Spontaneous basilar-membrane oscillation (SBMO) and coherent reflection. (33/139)

In a previous report (in JARO) we have described a relatively high-frequency (15 kHz) spontaneous oscillation of the basilar membrane (SBMO) in a guinea pig ear; this oscillation was accompanied by a spontaneous otoacoustic emission (SOAE) at the same frequency. During the spontaneous oscillation and after it had subsided, the mechanical frequency response of the basilar membrane was measured by way of a wide-band random-noise stimulus, and it showed a number of spectral peaks, one of which having the frequency of the original oscillation. This pattern of peaks cannot be explained by assuming a single place of reflection in the cochlea. In this paper the process of 'coherent reflection' is artificially evoked in a three-dimensional model of the cochlea by imposing random place-fixed irregularities to the basilar-membrane impedance. It is shown that in the model a series of peaks arises in the frequency spectrum of the basilar-membrane response which phenomenon resembles the one found in the experimental animal. It is also shown that these peaks are actually due to superposition of the primary wave and a wave resulting from 'coherent reflection' which is reflected at the stapes. When the intensity of the acoustic stimulus signal is increased, the relative sizes of these peaks in the simulation diminish in about the same way as in the experiment. It is concluded that coherent reflection most likely is the cause of the 'extra peaks', and that this concept can also explain the observed level dependence of these peaks. The findings of this study lead to a minor refinement regarding the actual requirements for coherent reflection to arise.  (+info)

Efferent-mediated control of basilar membrane motion. (34/139)

Medial olivocochlear efferent (MOCE) neurones innervate the outer hair cells (OHCs) of the mammalian cochlea, and convey signals that are capable of controlling the sensitivity of the peripheral auditory system in a frequency-specific manner. Recent methodological developments have allowed the effects of the MOCE system to be observed in vivo at the level of the basilar membrane (BM). These observations have confirmed earlier theories that at least some of the MOCE's effects are mediated via the cochlea's mechanics, with the OHCs acting as the mechanical effectors. However, the new observations have also provided some unexpected twists: apparently, the MOCEs can enhance the BM's responses to some sounds while inhibiting its responses to others, and they can alter the BM's response to a single sound using at least two separate mechanisms. Such observations put new constraints on the way in which the cochlea's mechanics, and the OHCs in particular, are thought to operate.  (+info)

Chlorpromazine alters cochlear mechanics and amplification: in vivo evidence for a role of stiffness modulation in the organ of corti. (35/139)

Although prestin-mediated outer hair cell (OHC) electromotility provides mechanical force for sound amplification in the mammalian cochlea, proper OHC stiffness is required to maintain normal electromotility and to transmit mechanical force to the basilar membrane (BM). To investigate the in vivo role of OHC stiffness in cochlear amplification, chlorpromazine (CPZ), an antipsychotic drug that alters OHC lateral wall biophysics, was infused into the cochleae in living guinea pigs. The effects of CPZ on cochlear amplification and OHC electromotility were observed by measuring the acoustically and electrically evoked BM motions. CPZ significantly reduced cochlear amplification as measured by a decline of the acoustically evoked BM motion near the best frequency (BF) accompanied by a loss of nonlinearity and broadened tuning. It also substantially reduced electrically evoked BM vibration near the BF and at frequencies above BF (< or =80 kHz). The high-frequency notch (near 50 kHz) in the electrically evoked BM response shifted toward higher frequency in a CPZ concentration-dependent manner with a corresponding phase change. In contrast, salicylate resulted in a shift in this notch toward lower frequency. These results indicate that CPZ reduces OHC-mediated cochlear amplification probably via its effects on the mechanics of the OHC plasma membrane rather than via a direct effect on the OHC motor, prestin. Through modeling, we propose that with a combined OHC somatic and hair bundle forcing, the upward-shift of the approximately 50-kHz notch in the electrically-evoked BM motion may indicate stiffness increase of the OHCs that is responsible for the reduced cochlear amplification.  (+info)

Sharpened cochlear tuning in a mouse with a genetically modified tectorial membrane. (36/139)

Frequency tuning in the cochlea is determined by the passive mechanical properties of the basilar membrane and active feedback from the outer hair cells, sensory-effector cells that detect and amplify sound-induced basilar membrane motions. The sensory hair bundles of the outer hair cells are imbedded in the tectorial membrane, a sheet of extracellular matrix that overlies the cochlea's sensory epithelium. The tectorial membrane contains radially organized collagen fibrils that are imbedded in an unusual striated-sheet matrix formed by two glycoproteins, alpha-tectorin (Tecta) and beta-tectorin (Tectb). In Tectb(-/-) mice the structure of the striated-sheet matrix is disrupted. Although these mice have a low-frequency hearing loss, basilar-membrane and neural tuning are both significantly enhanced in the high-frequency regions of the cochlea, with little loss in sensitivity. These findings can be attributed to a reduction in the acting mass of the tectorial membrane and reveal a new function for this structure in controlling interactions along the cochlea.  (+info)

Two-tone distortion at different longitudinal locations on the basilar membrane. (37/139)

When listening to two tones at frequency f1 and f2 (f2>f1), one can hear pitches not only at f1 and f2 but also at distortion frequencies f2-f1, (n+1)f1-nf2, and (n+1)f2-nf1 (n=1,2,3...). Such two-tone distortion products (DPs) also can be measured in the ear canal using a sensitive microphone. These ear-generated sounds are called otoacoustic emissions (OAEs). In spite of the common applications of OAEs, the mechanisms by which these emissions travel out of the cochlea remain unclear. In a recent study, the basilar membrane (BM) vibration at 2f1-f2 was measured as a function of the longitudinal location, using a scanning laser interferometer. The data indicated a forward traveling wave and no measurable backward wave. However, this study had a relatively high noise floor and high stimulus intensity. In the current study, the noise floor of the BM measurement was significantly decreased by using reflective beads on the BM, and the vibration was measured at relatively low intensities at more than one longitudinal location. The results show that the DP phase at a basal location leads the phase at an apical location. The data indicate that the emission travels along the BM from base to apex as a forward traveling wave, and no backward traveling wave was detected under the current experimental conditions.  (+info)

Similarity of traveling-wave delays in the hearing organs of humans and other tetrapods. (38/139)

Transduction of sound in mammalian ears is mediated by basilar-membrane waves exhibiting delays that increase systematically with distance from the cochlear base. Most contemporary accounts of such "traveling-wave" delays in humans have ignored postmortem basilar-membrane measurements in favor of indirect in vivo estimates derived from brainstem-evoked responses, compound action potentials, and otoacoustic emissions. Here, we show that those indirect delay estimates are either flawed or inadequately calibrated. In particular, we argue against assertions based on indirect estimates that basilar-membrane delays are much longer in humans than in experimental animals. We also estimate in vivo basilar-membrane delays in humans by correcting postmortem measurements in humans according to the effects of death on basilar-membrane vibrations in other mammalian species. The estimated in vivo basilar-membrane delays in humans are similar to delays in the hearing organs of other tetrapods, including those in which basilar membranes do not sustain traveling waves or that lack basilar membranes altogether.  (+info)

Laser-induced collagen remodeling and deposition within the basilar membrane of the mouse cochlea. (39/139)

The cochlea is the mammalian organ of hearing. Its predominant vibratory element, the basilar membrane, is tonotopically tuned, based on the spatial variation of its mass and stiffness. The constituent collagen fibers of the basilar membrane affect its stiffness. Laser irradiation can induce collagen remodeling and deposition in various tissues. We tested whether similar effects could be induced within the basilar membrane. Trypan blue was perfused into the scala tympani of anesthetized mice to stain the basilar membrane. We then irradiated the cochleas with a 694-nm pulsed ruby laser at 15 or 180 Jcm(2). The mice were sacrificed 14 to 16 days later and collagen organization was studied. Polarization microscopy revealed that laser irradiation increased the birefringence within the basilar membrane in a dose-dependent manner. Electron microscopy demonstrated an increase in the density of collagen fibers and the deposition of new fibrils between collagen fibers after laser irradiation. As an assessment of hearing, auditory brainstem response (ABR) thresholds were found to increase moderately after 15 Jcm(2) and substantially after 180 Jcm(2). Our results demonstrate that collagen remodeling and new collagen deposition occurs within the basilar membrane after laser irradiation in a similar fashion to that found in other tissues.  (+info)

Concentration gradient along the scala tympani after local application of gentamicin to the round window membrane. (40/139)

OBJECTIVES: The distribution of gentamicin along the fluid spaces of the cochlea after local applications has never previously been demonstrated. Computer simulations have predicted that significant basal-apical concentration gradients might be expected, and histologic studies indicate that hair cell damage is greater at the base than at the apex after local gentamicin application. In the present study, gradients of gentamicin along the cochlea were measured. METHODS: A recently developed method of sampling perilymph from the cochlear apex of guinea pigs was used in which the samples represent fluid originating from different regions along the scala tympani. Gentamicin concentration was determined in sequential apical samples that were taken after up to 3 hours of local application to the round window niche. RESULTS: Substantial gradients of gentamicin along the length of the scala tympani were demonstrated and quantified, averaging more than 4,000 times greater concentration at the base compared with the apex at the time of sampling. Peak concentrations and gradients for gentamicin varied considerably between animals, likely resulting from variations in round window membrane permeability and rates of perilymph flow. CONCLUSIONS: The large gradients for gentamicin demonstrated here in guinea pigs account for how it is possible to suppress vestibular function in some patients with a local application of gentamicin without damaging auditory function. Variations in round window membrane permeability and in perilymph flow could account for why hearing losses are observed in some patients.  (+info)