Preservation of Neural Sensitivity after Noise-Induced Suppression of Sensory Function

Abstract

Background: Permanent loss of outer hair cell (OHC) amplification may occur within days of acoustic overexposure. This loss of sensory function typically results in an immediate loss of neural sensitivity although neurodegeneration occurs months or years after damage to OHCs. This delay in neurodegeneration might provide an opportunity to preserve neural sensitivity although OHC amplification is permanently lost. Purpose: To test the hypothesis that neural functions can be preserved after permanent and severe loss of OHC amplification. To begin to address this possibility, an animal model of severe permanent loss of both OHC and neural functions was established. Research Design: This research employed a 4 × 4 split-plot factorial design, with four levels of the within-subject factor (time: baseline, 1-day, 1-week, and 1-mo postnoise exposure) and four levels of the between-subject factor (experimental groups: control, noise exposed, therapy, and noise exposed + therapy). Study Sample: Twenty-six hooded male Long-Evans rats (263 ± 63 g) served as subjects for this experiment. All animals exhibited baseline auditory function that approximated normative values for rats of the same strain. Data Collection and Analysis: Distortion product otoacoustic emissions and auditory brainstem responses were used to assay and differentiate OHC versus neural functions. Factorial analysis of variances was computed to identify statistically significant main effects and Dunnett testing was employed in post hoc computations. Intervention: To rescue neural function after permanent loss of OHC amplification, small molecular weight carboxy alkyl esters were employed after noise injury. Results: The results revealed that in the presence of permanent loss of OHC amplification, the loss of neural sensitivity could be rescued. In addition, auditory brainstem response wave I amplitudes at suprathreshold levels were rescued from noise-induced depletion into the biologic noise floor. Conclusion: Since mammalian OHCs do not regenerate after damage, these results encourage further experiments aimed at preserving neural functions following noise injury.