Abstract
The compressive nonlinearity of cochlear signal transduction, reflecting outer-hair-cell function, manifests as suppressive spectral interactions; e.g., two-tone suppression. Moreover, for broadband sounds, there are multiple interactions between frequency components. These frequency-dependent nonlinearities are important for neural coding of complex sounds, such as speech. Acoustic-trauma-induced outer-hair-cell damage is associated with loss of nonlinearity, which auditory prostheses attempt to restore with, e.g., "multi-channel dynamic compression" algorithms.Neurophysiological data on suppression in hearing-impaired (HI) mammals are limited. We present data on firing-rate suppression measured in auditory-nerve-fiber responses in a chinchilla model of noise-induced hearing loss, and in normal-hearing (NH) controls at equal sensation level. Hearing-impaired (HI) animals had elevated single-fiber excitatory thresholds (by ~ 20-40 dB), broadened frequency tuning, and reduced-magnitude distortion-product otoacoustic emissions; consistent with mixed inner- and outer-hair-cell pathology. We characterized suppression using two approaches: adaptive tracking of two-tone-suppression threshold (62 NH, and 35 HI fibers), and Wiener-kernel analyses of responses to broadband noise (91 NH, and 148 HI fibers). Suppression-threshold tuning curves showed sensitive low-side suppression for NH and HI animals. High-side suppression thresholds were elevated in HI animals, to the same extent as excitatory thresholds. We factored second-order Wiener-kernels into excitatory and suppressive sub-kernels to quantify the relative strength of suppression. We found a small decrease in suppression in HI fibers, which correlated with broadened tuning. These data will help guide novel amplification strategies, particularly for complex listening situations (e.g., speech in noise), in which current hearing aids struggle to restore intelligibility.