Binaural hearing refers to the coordinated use of information from the two ears for auditory perceptions such as sound location. The goals of this study are to determine the neural bases for the behavioral deficits in binaural hearing produced by early developmental exposure to conductive hearing loss (CHL). Children that have experienced CHL early in life, particularly unilateral, often show impairments in binaural hearing abilities that persist even after the CHL has been resolved and hearing sensitivity in both ears is normal. Binaural hearing enhances the perceptual ability to separate and selectively attend to particular sources, such as speech, in the presence of competing sounds. While binaural hearing abilities often recover, a return to normal hearing can take months or even years. Because language is learned in noisy reverberant environments, like classrooms, persistent binaural impairments may contribute to deficits in language and speech. Decades of studies of the neural consequences of CHL in animal models have determined how only the most basic of monaural and binaural neuronal response properties are altered at several levels of the auditory system. Nevertheless, the persistent binaural behavioral deficits in humans have defied explanation based on these basic response properties. The proposed experiments use the novel framework of information theory to test the hypothesis that early CHL persistently alters the capacity of neurons in the inferior colliculus to carry information about the acoustical cues to sound location and that this capacity recovers with exposure to normal hearing after resolution of the CHL. The inferior colliculus, a midbrain nucleus known to be important for binaural hearing, has been implicated by clinical studies in children that have experienced early CHL as a site for the neural deficits associated with the persistent impairments in binaural hearing. The proposed experiments are designed to determine which aspects of responses of inferior colliculus neurons are affected by experimentally- induced CHL to produce the reduced information carrying capacities, reflected by changes in overall responsiveness, reliability, and general sensitivity to the localization cues. As one way to link these results to clinical data, we will correlate changes in the information carrying capabilities of inferior colliculus neurons with changes in the binaural interaction components of the non-invasively measured auditory brainstem response (ABR). These components of the ABR have proven to be predictive of the persistent binaural hearing impairments due to CHL in clinical studies. A behavioral assay will be used to quantify deficits in binaural hearing and its recovery. Overall this work has both biological and clinical significance. From a biological perspective, we will determine which particular aspects of responses of inferior colliculus neurons are affected by experimentally-induced unilateral CHL to produce the reduced information carrying capacities. Of clinical significance, we will determine whether and how the altered neural information processing in the inferior colliculus is correlated with attributes of the binaural evoked potentials and sound localization behavior.
Common problems that arise during infancy such as middle ear disease (otitis media with effusion, or simply ear infections) can lead to deficits in binaural hearing, due to the associated conductive hearing losses, that have been shown to lead to future language, learning, and social disabilities. Basic studies of the mammalian binaural auditory pathway will determine if, where, and how long the binaural system is plastic and the time course over which it may recover from early deficits. A thorough understanding of normal and abnormal development will facilitate the design of new and better ways to identify, prevent, and possibly to treat early- onset hearing loss.
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