Improving Auditory Responses After Hearing Loss

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2022-05-01T05:00:00.000Z

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Abstract

Noise-induced hearing loss is a common and debilitating neurological injury. Exposure to loud sounds can result in damage to cochlear structures and subsequently to losses in the transduction of acoustic signals into neural activity. The loss of neural activity leads to auditory pathways having less information available to them to process and evaluate any given acoustic scene. For patients with noise-induced hearing loss, the degradation of acoustic processing leads to difficulties in communication. Challenges in communication for patients with noise-induced hearing loss arise from trouble understanding speech—especially in noisy environments. Ineffective communication can lead to lost productivity and social withdrawal, which profoundly degrade the quality of life for people with noise-induced hearing loss. In addition to the loss of acoustic input, noise-induced hearing loss also results in adaptive changes throughout the auditory pathway. The nature and impact of these adaptations remains unclear and techniques which can probe these adaptations by precisely modulating neural activity are needed. Vagus nerve stimulation (VNS) paired with sound presentation has been shown to induce stimulus-specific plasticity in the auditory cortex. To explore the possibility that VNS paired with sounds might enhance neural responses to auditory cues following noise-induced hearing loss, a rodent model of noise-induced hearing loss was established. The model covered a wide range of behavioral impairments and demonstrated behavioral deficits in speech sound detection and discrimination. Importantly, rats with severe hearing loss demonstrated behavioral deficits most akin to clinical complaints—difficulty discriminating speech in the presence of noise. The present rodent model was then used to evaluate the ability of VNS paired with speech sound presentation to alter neural responses to speech sounds following noise-induced hearing loss. For rats with moderate hearing loss and which had intact neural responses to speech sounds, VNS-speech pairing did not significantly alter the neural responses to speech sounds. However, for rats with severe noiseinduced hearing loss, VNS-speech pairing doubled the response strength to the consonant portion of the speech sound, significantly improved neural discriminability, and did not alter the response to the vowel. For rats with profound hearing loss, the response strength to the vowel portion of the speech sounds was doubled and neural detection improved. Taken together, these findings suggest that when neural responses are present but weakened, such as with the consonant portion in the severe group or the vowel in profound group, VNS-speech pairing can strengthen those responses. However, when responses are absent, such as with the lack of any evoked response to the consonant in the profound group, VNS-speech pairing does not strengthen a response which is not present. Where responses were robust, such as with the moderate group and the vowel response in severe rats, VNS-speech paring does not interfere with those responses. This proof-of-concept work demonstrates that the auditory pathways remain plastic following noise-induced hearing loss and that they are manipulable using VNS-speech pairing. Future work is needed to establish if the plastic changes induced by VNS-speech pairing result in improved behavioral outcomes.

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Biology, Neuroscience

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