Author: Adam Christopher Dziorny
Publisher:
Published: 2009
Total Pages: 464
ISBN-13:
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"Each year as many as 3/1000 children are diagnosed with congenital sensorineural hearing loss. Common in these children are delays in grammar comprehension, vocabulary retention and speech development, related to temporal processing abilities. Studies in a mouse model of congenital sensorineural hearing loss suggest that early exposure to an augmented acoustic environment (AAE) limits outer hair cell death and maintains peripheral auditory thresholds. However, there have been no studies on the effects of AAE on neural encoding in the central auditory system. The goal of these experiments is to investigate midbrain auditory processing in a mouse model (the DBA strain) of sensorineural hearing loss, and determine the effects of AAE exposure. It is clear that sound exposure during the early developmental period has profound effects on neural processing in the central auditory system of normal-hearing subjects. Questions remain on the effects of such sound exposure on a model of hearing impairment. In Aim I of this study we presented a novel temporal AAE containing silent gaps embedded in noise bursts to DBA mice and examined the frequency representation, intensity encoding and temporal processing in the auditory midbrain. Mice were exposed to a traditional AAE stimulus, a novel temporal AAE stimulus, or no stimulus from birth to P30. Auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) were recorded to assess peripheral auditory function. To assess the effects on central auditory processing we recorded neural activity from a 16-channel electrode in the inferior colliculus (IC). We confirmed peripheral preservation with AAE exposure, and expanded these results to demonstrate outer hair cell functional preservation. In the midbrain we demonstrated that IC neurons showed decreased thresholds, that high best-frequency units were maintained, tuning sharpness was improved, excitatory drive was increased and most importantly, units displayed shorter neural gap thresholds. Additionally, only mice exposed to our novel temporal AAE demonstrated significantly shortened mean gap threshold at low carrier levels, and in the presence of continuous background noise. To be useful as a therapeutic intervention the effect of onset time on central auditory function must be examined. Additionally, it is not known if the improvements provided by AAE exposure will remain after exposure cessation. In Aim II of this study we asked whether delaying the exposure onset or altering its duration influence the improvements in neural processing noted above. Again DBA mice were exposed to a traditional AAE stimulus or no stimulus from birth to P60. Two additional groups were included, one exposed for 30 days followed by 30 days of no exposure (On/Off), the other not exposed until P30 followed by 30 days of exposure (Off/On). All animals were tested at P60. Again ABRs and DPOAEs were recorded to assess peripheral auditory function, and central auditory processing was measured using a 16-channel electrode in the IC. We determined that the onset time of exposure is of little importance in demonstrating improvements in both peripheral and central auditory system. However, continued exposure is essential to maintain the beneficial effects and limit functional loss. Our results demonstrate that AAE preserves peripheral structure and function and improves central auditory processing, that a targeted temporal AAE can improve neural correlates of temporal processing, and that the timing of AAE is essential in delaying the progression of sensorineural hearing loss. These experiments pave the way for possible therapeutic intervention in children suffering congenital sensorineural hearing loss."--Leaves v-vi.
