Abstract

BackgroundNoise induced injury of the cochlea causes shifts in activation thresholds and changes of frequency response in the inferior colliculus (IC). Noise overexposure also induces pathological changes in the cochlea, and is highly correlated to hearing loss. However, the underlying mechanism has not been fully elucidated. In this study, we hypothesized that overexposure to noise induces substantial electrophysiological changes in the IC of guinea pigs.ResultsDuring the noise exposure experiment, the animals were undergoing a bilateral exposure to noise. Additionally, various techniques were employed including confocal microscopy for the detection of cochlea hair cells and single neuron recording for spontaneous firing activity measurement. There were alterations among three types of frequency response area (FRA) from sound pressure levels, including V-, M-, and N-types. Our results indicate that overexposure to noise generates different patterns in the FRAs. Following a short recovery (one day after the noise treatment), the percentage of V-type FRAs considerably decreased, whereas the percentage of M-types increased. This was often caused by a notch in the frequency response that occurred at 4 kHz (noise frequency). Following a long recovery from noise exposure (11–21 days), the percentage of V-types resumed to a normal level, but the portion of M-types remained high. Interestingly, the spontaneous firing in the IC was enhanced in both short and long recovery groups.ConclusionOur data suggest that noise overexposure changes the pattern of the FRAs and stimulates spontaneous firing in the IC in a unique way, which may likely relate to the mechanism of tinnitus.

Highlights

  • Noise induced injury of the cochlea causes shifts in activation thresholds and changes of frequency response in the inferior colliculus (IC)

  • ABR thresholds in noise exposure group Prior to noise exposure, the average auditory brainstem response (ABR) threshold was screened using 2, 4, 8, and 16 kHz

  • One day after noise overexposure, the ABR thresholds were raised at all the above frequencies compared to pre-exposure levels (P < 0.01 from 13 animals)

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Summary

Introduction

Noise induced injury of the cochlea causes shifts in activation thresholds and changes of frequency response in the inferior colliculus (IC). The reorganization of the frequency topographic map (FTM) has shown to be a direct outcome from hearing loss [4,5,6,7] This could be associated with an increase of spontaneous firing in the brain auditory center [8,9]. Topographic plasticity in the adult central auditory system has been well documented using a wide variety of techniques that result in partial ablation within the periphery of the auditory system These techniques include mechanical disruption of the organ of Corti [5,6] and spiral ganglion [7,12], administration of cochleotoxic drugs [4,13,14], and exposure to high intensity sounds [15,16]

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