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.
Key Words
noise-induced hearing loss - otoprotection - repair
