When stimulated by tones, the ear appears to emit tones of its own, stimulus-frequency otoacoustic emissions (SFOAEs). SFOAEs were measured in 17 chinchillas and their group delays were compared with a place map of basilar-membrane vibration group delays measured at the characteristic frequency. The map is based on Wiener-kernel analysis of responses to noise of auditory-nerve fibers corroborated by measurements of vibrations at several basilar-membrane sites. SFOAE group delays were similar to, or shorter than, basilar-membrane group delays for frequencies >4 kHz and <4 kHz, respectively. Such short delays contradict the generally accepted "theory of coherent reflection filtering" [Zweig and Shera, J. Acoust. Soc. Am. 98, 2018-2047 (1995)], which predicts that the group delays of SFOAEs evoked by low-level tones approximately equal twice the basilar-membrane group delays. The results for frequencies higher than 4 kHz are compatible with hypotheses of SFOAE propagation to the stapes via acoustic waves or fluid coupling, or via reverse basilar membrane traveling waves with speeds corresponding to the signal-front delays, rather than the group delays, of the forward waves. The results for frequencies lower than 4 kHz cannot be explained by hypotheses based on waves propagating to and from their characteristic places in the cochlea.

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Objectives The purpose of this study was to obtain behavioral hearing thresholds for frequencies between 0.125 and 20 kHz from a large population between 10 and 65 years old using a clinically feasible calibration method expected to compensate well for variations in the distance between the eardrum and an insert-type sound source. Previous reports of hearing thresholds in the extended high frequencies (> 8 kHz) have either used calibration techniques known to be inaccurate or specialized equipment not suitable for clinical use. Design Hearing thresholds were measured from 352 human subjects between 10 to 65 years old having clinically normal hearing thresholds (< 20 dB HL) up to 4 kHz. An otoacoustic emission probe fitted with custom sound sources was used and the stimulus levels individually tailored based on an estimate of the insertion depth of the measurement probe. The calibrated stimulus levels were determined based on measurements made at various depths of insertion in a standard ear simulator. Threshold values were obtained for 21 frequencies between 0.125 and 20 kHz using a modified Békésy technique. Forty six of the subjects returned for a second measurement months later from the initial evaluation. Results In agreement with previous reports hearing thresholds at extended high frequencies were found to be sensitive to age related changes in auditory function. In contrast with previous reports, no gender differences were found in average hearing thresholds at most evaluated frequencies. Two aging processes, one faster than the other in time scale, appear to influence hearing thresholds in different frequency ranges. The standard deviation of test-retest threshold difference for all evaluated frequencies was 5~10 dB, comparable to that reported in the literature for similar measurement techniques, but smaller than that observed for data obtained using the standard clinical procedure. Conclusions The depth-compensated ear-simulator-based calibration method and the modified Békésy technique allow reliable measurement of hearing thresholds over the entire frequency range of human hearing. Hearing thresholds at the extended high frequencies are sensitive to aging and reveal subtle differences, which are not evident in the frequency range evaluated regularly (8 kHz and below). Previously-reported gender-related differences in hearing thresholds may be related to ear canal acoustics and the calibration procedure and not due to differences in hearing sensitivity.

Low-noise microphones designed to measure otoacoustic emissions from the human ear canal typically sample the sound field in the canal some 15–20 mm away from the eardrum. The input sound levels to the middle ear are usually defined as the sound-pressure level ‘‘at the eardrum.’’ However, the well-known phenomenon of standing waves produces a spatially nonuniform pressure for frequencies above 2–3 kHz. This phenomenon is demonstrated using physical simulation with a commonly used emission probe and the interpretation of the results are confirmed by simple acoustical theory. In addition, it is shown large (±20 dB) errors in the estimated eardrum sound pressure result from varying the position of the sound source in the canal. Theory, physical simulations and measurements in human ear canals are used to characterize the errors using various calibration procedures commonly employed in otoacoustic emission studies. It is predicted that the reliability of measurements of high-frequency stimulated otoacoustic emissions will be improved if the stimulus sound-pressure levels were measured near the eardrum.

The reliability of nine measures of the stimulus level in the human ear canal was compared by measuring the sensitivity of behavioral hearing thresholds to changes in the depth of insertion of an otoacoustic emission probe. Four measures were the ear-canal pressure, the eardrum pressure estimated from it and the pressure measured in an ear simulator with and without compensation for insertion depth. The remaining five quantities were derived from the ear-canal pressure and the Thévenin-equivalent source characteristics of the probe: Forward pressure, initial forward pressure, the pressure transmitted into the middle ear, eardrum sound pressure estimated by summing the magnitudes of the forward and reverse pressure (integrated pressure) and absorbed power. Two sets of behavioral thresholds were measured in 26 subjects from 0.125 to 20 kHz, with the probe inserted at relatively deep and shallow positions in the ear canal. The greatest dependence on insertion depth was for transmitted pressure and absorbed power. The measures with the least dependence on insertion depth throughout the frequency range (best performance) included the depth-compensated simulator, eardrum, forward, and integrated pressures. Among these, forward pressure is advantageous because it quantifies stimulus phase.

␣-Tectorin (TECTA), ␤-tectorin (TECTB), and carcinoembryonic antigen-related cell adhesion molecule 16 (CEACAM) are secreted glycoproteins that are present in the tectorial membrane (TM), an extracellular structure overlying the hearing organ of the inner ear, the organ of Corti. Previous studies have shown that TECTA and TECTB are both required for formation of the striated-sheet matrix within which collagen fibrils of the TM are imbedded and that CEACAM16 interacts with TECTA. To learn more about the structural and functional significance of CEACAM16, we created a Ceacam16-null mutant mouse. In the absence of CEACAM16, TECTB levels are reduced, a clearly defined striated-sheet matrix does not develop, and Hensen's stripe, a prominent feature in the basal two-thirds of the TM in WT mice, is absent. CEACAM16 is also shown to interact with TECTB, indicating that it may stabilize interactions between TECTA and TECTB. Although brain-stem evoked responses and distortion product otoacoustic emissions are, for most frequencies, normal in young mice lacking CEACAM16, stimulus-frequency and transiently evoked emissions are larger. We also observed spontaneous otoacoustic emissions (SOAEs) in 70% of the homozygous mice. This incidence is remarkable considering that Ͻ3% of WT controls have SOAEs. The predominance of SOAEs Ͼ15 kHz correlates with the loss of Hensen's stripe. Results from mice lacking CEACAM16 are consistent with the idea that the organ of Corti evolved to maximize the gain of the cochlear amplifier while preventing large oscillations. Changes in TM structure appear to influence the balance between energy generation and dissipation such that the system becomes unstable.

Membrane recycling in the mechanoreceptive sensory cells of the mammalian cochlea was studied by observing membrane-bound horseradish peroxidase (HRP) reaction product following brief in vivo exposure to the enzyme. In the inner hair cell (IHC), peroxidase was taken up into coated vesicles and became incorporated into synaptic vesicles surrounding presynaptic bodies, but much HRP was also transported to the apical zone where reaction product appeared in all components of the Golgi complex. Neither the subsurface cisternae nor a tubular network associated with clusters of mitochondria were labelled. Outer hair cells (OHCs) showed considerably less membrane-bound reaction product than IHCs, indicating less rapid plasmalemmal recycling. Most membrane-bound reaction product was contained in coated vesicles and small vacuoles in the synaptic zone, but was occasionally seen in multivesicular bodies in the most apical zone. No labelled organelles were detected in the large central region of the OHC. A diffuse staining of the cytoplasm, particularly pronounced in OHCs, often interfered with the evaluation of membrane-bound reaction product in OHCs. This staining pattern could be qualitatively reproduced in both IHCs and OHCs by incubating fixed segments of the organ of Corti in oxidized diaminobenzidine. The presence of labelled synaptic vesicles associated with presynaptic bodies of IHCs and OHCs suggests that they are formed from membrane retrieved from the plasmalemma. We found no evidence that the subsurface cisternae of IHCs or the laminated cisternae of OHCs are derived from the cell surface as they never contained reaction product.

Distortion-product otoacoustic emissions (DPOAEs) elicited with stimulus frequencies less than or equal to 8 kHz have been used in hearing clinics to assess whether the middle ear and cochlea are normal, but high-frequency hearing (>4 kHz) is most vulnerable to cochlear pathology. It might prove useful to measure DPOAEs with even higher frequency stimuli (>8 kHz), but there have been few reports of such studies in humans. DPOAEs have been measured in other mammals to the upper range of hearing sensitivity. The purpose of this study was to compare some characteristics of DPOAEs in human subjects elicited with high-frequency stimuli with those that have been extensively measured with lower-frequency stimuli. The primary goal was to establish if the same phenomenon responsible for the behavior of low-frequency DPOAEs is responsible for the behavior of high-frequency DPOAEs. Specifically, the DPOAE level with stimuli varied from 2 to 20 kHz, growth functions of DPOAEs, effects of varying the primary frequency ratio (f2/f1) on the DPOAE level, and DPOAE group delay were determined. Because the behaviors appeared to vary smoothly with stimulus frequency, the study suggests that emissions measured from 2 to 20 kHz were the product of the same biological process.