Significant perceptual and physiological aspects of sensorineural hearing loss (SNHL) remain hidden from standard clinical diagnostics (i.e., pure tone audiometry, which measures the ear's sensitivity in quiet). Suprathreshold deficits in temporal processing occur in many listeners with SNHL, even at frequencies with a normal audiometric threshold. Furthermore, significant permanent cochlear synaptopathy (up to 50% loss) can occur in noise-exposed ears that only experience a temporary threshold shift. The current proposal provides a systematic approach to directly link physiological and behavioral effects of noise-induced hearing loss in cases of both temporary and permanent threshold shift. These experiments were designed based on evidence from the auditory nerve that physiological deficits in temporal coding due to SNHL may be hidden in quiet conditions, may be different for narrowband vs. broadband sounds, and may be more prominent in the slowly varying fluctuations in sound (temporal envelope) than in the rapidly varying fine-structure.
Specific Aim 1 is to quantify the effects of permanent noise-induced hearing loss on temporal coding in the ventral cochlear nucleus, which is the first processing station of the ascending auditory brainstem pathway and an obligatory synapse of all auditory-nerve fibers. The balance of fine-structure/envelope strength and tonotopicity will be measured from responses to broadband noise recorded from single neurons in the ventral cochlear nucleus of anesthetized chinchillas. Neurometric analyses will quantify the effects of hearing loss on envelope modulation detection and discrimination thresholds, vs. modulation depth and background-noise level.
Specific Aim 2 is to quantify the effects of synaptopathy following temporary threshold shift on auditory-nerve and ventral-cochlear- nucleus responses. Immunohistochemical techniques will be used to quantify synaptopathy and to evaluate sensitivity of non-invasive physiological assays to cochlear-synapse loss. The same single-neuron measures as in Aim 1 will be made for both synaptopathic and non-synaptopathic noise exposures.
Specific Aim 3 is to relate behavioral and physiological consequences of noise exposure. Chinchillas will be trained to perform detection and discrimination tasks in background noise. Tone detection, intensity discrimination, and envelope modulation detection and discrimination will be measured. Psychometric (Aim 3) and neurometric (Aims 1 and 2) thresholds will be compared. We hypothesize that hair-cell dysfunction and cochlear synaptopathy will alter envelope more than fine-structure coding, and that this imbalance in temporal coding will be perceptually relevant at low modulation depths associated with listening in noise. No matter whether this hypothesis is supported or refuted, these fundamental data will be extremely useful for linking physiological and perceptual effects of sensorineural hearing loss. By closely coordinating these behavioral and physiological measures with collaborators studying human perceptual deficits after noise exposure, we maximize the potential for translating our animal results to diagnostic and prevalence measures of hidden hearing loss in humans.
Noise exposure is the main cause of preventable hearing loss worldwide, occurring in the workplace, such as in noisy factories, and recreationally, through the use of personal music players and attendance at live music events. Significant physiological aspects of sensorineural hearing loss remain hidden from current audiologic diagnostics. The data collected in these experiments will help to bridge this gap by relating physiological, anatomical, and behavioral consequences of noise exposures and will thus ultimately contribute to the development of new, more sensitive clinical diagnostics.
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