Psychophysical estimates of cochlear function suggest that normal-hearing listeners exhibit a compressive basilar-membrane (BM) response. Listeners with moderate to severe sensorineural hearing loss may exhibit a linearized BM response along with reduced gain, suggesting the loss of an active cochlear mechanism. This study investigated how the BM response changes with increasing hearing loss by comparing psychophysical measures of BM compression and gain for normal-hearing listeners with those for listeners who have mild to moderate sensorineural hearing loss. Data were collected from 16 normal-hearing listeners and 12 ears from 9 hearing-impaired listeners. The forward masker level required to mask a fixed low-level, 4000-Hz signal was measured as a function of the masker-signal interval using a masker frequency of either 2200 or 4000 Hz. These plots are known as temporal masking curves (TMCs). BM response functions derived from the TMCs showed a systematic reduction in gain with degree of hearing loss. Contrary to current thinking, however, no clear relationship was found between maximum compression and absolute threshold.

Cochlear nonlinearity was estimated over a wide range of center frequencies and levels in listeners with normal hearing, using a forward-masking method. For a fixed low-level probe, the masker level required to mask the probe was measured as a function of the masker-probe interval, to produce a temporal masking curve (TMC). TMCs were measured for probe frequencies of 500, 1000, 2000, 4000, and 8000 Hz, and for masker frequencies 0.5, 0.7, 0.9, 1.0 (on frequency), 1.1, and 1.6 times the probe frequency. Across the range of probe frequencies, the TMCs for on-frequency maskers showed two or three segments with clearly distinct slopes. If it is assumed that the rate of decay of the internal effect of the masker is constant across level and frequency, the variations in the slopes of the TMCs can be attributed to variations in cochlear compression. Compression-ratio estimates for on-frequency maskers were between 3:1 and 5:1 across the range of probe frequencies. Compression did not decrease at low frequencies. The slopes of the TMCs for the lowest frequency probe (500 Hz) did not change with masker frequency. This suggests that compression extends over a wide range of stimulus frequencies relative to characteristic frequency in the apical region of the cochlea.

A revised computational model of the inner-hair cell (IHC) and auditory-nerve (AN) complex is presented and evaluated. Building on previous models, the algorithm is intended as a component for use in more comprehensive models of the auditory periphery. It combines smaller components that aim to be faithful to physiology in so far as is practicable and known. Transduction between cochlear mechanical motion and IHC receptor potential (RP) is simulated using a modification of an existing biophysical IHC model. Changes in RP control the opening of calcium ion channels near the synapse, and local calcium levels determine the probability of the release of neurotransmitter. AN adaptation results from transmitter depletion. The exact timing of AN action potentials is determined by the quantal and stochastic release of neurotransmitter into the cleft. The model reproduces a wide range of animal RP and AN observations. When the input to the model is taken from a suitably nonlinear simulation of the motion of the cochlear partition, the new algorithm is able to simulate the rate-intensity functions of low-, medium-, and high-spontaneous rate AN fibers in response to stimulation both at best frequency and at other frequencies. The variation in fiber type arises in large part from the manipulation of a single parameter in the model: maximum calcium conductance. The model also reproduces quantitatively phase-locking characteristics, relative refractory effects, mean-to-variance ratio, and first- and second-order discharge history effects.

Animal studies demonstrate that noise exposure can permanently damage the synapses between inner hair cells and auditory nerve fibers, even when outer hair cells are intact and there is no clinically relevant permanent threshold shift. Synaptopathy disrupts the afferent connection between the cochlea and the central auditory system and is predicted to impair speech understanding in noisy environments and potentially result in tinnitus and/or hyperacusis. While cochlear synaptopathy has been demonstrated in numerous experimental animal models, synaptopathy can only be confirmed through post-mortem temporal bone analysis, making it difficult to study in living humans. A variety of non-invasive measures have been used to determine whether noise-induced synaptopathy occurs in humans, but the results are conflicting. The overall objective of this article is to synthesize the existing data on the functional impact of noise-induced synaptopathy in the human auditory system. The first section of the article summarizes the studies that provide evidence for and against noise-induced synaptopathy in humans. The second section offers potential explanations for the differing results between studies. The final section outlines suggested methodologies for diagnosing synaptopathy in humans with the aim of improving consistency across studies.