Existing auditory system models focus on the ascending path from the cochlea to the midbrain and auditory cortex. However, there exist several feedback paths connecting different auditory pathway stages from the auditory cortex to the cochlea, referred to as the efferent system. We have implemented a dynamic, closed-loop gain-control system into an existing auditory model to simulate parts of the efferent system. Inputs to this control system are auditory nerve (AN) and midbrain spike rates that encode stimulus level and AN fluctuation patterns, respectively. Data from a previous physiological study shows that midbrain cells with band-enhanced modulation transfer functions have rates that increase over time in response to amplitude-modulated stimuli. This trend does not occur in a model without efferent pathways. We adjusted parameters of the model with efferent control paths so that it could simulate the increasing midbrain rate with the same time constant (~140ms) as physiological data.

Forward masking is generally greater for Gaussian noise (GN) than for low-fluctuation noise (LFN) maskers for listeners with and without sensorineural hearing loss (SNHL). Because older age and SNHL may affect recovery from masker envelope fluctuations differently, the current study explored which of these two factors contributed more substantially to the persistence of GN disruption. GN disruption was measured using three masker-signal delays (25, 75, and 150 ms) for three adult participant groups: younger listeners with normal hearing (YNH), older participants with normal, or near-normal, hearing (ONH), and older participants with sensorineural hearing loss (OSNHL). The role of underlying mechanisms was tested using a computational model for midbrain neurons. The primary result suggests that older listeners with normal or near normal hearing may be more susceptible to the deleterious effects of masker-envelope fluctuations than younger listeners with normal hearing. Results from the computational model propose that there may be a larger influence of efferent feedback and saturation of inner hair cells on GN disruption than previously expected.

The focus of most existing auditory models is on the afferent system. The auditory efferent system contains descending projections from several levels of the auditory pathway, from the auditory cortex to the brainstem, that control gain in the cochlea. We developed a model with a time-varying, gain-control signal from the efferent system that includes sub-cortical ascending and descending neural pathways. The medial olivocochlear (MOC) efferent stage of the model receives excitatory projections from both fluctuation-sensitive neurons in the inferior colliculus (IC) and wide-dynamic-range neurons in the cochlear nucleus (CN). The response of the model MOC stage controlled cochlear gain dynamically. Changes in the rates of IC neurons in awake rabbit to long-duration amplitude-modulated (AM) noise were employed to adjust the parameters of the proposed model. In response to AM stimuli, physiological response rates of most IC neurons with band-enhanced (BE) modulation transfer functions (MTFs) increased over a time course consistent with the dynamics of the MOC efferent feedback. The time constant of the MOC model that best matched the IC physiology was compared to available descriptions of the MOC. Responses of the proposed subcortical model to AM noise simulate the trend of increasing rate over time, while the model without the efferent system did not show this trend.

Simultaneous tone-in-noise detection has been studied extensively, but typically without consideration of the medial olivocochlear (MOC) efferents. We are testing hypotheses for masked detection using a central auditory model with a signal from midbrain to MOC. Masked tones are encoded in the rate profile of band-enhanced (BE) inferior colliculus (IC) neurons, which are excited by a range of modulation frequencies. Peripheral responses to noise are characterized by large fluctuations, an effective stimulus for BE IC neurons. In contrast, peripheral channels tuned near the tone have smaller fluctuations: addition of the tone flattens the signal envelope and also pushes the inner hair cell (IHC) transduction nonlinearity further into saturation. Excitatory projections to MOC from noise-driven BE IC cells would decrease cochlear gain, reducing IHC saturation, and resulting in larger fluctuations and IC rates. In contrast, tone-plus-noise-driven channels would reduce MOC excitation, resulting in relatively higher cochlear gain, more saturation, and ultimately lower IC rates. Thus, the descending signal from IC BE cells to MOC is hypothesized to enhance contrast in the IC rate profile. Because efferents have slow dynamics, timing is an important factor. Therefore, we focus on model sensitivity to masked tones of different durations for comparison to psychophysical trends.

Forward masking is generally greater for Gaussian noise (GN) than for low-fluctuation noise maskers, i.e., GN disruption. Because the minimal hearing loss that is associated with older age may affect GN disruption differently than more significant hearing loss, the current study explored the contribution of minimal hearing loss associated with older age to GN disruption. GN disruption was measured using three masker-signal delays (25, 75, and 150 ms) for three adult groups: younger participants with normal hearing (NH), older participants with minimal hearing loss, and older participants with sensorineural hearing loss. The role of underlying mechanisms was tested using a computational model for midbrain neurons. The primary result suggests that older listeners with mild threshold elevations that typically occur with age may be more susceptible to the deleterious effects of masker envelope fluctuations than younger listeners with NH. Results from the computational model indicate that there may be a larger influence of efferent feedback and saturation of inner hair cells on forward masking and GN disruption than previously considered.