Reorganization of receptive fields following hearing loss in inferior colliculus neurons

Abstract

We explored frequency and intensity encoding in the inferior colliculus of the C57 mouse model of sensorineural hearing loss. Consistent with plasticity reported in the IC of other models of hearing loss, frequency response areas (FRAs) in hearing impaired (HI) mice were broader with fewer highfrequency units than normal-hearing (NH) mice. The broad FRAs recorded from HI mice had lower cutoffs on the low frequency edge of the FRA. Characteristic frequency (CF) and sharpness of tuning (Q10) calculated from the FRA were used to divide the sample into 4 categories: low-CF sharp-FRA, low-CF broad-FRA, high-CF sharp-FRA, and high-CF broad-FRA units. Rate-intensity functions (RIFs) for CF tones and noise were used to determine the minimum and maximum response counts as well as the sound pressure levels resulting in 10%, 50%, and 90% of the maximum spike count. Tone RIFs of broad FRA units were shifted to the right of tone RIFs of sharp FRA units in both NH and HI mouse IC, regardless of the unit CF. The main effects of hearing loss were seen in the noise RIFs. The low-CF broad-FRA units in HI mice had elevated response to noise, and the high-CF sharp-FRA units in HI mice had lower maximum rates, as compared to the units recorded from NH mice. These results suggest that, as the IC responds to peripheral hearing loss with changes in the representation of frequency, an altered balance between inhibitory and excitatory inputs to the neurons recorded from the HI mice alter aspects of the units' intensity encoding. This altered balance likely occurs, at least in part, outside of the IC. Keywords plasticity; sensorineural hearing loss; C57 mouse; intensity encoding; central auditory nervous system Sensorineural hearing loss occurs in almost 10% of the US population. One of the most debilitating side effects of this condition is difficulty with word comprehension, particularly when the listening environment is noisy (Needleman and Crandell, 1995). Treatment of hearing loss includes amplification, but it cannot be assumed that amplification restores normal perception. For instance, hearing loss alters the frequency tuning curves and rate-intensity functions (RIFs) in central auditory neurons (Willott, 1984, Willott, 1986, and these deficits cannot be compensated by simple amplification alone. In addition, the sensitivity of the auditory system of hearing impaired listeners may be altered by long-term amplification. ForCorresponding Author: Joseph P. Walton, Department of Otolaryngology and Neurobiology and Anatomy, University of Rochester Medical School, 601 Elmwood Ave., Rochester, NY 14642, USA, Joseph_Walton@URMC.rochester.edu, PHONE: 585-275-1248, FAX: 585-244-4103. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that durin...

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Developmental Hearing Loss Disrupts Synaptic Inhibition: Implications for Auditory Processing

“…Hearing loss can broaden tuning curves of single cells, shift CFs and lead to global changes in tonotopy. For example, frequency tuning curves of IC neurons become broader following noise- and drug-induced hearing loss [78–82] and in mice with congenital SNHL [83]. Partial hair cell damage within regions of the cochlea also leads to a reorganization of the cortical tonotopy [81,84–88].…”

Plasticity of serotonergic innervation of the inferior colliculus in mice following acoustic trauma

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