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• W2300314283 abstract "Each year as many as 3/1000 children are diagnosedwith congenital sensorineural hearing loss. Common in thesechildren are delays in grammar comprehension, vocabulary retentionand speech development, related to temporal processing abilities.Studies in a mouse model of congenital sensorineural hearing losssuggest that early exposure to an augmented acoustic environment(AAE) limits outer hair cell death and maintains peripheralauditory thresholds. However, there have been no studies on theeffects of AAE on neural encoding in the central auditory system.The goal of these experiments is to investigate midbrain auditoryprocessing in a mouse model (the DBA strain) of sensorineuralhearing loss, and determine the effects of AAE exposure. It isclear that sound exposure during the early developmental period hasprofound effects on neural processing in the central auditorysystem of normal-hearing subjects. Questions remain on the effectsof such sound exposure on a model of hearing impairment. In Aim Iof this study we presented a novel temporal AAE containing silentgaps embedded in noise bursts to DBA mice and examined thefrequency representation, intensity encoding and temporalprocessing in the auditory midbrain. Mice were exposed to atraditional AAE stimulus, a novel temporal AAE stimulus, or nostimulus from birth to P30. Auditory brainstem responses (ABRs) anddistortion product otoacoustic emissions (DPOAEs) were recorded toassess peripheral auditory function. To assess the effects oncentral auditory processing we recorded neural activity from a16-channel electrode in the inferior colliculus (IC). We confirmedperipheral preservation with AAE exposure, and expanded theseresults to demonstrate outer hair cell functional preservation. Inthe midbrain we demonstrated that IC neurons showed decreasedthresholds, that high best-frequency units were maintained, tuningsharpness was improved, excitatory drive was increased and mostimportantly, units displayed shorter neural gap thresholds.Additionally, only mice exposed to our novel temporal AAEdemonstrated significantly shortened mean gap threshold at lowcarrier levels, and in the presence of continuous backgroundnoise. To be useful as a therapeutic intervention the effect ofonset time on central auditory function must be examined.Additionally, it is not known if the improvements provided by AAEexposure will remain after exposure cessation. In Aim II of thisstudy we asked whether delaying the exposure onset or altering itsduration influence the improvements in neural processing notedabove. Again DBA mice were exposed to a traditional AAE stimulus orno 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 ofexposure (Off/On). All animals were tested at P60. Again ABRs andDPOAEs were recorded to assess peripheral auditory function, andcentral auditory processing was measured using a 16-channelelectrode in the IC.…" @default.
• W2300314283 created "2016-06-24" @default.
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• W2300314283 date "2010-01-01" @default.
• W2300314283 modified "2023-09-23" @default.
• W2300314283 title "Neural correlates of auditory processing following exposure to an augmented acoustic environment" @default.
• W2300314283 hasPublicationYear "2010" @default.
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