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展性听力损失而限制感知能力的神经机制。在听觉系统中，儿童慢性中耳感染（中耳炎）在发育过程中导致波动性传导性听力损失（HLC）。听力损失的持续时间与包括言语处理缺陷在内的持续性知觉问题相关。时变听觉信号的处理特别容易受到早期听力损失的影响。最近在动物身上的研究

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.