍的研究表明，这些语音成分的一个子集的神经处理受到损害，这导致了直接的治疗干预。这项提议将确定哪些刺激参数会引起因早期听力损失而改变的反应。了解慢性传导性听力损失所致损害的神经基础是为干预和补救提供靶点的必要步骤。

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.