Cochlear Gain Research Articles

Effects of ipsilateral, contralateral, and bilateral noise precursors on psychoacoustical tuning curves in humans

Cochlear tuning and hence auditory frequency selectivity are thought to change in noisy environments by activation of the medial olivocochlear reflex (MOCR). In humans, auditory frequency selectivity is often assessed using psychoacoustical tuning curves (PTCs), a plot of the level required for pure-tone maskers to just mask a fixed-level pure-tone probe as a function of masker frequency. Sometimes, however, the stimuli used to measure a PTC are long enough that they can activate the MOCR by themselves and thus affect the PTC. Here, PTCs for probe frequencies of 500 Hz and 4 kHz were measured in forward masking using short maskers (30 ms) and probes (10 ms) to minimize the activation of the MOCR by the maskers or the probes. PTCs were also measured in the presence of long (300 ms) ipsilateral, contralateral, and bilateral broadband noise precursors to investigate the effect of the ipsilateral, contralateral, and bilateral MOCR on PTC tuning. Four listeners with normal hearing participated in the experiments. At 500 Hz, ipsilateral and bilateral precursors sharpened the PTCs by decreasing the thresholds for maskers with frequencies at or near the probe frequency with minimal effects on thresholds for maskers remote in frequency from the probe. At 4 kHz, by contrast, ipsilateral and bilateral precursors barely affected thresholds for maskers near the probe frequency but broadened PTCs by reducing thresholds for maskers far from the probe. Contralateral precursors barely affected PTCs. An existing computational model was used to interpret the results. The model suggested that despite the apparent differences, the pattern of results is consistent with the ipsilateral and bilateral MOCR inhibiting the cochlear gain similarly at the two probe frequencies and more strongly than the contralateral MOCR.

Measuring and modeling Gaussian noise disruption across frequency, level, and hearing status

Recent work suggested that older listeners with minimal hearing loss exhibit more forward masking for a highly fluctuating Gaussian noise (GN) masker relative to a low-fluctuation noise (LFN) masker. This threshold difference (GN–LFN) is referred to as GN disruption and was previously attributed to time-varying cochlear gain resulting from feedback control by the medial olivocochlear (MOC) system. However, thus far, masker conditions have been limited to 80 dB SPL at 4 kHz. The current study aims to challenge the hypothesis that the physiological basis of GN disruption is the MOC system using behavioral measures and computational models across multiple target and masker frequencies (0.5, 1, 2, and 4 kHz), masker levels (80-, 65-, and 50-dB SPL), masker-signal delays (25- and 75-ms), participant age ranges (18–30 and 60–75), and hearing statuses (normal hearing, sensorineural hearing loss). Additionally, speech recognition using IEEE sentences will be measured with GN and LFN maskers. Although testing will not be completed until 2025, preliminary data from 20 younger participants with normal hearing suggest that GN disruption is greater for higher than lower masker and probe frequencies, that GN disruption is similar across masker levels, and that refinements to the computational model are needed to more accurately predict GN disruption.

Noise within: Signal-to-noise enhancement via coherent wave amplification in the mammalian cochlea.

The extraordinary sensitivity of the mammalian inner ear has captivated scientists for decades, largely due to the crucial role played by the outer hair cells (OHCs) and their unique electromotile properties. Typically arranged in three rows along the sensory epithelium, the OHCs work in concert via mechanisms collectively referred to as the "cochlear amplifier" to boost the cochlear response to faint sounds. While simplistic views attribute this enhancement solely to the OHC-based increase in cochlear gain, the inevitable presence of internal noise requires a more rigorous analysis. Achieving a genuine boost in sensitivity through amplification requires that signals be amplified more than internal noise, and this requirement presents the cochlea with an intriguing challenge. Here we analyze the effects of spatially distributed cochlear-like amplification on both signals and internal noise. By combining a straightforward mathematical analysis with a simplified model of cochlear mechanics designed to capture the essential physics, we generalize previous results about the impact of spatially coherent amplification on signal degradation in active gain media. We identify and describe the strategy employed by the cochlea to amplify signals more than internal noise and thereby enhance the sensitivity of hearing. For narrow-band signals, this effective, wave-based strategy consists of spatially amplifying the signal within a localized cochlear region, followed by rapid attenuation. Location-dependent wave amplification and attenuation meet the necessary conditions for amplifying near-characteristic frequency (CF) signals more than internal noise components of the same frequency. Our analysis reveals that the sharp wave cutoff past the CF location greatly reduces noise contamination. The distinctive asymmetric shape of the "cochlear filters" thus underlies a crucial but previously unrecognized mechanism of cochlear noise reduction.

Subcortical auditory model including efferent dynamic gain control with inputs from cochlear nucleus and inferior colliculus.

An auditory model has been developed with a time-varying, gain-control signal based on the physiology of the efferent system and subcortical neural pathways. The medial olivocochlear (MOC) efferent stage of the model receives excitatory projections from fluctuation-sensitive model neurons of the inferior colliculus (IC) and wide-dynamic-range model neurons of the cochlear nucleus. The response of the model MOC stage dynamically controls cochlear gain via simulated outer hair cells. In response to amplitude-modulated (AM) noise, firing rates of most IC neurons with band-enhanced modulation transfer functions in awake rabbits increase over a time course consistent with the dynamics of the MOC efferent feedback. These changes in the rates of IC neurons in awake rabbits were employed to adjust the parameters of the efferent stage of the proposed model. Responses of the proposed model to AM noise were able to simulate the increasing IC rate over time, whereas the model without the efferent system did not show this trend. The proposed model with efferent gain control provides a powerful tool for testing hypotheses, shedding insight on mechanisms in hearing, specifically those involving the efferent system.

Distortion Product Otoacoustic Emissions in Mice Above and Below the Eliciting Primaries.

Normal hearing is associated with cochlear nonlinearity. When two tones (f1 and f2) are presented, the intracochlear response contains additional components that can be recorded from the ear canal as distortion product otoacoustic emissions (DPOAEs). Although the most prominent intermodulation distortion component is at 2f1-f2, other cubic distortion products are also generated. Because these measurements are noninvasive, they are used in humans and in animal models to detect hearing loss. This study evaluated how loss of sensitivity affects DPOAEs with frequencies above and below the stimulating primaries, i.e., for upper sideband (USB) components like 2f2-f1 and for lower sideband (LSB) components like 2f1-f2. DPOAEs were recorded in several mouse mutants with varying degrees of hearing loss associated with structural changes to the tectorial membrane (TM), or with loss of outer hair cell (OHC) somatic electromotility due to lack of prestin or to the expression of a non-functional prestin. In mice with changes in sensitivity, magnitude reductions were observed for 2f1-f2 relative to controls with mice lacking prestin showing the greatest changes. In contrast, 2f2-f1 was minimally affected by reductions in cochlear gain due to changes in the TM or by the loss of OHC somatic electromotility. In addition, TM mutants with spontaneous otoacoustic emissions (SOAEs) generated larger responses than controls at 2f2-f1 when its frequency was similar to that for the SOAEs. Although cochlear pathologies appear to affect USB and LSB DPOAEs in different ways, both 2f1-f2 and 2f2-f1 reflect nonlinearities associated with the transducer channels. However, in mice, the component at 2f2-f1 does not appear to receive enhancement due to prestin's motor action.

Effects of sensorineural hearing loss on formant-frequency discrimination: Measurements and models

This study concerns the effect of hearing loss on discrimination of formant frequencies in vowels. In the response of the healthy ear to a harmonic sound, auditory-nerve (AN) rate functions fluctuate at the fundamental frequency, F0. Responses of inner-hair-cells (IHCs) tuned near spectral peaks are captured (or dominated) by a single harmonic, resulting in lower fluctuation depths than responses of IHCs tuned between spectral peaks. Therefore, the depth of neural fluctuations (NFs) varies along the tonotopic axis and encodes spectral peaks, including formant frequencies of vowels. This NF code is robust across a wide range of sound levels and in background noise. The NF profile is converted into a rate-place representation in the auditory midbrain, wherein neurons are sensitive to low-frequency fluctuations. The NF code is vulnerable to sensorineural hearing loss (SNHL) because capture depends upon saturation of IHCs, and thus the interaction of cochlear gain with IHC transduction. In this study, formant-frequency discrimination limens (DLFFs) were estimated for listeners with normal hearing or mild to moderate SNHL. The F0 was fixed at 100 Hz, and formant peaks were either aligned with harmonic frequencies or placed between harmonics. Formant peak frequencies were 600 and 2000 Hz, in the range of first and second formants of several vowels. The difficulty of the task was varied by changing formant bandwidth to modulate the contrast in the NF profile. Results were compared to predictions from model auditory-nerve and inferior colliculus (IC) neurons, with listeners’ audiograms used to individualize the AN model. Correlations between DLFFs, audiometric thresholds near the formant frequencies, age, and scores on the Quick speech-in-noise test are reported. SNHL had a strong effect on DLFF for the second formant frequency (F2), but relatively small effect on DLFF for the first formant (F1). The IC model appropriately predicted substantial threshold elevations for changes in F2 as a function of SNHL and little effect of SNHL on thresholds for changes in F1.

The effects of broadband elicitor duration on a psychoacoustic measure of cochlear gain reduction.

Physiological and psychoacoustic studies of the medial olivocochlear reflex (MOCR) in humans have often relied on long duration elicitors (>100 ms). This is largely due to previous research using otoacoustic emissions (OAEs) that found multiple MOCR time constants, including time constants in the 100s of milliseconds, when elicited by broadband noise. However, the effect of the duration of a broadband noise elicitor on similar psychoacoustic tasks is currently unknown. The current study measured the effects of ipsilateral broadband noise elicitor duration on psychoacoustic gain reduction estimated from a forward-masking paradigm. Analysis showed that both masker type and elicitor duration were significant main effects, but no interaction was found. Gain reduction time constants were ∼46 ms for the masker present condition and ∼78 ms for the masker absent condition (ranging from ∼29 to 172 ms), both similar to the fast time constants reported in the OAE literature (70-100 ms). Maximum gain reduction was seen for elicitor durations of ∼200 ms. This is longer than the 50-ms duration which was found to produce maximum gain reduction with a tonal on-frequency elicitor. Future studies of gain reduction may use 150-200 ms broadband elicitors to maximally or near-maximally stimulate the MOCR.

Testing phenomenological auditory-nerve model predictions for selective inner- and outer-hair-cell dysfunction

Sensorineural hearing loss (SNHL) effects on neural coding and perception have been largely associated with outer-hair-cell (OHC) dysfunction (e.g., reduced cochlear gain, reduced compression, broadened tuning). However, both inner-hair-cell (IHC) and OHC dysfunction occur in common hearing-loss etiologies, e.g., noise-induced and age-related (metabolic). Although IHC effects are largely ignored based on the insensitivity of audiograms to IHC loss up to 80%, the same selective IHC damage affects suprathreshold hearing (e.g., tone-in-noise detection, EFRs to periodic stimuli). Phenomenological auditory-nerve (AN) models are useful for studying neural-coding effects of SNHL, but their parametric control of OHC and IHC function (e.g., cohc and cihc parameters, Bruce et al., 2018) are designed based on data from animals with noise-induced hearing loss (OHC/IHC dysfunction combined). Although this approach has proven successful for OHC effects, testing of IHC-based effects has been largely indirect. Here, we compare model predictions to our previously collected AN-fiber responses to amplitude-modulated stimuli in animals with either carboplatin-induced selective IHC dysfunction or gentamicin-induced selective OHC damage to provide more direct testing of IHC and OHC effects. Model parameters were estimated from histology, ABR thresholds, AN-fiber rates, and spike-train statistical metrics (e.g., vector strength, discriminability, mutual information).

Contralateral inhibition of distortion product otoacoustic emissions in young noise-exposed Veterans.

Although animal models show a clear link between noise exposure and damage to afferent cochlear synapses, the relationship between noise exposure and efferent function appears to be more complex. Animal studies indicate that high intensity noise exposure reduces efferent medial olivocochlear (MOC) reflex strength, whereas chronic moderate noise exposure is associated with a conditioning effect that enhances the MOC reflex. The MOC reflex is predicted to improve speech-in-noise perception and protects against noise-induced auditory damage by reducing cochlear gain. In humans, MOC reflex strength can be estimated by measuring contralateral inhibition of distortion product otoacoustic emissions (DPOAEs). The objective of this study was to determine the impact of military noise exposure on efferent auditory function by measuring DPOAE contralateral inhibition in young Veterans and non-Veterans with normal audiograms. Compared with non-Veteran controls, Veterans with high levels of reported noise exposure demonstrated a trend of reduced contralateral inhibition across a broad frequency range, suggesting efferent damage. Veterans with moderate noise exposure showed trends of reduced inhibition from 3 to 4 kHz but greater inhibition from 1 to 1.5 kHz, consistent with conditioning. These findings suggest that, in humans, the impact of noise exposure on the MOC reflex differs depending on the noise intensity and duration.

Synaptopathy in Guinea Pigs Induced by Noise Mimicking Human Experience and Associated Changes in Auditory Signal Processing.

Noise induced synaptopathy (NIS) has been researched extensively since a large amount of synaptic loss without permanent threshold shift (PTS) was found in CBA mice after a brief noise exposure. However, efforts to translate these results to humans have met with little success—and might not be possible since noise exposure used in laboratory animals is generally different from what is experienced by human subjects in real life. An additional problem is a lack of morphological data and reliable functional methods to quantify loss of afferent synapses in humans. Based on evidence for disproportionate synaptic loss for auditory nerve fibers (ANFs) with low spontaneous rates (LSR), coding-in-noise deficits (CIND) have been speculated to be the major difficulty associated with NIS without PTS. However, no robust evidence for this is available in humans or animals. This has led to a re-examination of the role of LSR ANFs in signal coding in high-level noise. The fluctuation profile model has been proposed to support a role for high-SR ANFs in the coding of high-level noise in combination with efferent control of cochlear gain. This study aimed to induce NIS by a low-level, intermittent noise exposure mimicking what is experienced in human life and examined the impact of the NIS on temporal processing under masking. It also evaluated the role of temporal fluctuation in evoking efferent feedback and the effects of NIS on this feedback.

A Modelling Study on the Comparison of Predicted Auditory Nerve Firing Rates for the Personalized Indication of Cochlear Implantation

The decision of whether to perform cochlear implantation is crucial because implantation cannot be reversed without harm. The aim of the study was to compare model-predicted time–place representations of auditory nerve (AN) firing rates for normal hearing and impaired hearing with a view towards personalized indication of cochlear implantation. AN firing rates of 1024 virtual subjects with a wide variety of different types and degrees of hearing impairment were predicted. A normal hearing reference was compared to four hearing prosthesis options, which were unaided hearing, sole acoustic amplification, sole electrical stimulation, and a combination of the latter two. The comparisons and the fitting of the prostheses were based on a ‘loss of action potentials’ (LAP) score. Single-parameter threshold analysis suggested that cochlear implantation is indicated when more than approximately two-thirds of the inner hair cells (IHCs) are damaged. Second, cochlear implantation is also indicated when more than an average of approximately 12 synapses per IHC are damaged due to cochlear synaptopathy (CS). Cochlear gain loss (CGL) appeared to shift these thresholds only slightly. Finally, a support vector machine predicted the indication of a cochlear implantation from hearing loss parameters with a 10-fold cross-validated accuracy of 99.2%.

Synaptic plasticity of inhibitory synapses onto medial olivocochlear efferent neurons.

The descending auditory system modulates the ascending system at every level. The final descending, or efferent, stage comprises lateral olivocochlear and medial olivocochlear (MOC) neurons. MOC somata in the ventral brainstem project axons to the cochlea to synapse onto outer hair cells (OHC), inhibiting OHC‐mediated cochlear amplification. MOC suppression of OHC function is implicated in cochlear gain control with changing sound intensity, detection of salient stimuli, attention and protection against acoustic trauma. Thus, sound excites MOC neurons to provide negative feedback of the cochlea. Sound also inhibits MOC neurons via medial nucleus of the trapezoid body (MNTB) neurons. However, MNTB–MOC synapses exhibit short‐term depression, suggesting reduced MNTB–MOC inhibition during sustained stimuli. Further, due to high rates of both baseline and sound‐evoked activity in MNTB neurons in vivo, MNTB–MOC synapses may be tonically depressed. To probe this, we characterized short‐term plasticity of MNTB–MOC synapses in mouse brain slices. We mimicked in vivo‐like temperature and extracellular calcium conditions, and in vivo‐like activity patterns of fast synaptic activation rates, sustained activation and prior tonic activity. Synaptic depression was sensitive to extracellular calcium concentration and temperature. During rapid MNTB axon stimulation, postsynaptic currents in MOC neurons summated but with concurrent depression, resulting in smaller, sustained currents, suggesting tonic inhibition of MOC neurons during rapid circuit activity. Low levels of baseline MNTB activity did not significantly reduce responses to subsequent rapid activity that mimics sound stimulation, indicating that, in vivo, MNTB inhibition of MOC neurons persists despite tonic synaptic depression.Key points Inhibitory synapses from the medial nucleus of the trapezoid body (MNTB) onto medial olivocochlear (MOC) neurons exhibit short‐term plasticity that is sensitive to calcium and temperature, with enhanced synaptic depression occurring at higher calcium concentrations and at room temperature.High rates of background synaptic activity that mimic the upper limits of spontaneous MNTB activity cause tonic synaptic depression of MNTB–MOC synapses that limits further synaptic inhibition.High rates of activity at MNTB–MOC synapses cause synaptic summation with concurrent depression to yield a response with an initial large amplitude that decays to a tonic inhibition.

Examining potential sources of variability in behavioral measures of cochlear gain and gain reduction in listeners with normal hearing or minimal cochlear hearing loss

This study examined the relationship between clinical measures of auditory function and psychoacoustic measures related to cochlear function. Listeners’ audiometric thresholds for long tones ranged from well within the clinically normal range to just above this range. Where thresholds were elevated, other clinical tests were consistent with a cochlear origin. Because the medial olivocochlear reflex decreases cochlear gain in response to sound, measures were made with short stimuli. Signal frequencies were from 1 to 8 kHz. One point on the lower leg of the input/output function was measured by finding threshold masker level for a masker almost one octave below the signal frequency needed to mask a signal at 5 dB SL. Gain reduction was estimated by presenting a pink broadband noise precursor before the signal and masker and measuring the change in signal threshold as a function of precursor level. In a previous presentation, it was shown that the estimate of gain reduction decreased as quiet threshold increased, but was not solely determined by the amount of gain. In this presentation, the relationship between gain reduction and clinical otoacoustic emission and middle-ear muscle reflex measurements was examined to determine whether these explained some of the variability. [Work supported by NIH (NIDCD) R01 DC008327 (EAS) and NIH(NIDCD) T32 DC016853 (WBS).]

Immunohistochemistry localises myosin-7a to cochlear efferent boutons.

Background: Myosin 7a is an actin-binding motor protein involved in the formation of hair-cell stereocilia both in the cochlea and in the vestibular system. Mutations in myosin 7a are linked to congenital hearing loss and are present in 50% of Type-1 Usher syndrome patients who suffer from progressive hearing loss and vestibular system dysfunction. Methods: Myosin 7a is often used to visualise sensory hair cells due to its well characterised and localised expression profile. We thus conducted myosin-7a immunostaining across all three turns of the adult rat organ of Corti to visualise hair cells. Results: As expected, we observed myosin 7a staining in both inner and outer hair cells. Unexpectedly, we also observed strong myosin 7a staining in the medial olivocochlear efferent synaptic boutons contacting the outer hair cells. Efferent bouton myosin-7a staining was present across all three turns of the cochlea. We verified this localisation by co-staining with a known efferent bouton marker, the vesicular acetylcholine transporter. Conclusions: In addition to its role in stereocilia formation and maintenance, myosin 7a or certain myosin-7a expression variants might play a role in efferent synaptic transmission in the cochlea and thus ultimately influence cochlear gain regulation. Our immunohistochemistry results should be validated with other methods to confirm these serendipitous findings.

Immunohistochemistry localises myosin-7a to cochlear efferent boutons

Background: Myosin 7a is an actin-binding motor protein involved in the formation of hair-cell stereocilia both in the cochlea and in the vestibular system. Mutations in myosin 7a are linked to congenital hearing loss and are present in 50% of Type-1 Usher syndrome patients who suffer from progressive hearing loss and vestibular system dysfunction. Methods: Myosin 7a is often used to visualise sensory hair cells due to its well characterised and localised expression profile. We thus conducted myosin-7a immunostaining across all three turns of the adult rat organ of Corti to visualise hair cells. Results: As expected, we observed myosin 7a staining in both inner and outer hair cells. Unexpectedly, we also observed strong myosin 7a staining in the medial olivocochlear efferent synaptic boutons contacting the outer hair cells. Efferent bouton myosin-7a staining was present across all three turns of the cochlea. We verified this localisation by co-staining with a known efferent bouton marker, the vesicular acetylcholine transporter. Conclusions: In addition to its role in stereocilia formation and maintenance, myosin 7a or certain myosin-7a expression variants might play a role in efferent synaptic transmission in the cochlea and thus ultimately influence cochlear gain regulation. Our immunohistochemistry results should be validated with other methods to confirm these serendipitous findings.

Immunohistochemistry localises myosin-7a to cochlear efferent boutons

Background: Myosin 7a is an actin-binding motor protein involved in the formation of hair-cell stereocilia both in the cochlea and in the vestibular system. Mutations in myosin 7a are linked to congenital hearing loss and are present in 50% of Type-1 Usher syndrome patients who suffer from progressive hearing loss and vestibular system dysfunction. Methods: Myosin 7a is often used to visualise sensory hair cells due to its well characterised and localised expression profile. We thus conducted myosin-7a immunostaining across all three turns of the adult rat organ of Corti to visualise hair cells. Results: As expected, we observed myosin 7a staining in both inner and outer hair cells. Unexpectedly, we also observed strong myosin 7a staining in the medial olivocochlear efferent synaptic boutons contacting the outer hair cells. Efferent bouton myosin-7a staining was present across all three turns of the cochlea. We verified this localisation by co-staining with a known efferent bouton marker, the vesicular acetylcholine transporter. Conclusions: In addition to its role in stereocilia formation and maintenance, myosin 7a or certain myosin-7a expression variants might play a role in efferent synaptic transmission in the cochlea and thus ultimately influence cochlear gain regulation. Our immunohistochemistry results should be validated with other methods to confirm these serendipitous findings.

Magnitude of the contralateral efferent olivocochlear effect as a function of the frequency

BackgroundThe activation of the medial olivocochlear reflex reduces the cochlear gain, which is manifested perceptually as decreased auditory sensitivity. However, it has remained unclear whether the extent of this suppression varies according to the cochlear region involved. Here we aims to assess the magnitude of contralateral efferent suppression across human cochlea, at low levels, and its impact on hearing sensitivity. MethodsAssuming that acoustic stimulation activates the contralateral medial olivocochlear reflex, we evaluated the magnitude of the suppressive effect as a function of frequency in 17 subjects with normal hearing. Absolute thresholds were measured for bursts tones of various durations (10, 100, and 500 ms) and frequencies (250, 500, 1000, 4000, and 8000 Hz) in the presence or absence of contralateral white noise at 60 dB SPL. ResultsWe found that contralateral noise raised the absolute threshold for the burst tones evaluated. The effect was greater at lower than higher frequencies (3.85 dB at 250 Hz vs. 2.22 dB at 8000 Hz). ConclusionsOur findings suggest that in humans, the magnitude of this suppression varies according to the cochlear region stimulated, with a greater effect towards the apex (lower frequencies) than the base (higher frequencies) of the cochlea.

Fluid focusing and viscosity allow high gain and stability of the cochlear response.

This paper discusses the role of two-dimensional (2-D)/three-dimensional (3-D) cochlear fluid hydrodynamics in the generation of the large nonlinear dynamical range of the basilar membrane (BM) and pressure response, in the decoupling between cochlear gain and tuning, and in the dynamic stabilization of the high-gain BM response in the peak region. The large and closely correlated dependence on stimulus level of the BM velocity and fluid pressure gain [Dong, W., and Olson, E. S. (2013). Biophys. J. 105(4), 1067-1078] is consistent with a physiologically oriented schematization of the outer hair cell (OHC) mechanism if two hydrodynamic effects are accounted for: amplification of the differential pressure associated with a focusing phenomenon, and viscous damping at the BM-fluid interface. The predictions of the analytical 2-D Wentzel-Kramers-Brillouin (WKB) approach are compared to solutions of a 3-D finite element model, showing that these hydrodynamic phenomena yield stable high-gain response in the peak region and a smooth transition among models with different effectiveness of the active mechanism, mimicking the cochlear nonlinear response over a wide stimulus level range. This study explains how an effectively anti-damping nonlinear outer hair cells (OHC) force may yield large BM and pressure dynamical ranges along with an almost level-independent admittance.

Behavioral Measures of Cochlear Gain Reduction Depend on Precursor Frequency, Bandwidth, and Level.

Sensory systems adjust to the environment to maintain sensitivity to change. In the auditory system, the medial olivocochlear reflex (MOCR) is a known physiological mechanism capable of such adjustment. The MOCR provides efferent feedback between the brainstem and cochlea, reducing cochlear gain in response to sound. The perceptual effects of the MOCR are not well understood, such as how gain reduction depends on elicitor characteristics in human listeners. Physiological and behavioral data suggest that ipsilateral MOCR tuning is only slightly broader than it is for afferent fibers, and that the fibers feed back to the frequency region of the cochlea that stimulated them. However, some otoacoustic emission (OAE) data suggest that noise is a more effective elicitor than would be consistent with sharp tuning, and that a broad region of the cochlea may be involved in elicitation. If the elicitor is processed in a cochlear channel centered at the signal frequency, the growth of gain reduction with elicitor level would be expected to depend on the frequency content of the elicitor. In the current study, the effects of the frequency content and level of a preceding sound (called a precursor) on signal threshold was examined. The results show that signal threshold increased with increasing precursor level at a shallower slope for a tonal precursor at the signal frequency than for a tonal precursor nearly an octave below the signal frequency. A broadband noise was only slightly more effective than a tone at the signal frequency, with a relatively shallow slope similar to that of the tonal precursor at the signal frequency. Overall, these results suggest that the excitation at the signal cochlear place, regardless of elicitor frequency, determines the magnitude of ipsilateral cochlear gain reduction, and that it increases with elicitor level.

The effect of broadband elicitor laterality on psychoacoustic gain reduction across signal frequency.

There are psychoacoustic methods thought to measure gain reduction, which may be from the medial olivocochlear reflex (MOCR), a bilateral feedback loop that adjusts cochlear gain. Although studies have used ipsilateral and contralateral elicitors and have examined strength at different signal frequencies, these factors have not been examined within a single study. Therefore, basic questions about gain reduction, such as the relative strength of ipsilateral vs contralateral elicitation and the relative strength across signal frequency, are not known. In the current study, gain reduction from ipsilateral, contralateral, and bilateral elicitors was measured at 1-, 2-, and 4-kHz signal frequencies using forward masking paradigms at a range of elicitor levels in a repeated measures design. Ipsilateral and bilateral strengths were similar and significantly larger than contralateral strength across signal frequencies. Growth of gain reduction with precursor level tended to differ with signal frequency, although not significantly. Data from previous studies are considered in light of the results of this study. Behavioral results are also considered relative to anatomical and physiological data on the MOCR. These results indicate that, in humans, cochlear gain reduction is broad across frequencies and is robust for ipsilateral and bilateral elicitation but small for contralateral elicitation.