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Cochlear implantation leads to many structural changes within the cochlea which can impair residual hearing. In patients with preserved low-frequency hearing, a delayed hearing loss can occur weeks-to-years post-implantation. We explore whether stiffening of the basilar membrane (BM) may be a contributory factor in an animal model. Our objective is to map changes in morphology and Young's modulus of basal and apical areas of the BM after cochlear implantation, using quantitative nanomechanical atomic force microscopy (QNM-AFM) after cochlear implant surgery. Cochlear implantation was undertaken in the guinea pig, and the BM was harvested at four time-points: 1 day, 14 days, 28 days and 84 days post-implantation for QNM-AFM analysis. Auditory brainstem response thresholds were determined prior to implantation and termination. BM tissue showed altered morphology and a progressive increase in Young's modulus, mainly in the apex, over time after implantation. BM tissue from the cochlear base demonstrated areas of extreme stiffness which are likely due to micro-calcification on the BM. In conclusion, stiffening of the BM after cochlear implantation occurs over time, even at sites far apical to a cochlear implant., (Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.)

In the sensory epithelium, macrophages have been identified on the scala tympani side of the basilar membrane. These basilar membrane macrophages are the spatially closest immune cells to sensory cells and are able to directly respond to and influence sensory cell pathogenesis. While basilar membrane macrophages have been studied in acute cochlear stresses, their behavior in response to chronic sensory cell degeneration is largely unknown. Here we report a systematic observation of the variance in phenotypes, the changes in morphology and distribution of basilar membrane tissue macrophages in different age groups of C57BL/6J mice, a mouse model of age-related sensory cell degeneration. This study reveals that mature, fully differentiated tissue macrophages, not recently infiltrated monocytes, are the major macrophage population for immune responses to chronic sensory cell death. These macrophages display dynamic changes in their numbers and morphologies as age increases, and the changes are related to the phases of sensory cell degeneration. Notably, macrophage activation precedes sensory cell pathogenesis, and strong macrophage activity is maintained until sensory cell degradation is complete. Collectively, these findings suggest that mature tissue macrophages on the basilar membrane are a dynamic group of cells that are capable of vigorous adaptation to changes in the local sensory epithelium environment influenced by sensory cell status., Competing Interests: The authors declare no conflict of interest., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Cochlear implantation is an effective, established procedure for patients with profound deafness. Although implant electrodes have been considered as biocompatible prostheses, surgical insertion of the electrode induces various changes within the cochlea. Immediate changes include insertional trauma to the cochlea. Delayed changes include a tissue response consisting of inflammation, fibrosis and neo-osteogenesis induced by trauma and an immunologic reaction to a foreign body. The goal of this study was to evaluate the effect of these delayed changes on the word recognition scores achieved post-operatively. Seventeen temporal bones from patients who in life had undergone cochlear implantation were prepared for light microscopy. We digitally calculated the volume of fibrous tissue and new bone within the cochlea using Amira(®) three-dimensional reconstruction software and assessed the correlations of various clinical and histologic factors. The postoperative CNC word score was positively correlated with total spiral ganglion cell count. Fibrous tissue and new bone were found within the cochlea of all seventeen specimens. The postoperative CNC word score was negatively correlated with the % volume of new bone within the scala tympani, scala media/vestibuli and the cochlea, but not with the % volume of fibrous tissue. The % volume of new bone in the scala media/vestibuli was positively correlated with the degree of intracochlear insertional trauma, especially trauma to the basilar membrane. Our results revealed that the % volume of new bone as well as residual total spiral ganglion cell count are important factors influencing post-implant hearing performance. New bone formation may be reduced by limiting insertional trauma and increasing the biocompatibility of the electrodes., Competing Interests: The authors disclose no conflicts of interest., (Copyright © 2016 Elsevier B.V. All rights reserved.)

A cochlear implant (CI) restores partial hearing to profoundly deaf individuals. CI electrodes are inserted manually in the cochlea and surgeons rely on tactile feedback from the implant to determine when to stop the insertion. This manual insertion method results in a large degree of variability in surgical outcomes and intra-cochlear trauma. Additionally, implants often span only the basal turn. In the present study we report on the development of a new method to assist CI electrode insertion. The design objectives are (1) an automated and standardized insertion technique across patients with (2) more apical insertion than is possible by the contemporary methods, while (3) minimizing insertion trauma. The method relies on a viscous fluid flow through the cochlea to carry the electrode array with it. A small cochleostomy (∼100-150 um in diameter) is made in scala vestibuli (SV) and the round window (RW) membrane is opened. A flow of diluted Sodium Hyaluronate (also known as Hyaluronic Acid, (HA)) is set up from the RW to the SV opening using a perfusion pump that sets up a unidirectional flow. Once the flow is established an implant is dropped into the ongoing flow. Here we present a proof-of-concept study where we used this technique to insert silicone implants all the way to the cochlear apex in rats and gerbils. In light-microscopic histology, the implantation occurred without cochlear trauma. To further assess the ototoxicity of the HA perfusion, we measured compound action potential (CAP) thresholds following the perfusion of HA, and found that the CAP thresholds were substantially elevated. Thus, at this point the method is promising, and requires further development to become clinically viable., (Copyright © 2014 Elsevier B.V. All rights reserved.)

In this study, a three-dimensional finite-element model of the passive human cochlea was created. Dynamic behavior of the basilar membrane caused by the vibration of the stapes footplate was analyzed considering a fluid-structure interaction with the cochlear fluid. Next, the effects of a perilymphatic fistula (PLF) on the vibration of the cochlea were examined by making a small hole on the wall of the cochlea model. Even if a PLF existed in the scala vestibuli, a traveling wave was generated on the basilar membrane. When a PLF existed at the basal end of the cochlea, the shape of the traveling wave envelope showed no remarkable change, but the maximum amplitude became smaller at the entire frequency range from 0.5 to 5kHz and decreased with decreasing frequency. In contrast, when a PLF existed at the second turn of the cochlea, the traveling wave envelope showed a notch at the position of the PLF and the maximum amplitude also became smaller. This model assists in elucidating the mechanisms of hearing loss due to a PLF from the view of dynamics., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Several types of nonauditory cells recover from transitory mechanically induced microlesions in their cell membranes. We report evidence that hair cells in the auditory papilla of the alligator lizard suffered similar membrane wounding when exposed to noise loud enough to induce a temporary threshold shift. Lucifer yellow, a molecular marker that does not normally penetrate through the cell membrane into the cytoplasm, was introduced into the extracellular fluid bathing the basolateral membrane of the hair cells. We assessed the effect of loud noise on the function of the ear by measuring compound action potentials of the auditory nerve before exposure to the noise, immediately after cessation of the noise, and after recovering overnight. Hair cells that were exposed to the noise took up much more Lucifer yellow than hair cells that were not exposed. We propose that the Lucifer yellow entered the hair cells via noise-induced lesions in their cell membranes, and that the cells were able to survive and recover functionally.

Recent reports of the role of iron-catalyzed free radical formation in gentamicin ototoxicity and the successful attenuation of gentamicin ototoxicity by iron chelators led us to re-examine experimental material from a previously unpublished study of deferoxamine. Deferoxamine was injected i.m. into adult Japanese quail at either 300 or 750 mg/kg body weight for 30 days. Examination of sections from the basilar papilla at the light microscope level indicated that supporting cells were damaged after the lower drug dose, and that both supporting cells and hair cells were damaged after the higher drug dose. High, prolonged exposure to deferoxamine produced pathological changes similar to those seen in the basilar papilla after much lower, shorter doses of gentamicin. These results demonstrate that deferoxamine damages the quail inner ear and are consistent with the idea that the ototoxic actions of gentamicin may be mediated by iron chelation.

The time course of recovery of compound action potential (CAP) thresholds was observed in individual adult pigeons after severe acoustic trauma. Pigeons were overstimulated with a tone of 0.7 kHz and 136-142 dB SPL presented to one ear for 1 h under general anesthesia. Recovery of CAP audiograms was monitored at regular intervals after trauma. A new semi-stereotaxic approach to the peripheral part of the auditory nerve was developed. This permitted activity from single auditory nerve fibers to be recorded over a wide range of characteristic frequencies (CFs), including high CFs, without having to open the inner ear. Single unit recordings were made after three weeks and after 4 or more months of recovery. The time course of recovery, the single unit properties, and the morphological status of the basilar papilla were correlated. The CAP was abolished in all animals after overstimulation. Three groups of animals were identified according to the functional recovery of the CAP thresholds recorded at regular intervals with implanted electrodes: Group 1: Fast functional recovery starting immediately after trauma, followed by recovery to pre-exposure values within 3 weeks. Group 2: Slow functional recovery of threshold starting 1-2 weeks after trauma and ending 4-5 weeks after trauma. A mean residual hearing loss of 26.3 dB at 2 kHz remained. Group 3: No recovery of CAP thresholds up to 8 months after trauma. Three weeks after trauma, very few responsive neurons were found in groups 2 and 3. Tuning curves were very broad and sometimes irregular in shape. Thresholds were very high, around 120 dB SPL. Spontaneous firing rate was much reduced, especially in neurons with high CFs. After 4 or more months of recovery, the response properties of single units in group 1 had only partially recovered. Thresholds and sharpness of tuning of many single units were normal: however, in general they were still poorer than in control animals. Spontaneous firing rate was comparable to control animals. Neurons from animals in group 2 showed less recovery, especially at frequencies above the exposure frequency. Thresholds and sharpness of tuning were normal at frequencies below the exposure frequency, but were much poorer at frequencies above the exposure. Spontaneous firing rate was much reduced in fibers with high CFs. The basilar papilla in animals without recovery showed total loss of the sensory epithelium. The basal lamina of the basilar membrane, however, remained intact and was covered with cuboidal cells. In fast recovering animals, the papilla was repopulated with hair cells after 4 months. In slow recovering animals, short (abneural) hair cells were still missing over large parts of the papilla after 4 months of recovery. Residual short (abneural) hair cell loss was largest at two areas, one more basal and the other more apical to the characteristic place of the traumatizing frequency. The results show that functional recovery from severe damage to both short (abneural) and tall (neural) hair cells occurs in adult birds. However, the onset of recovery is delayed and the time course is slower than after destruction of short (abneural) hair cells alone. Furthermore recovery is incomplete, both functionally and morphologically. There are residual permanent hearing losses and regeneration of short (abneural) hair cells is incomplete.

Nitric oxide (NO) is a messenger molecule that mediates several physiological functions and pathological processes. Sodium nitroprusside (SNP), a potent vasodilator, when given clinically as an anti-hypertension agent, exerts its function by releasing NO. It was reported recently that SNP causes a loss of auditory nerve compound action potential (CAP) after topical application of SNP on guinea pig round window membrane (RWM). The current study was designed to investigate the ototoxic target of SNP through both electrophysiological and morphological approaches. The CAP threshold at frequencies ranging from 2 to 36 kHz, the cochlear microphonic quadratic distortion product (cmQDP, F2-F1, where F1 = 17.1 kHz; F2 = 18 kHz), and the cochlear microphonic (CM) at the frequency of F1 were recorded via a round window electrode before and up to 2 h after RWM application of 1 microliter of drug solution. Cochlear blood flow (CBF) and arterial blood pressure were monitored. The cochleae were then processed for morphological examination. The effect of SNP on endocochlear potential (EP) was also studied. Results showed that cmQDP, CM, and CAP, as well as EP, were suppressed in varying amounts, while CBF was substantially increased following drug application. Morphological evaluations showed swelling of the afferent inner radial dendrites within the basal cochlear turn in the higher concentration groups of SNP, while the hair cells presented no evidence of damage at the light microscopic level. The results indicate that SNP has an acute ototoxic effect in a concentration- and time-dependent manner. The targets of SNP ototoxicity are at least the afferent dendrites and stria vascularis.

The onset and development of distortion product otoacoustic emissions (DPE) representing cochlear amplifier activity were studied in neonatal hyperthyroid (n = 10) and control (n = 10) rat pups. These were compared to the onset and development of auditory nerve-brainstem evoked responses (ABR) representing overall cochlear function, and to morphological development of the ear. DPEs were recorded at an earlier postnatal age to high (8 kHz) frequencies and progressed to lower (3 kHz) frequencies with age. ABRs to high-intensity clicks were recorded at least 2 days before DPEs, although DPE onset at 8 kHz preceded adult-like ABR thresholds. Both ABR and DPEs appeared earlier in the hyperthyroid rats. Histological evidence showed earlier morphological development of the ear in these animals. ABR thresholds and DPE amplitudes matured at a slower rate in the experimental group despite their earlier onset. There was no difference in ABR and DPE thresholds between adult hyperthyroid and control rats. However, in the experimental group, DPEs had smaller amplitudes to high (70 dB SPL) and to low (50 dB SPL) stimulus intensities at low frequencies. Hence, despite thyroxine-injected rat pups having earlier onset of auditory structure and function (lower ABR thresholds and earlier functioning active cochlear amplifier), it appeared that neonatal hyperthyroidism affected the later state of the cochlea, such that DPEs, especially to low-frequency stimuli, were depressed during and after maturation.

There is evidence from several studies showing that sensory cells which are destroyed by trauma in the chick auditory epithelium are replaced by new cells. The fate of neurons that innervate the injured and degenerating sensory cells in the lesion, and the temporal sequence of re-innervation of regenerated hair cells are not well understood. This study examined efferent terminals in the chick auditory sensory epithelium following acoustic overstimulation using synapsin-specific immunocytochemistry. Chicks were exposed to an octave band noise (1.5 kHz center frequency, 116 dB SPL, 16 h) and killed on each day from 0 to 9 days postexposure. In the proximal half of control whole mounts of the basilar papillae, synapsin-specific immunoreactivity stained efferent terminals throughout the abneural portion of the sensory epithelium (the short hair cell region). In this area, the labeling appeared as 2-3 bouton-shaped clusters along the abneural edge of each hair cell. After acoustic overstimulation, a lesion was observed at the abneural edge of the papilla where many short hair cells were lost. The center of the lesion was located at 40% distance from the proximal end of each traumatized papilla. Synapsin-specific labeling was not found in sites where expanded supporting cells had replaced missing hair cells. Hair cells which survived the trauma exhibited a shrunken apical area, and synapsin-labeled boutons were observed near their basal domains. New hair cells, which first appeared in the papilla 4 days after trauma, were not initially associated with synapsin-labeled boutons. Regenerated hair cells first displayed contacts with synapsin-labeled boutons 7 days after trauma. Nine days after acoustic overstimulation, most new hair cells appeared to be associated with synapsin-labeled boutons which resembled the normal horseshoe configuration of efferent terminals. The data suggest that direct contact with functional efferent synapses is not necessary for the generation and differentiation of new hair cells.

The mechanical function of the basilar membrane (BM) in the mammalian cochlea has been newly debated after the discovery of frequency selectivity of single hair cells. Decisive information on this matter can be expected from hydropic ears, since hydrops presumably alters cochlear mechanics by (1) impeding BM motion and (2) uncoupling outer hair cell (OHC) stereocilia from the tectorial membrane (TM). Therefore hearing in Menière's disease (MD) was examined analysing data on epidemiology of MD types and audiogram types, 2f thresholds, over-recruitment, loudness intolerance, and otoacoustic emissions. Further, hearing in experimental hydrops (XH) was examined analysing data on: morphological changes on TM and OHCs in relation to hydrops duration; morphological and electrophysiological changes upon acoustic overstimulation. The results were unequivocal on two points: (1) co-occurrence of hydrops and normal hearing thresholds can appear both in MD and XH, (2) co-occurrence of non-hearing-loss hydrops and loudness hypersensitivity is typical both in MD and XH. The conclusion is that BM motion apparently is no necessary element in the chain of cochlear sound transmission but obviously is an auxiliary element for overload protection through resonant absorption. The results are further indicative of audiometric methods for an early detection of incipient MD.

Severe acoustic damage in the chick cochlea causes a destruction of both hair cells and supporting cells in a localized area on the basilar papilla. In this region, the sensory cells are replaced by a layer of flattened epithelial cells. We have employed scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM) to examine the structure and cytoskeletal changes involved in this process. Immunocytochemical staining for actin indicates that the flattened cells are derived from the hyaline cells normally located along the inferior edge of the basilar papilla. In control cochleae the hyaline cells contain dense bundles of actin filaments that anchor into the basal surface of the cells. The hyaline cells appear to redistribute into the severely damaged region by extending the actin bundles at their basal surfaces. Moreover, the efferent nerves that normally form a network among the hyaline cells move into the severely damaged area along with the hyaline cells. In moderately damaged cochleae, where only hair cells are lost, the hyaline cells do not spread into the damaged region. The functional role of this hyaline cell migration is unknown, but it may be involved in maintenance or repair of the severely damaged cochlea.

A novel immunocytochemical method was used to determine whether the sound-damaged adult quail ear can repair its tectorial membrane (TM) and to compare the repair in quail to that in chicks. Birds were exposed to an octave band noise with a center frequency of 1.5 kHz at 116 dB SPL for 4 h. The chicks were grouped based on recovery duration (0 and 7 days), while the quail were divided into 0-, 7-, and 14-day recovered groups. At the end of the recovery period, the animals were sacrificed, and their basilar papillae labeled with a TM-specific monoclonal primary antibody solution followed by a diaminobenzidine process. Examinations under a stereoscope revealed that a patch lesion devoid of TM was located on all 0-day recovered papillae. Seven days later, a honeycomb-patterned layer was observed covering the lesion. In 14-day recovered quail ears, the honeycomb layer appeared similar to that seen at 7 days post-exposure. These observations indicated that both chicks and quail were able to repair their TM within 7 days following exposure to intense sound.

A total of 39 cochleae, 10 non-exposed and 29 noise exposed cochleae, were analyzed in a scanning electronmicroscope. Inner hair cells (IHCs) localized on the modiolar side of the ordinary row of IHCs were described. The mean number of such extra IHCs was 11 per cochlea both for non-exposed and exposed ears, ranging from 0-37. They showed a bimodal distribution with a maximum number at apex and 6-9 mm from apex. The dimension of the cuticular plate was slightly but significantly larger than for the ordinary IHCs. The extra IHCs suffered significantly less damage to their stereocilia than the ordinary IHCs after short-term high-level noise exposure. There was a significant negative correlation between the number of extra IHCs and the size of the post exposure permanent threshold shift. There was no evidence of postexposure generation of extra IHCs in or near the region of hair cell damage. It was concluded that extra IHCs normally occur in rabbits and that they are less susceptible to noise trauma than ordinary IHCs. The negative correlation between extra IHC occurrence and noise susceptibility needs further analysis.

Morphologic changes in the tegmentum vasculosum (TV) of adult quail after high intensity sound exposure were studied. Quail were continuously exposed to 115 dB SPL, 1500 Hz pure tone in a sound field for 12 h and either sacrificed immediately (0 day), 1, 2, 3, 4, 6 or 10 days later. Serial sections through the basilar papilla at 100 micron intervals from base to apex were obtained for study with light microscopy and TEM. Significant morphologic changes were found within the TV of quail sacrificed on days 0-4. On a quantitative scale, the majority of recovery occurred within the first 24 h. After four days survival the tegmentum appeared nearly normal. This recovery correlates well with the temporal pattern of threshold shift recovery. These results demonstrate a temporal correlation between ultrastructural changes in the TV and functional recovery of hearing after intense sound exposure. A potential etiologic role of the TV in avian temporary threshold shift is suggested.

We assessed the effect a sound-induced cochlear lesion had on the tonotopic organization of the nucleus magnocellularis (NM) immediately after acoustic overexposure and following a twelve day recovery period. The acoustic overexposure was a 0.9 kHz tone at 120 dB sound pressure level (SPL) for 48 h. Initially after the acoustic overexposure, the tonotopic organization of the NM was statistically different from that of age-matched controls. Specifically, it appeared that the center frequencies of units in the frequency region of the NM associated with the acoustic overexposure had higher center frequencies than their control counterparts. Following a twelve day recovery period, when threshold sensitivity and frequency selectivity were operating normally, the tonotopic organization of the NM was not statistically different from age-matched controls. We suggest that the sound-induced changes in the tonotopic organization of the NM reflect peripheral damage in the basilar papilla. It has been well documented that similar exposure paradigms produce a loss of short hair cells and a degeneration of the tectorial membrane in the region of the basilar membrane associated with the overexposure. We postulate that the loss of these structures alters the micromechanics and tuning of the basilar membrane which is reflected in the observed changes in NM tonotopy. Following the recovery period, when those structures destroyed by the overexposure had regenerated and basilar membrane micromechanics were operating normally, the tonotopic organization of the NM returned to normal.

Behavioral investigations of Belgian Waterslager canaries (BWCs) have demonstrated a congenital hearing impairment that primarily affects high frequencies. Research into the surface anatomy of the basilar papilla of these birds has pointed to the hair cells as the site of the lesion. Given that the basilar papilla and the vestibular organs both develop from the otocyst, we were interested in ascertaining whether the vestibular sensory epithelia also displayed abnormal hair cells. The inner ear of adult BWCs was examined by scanning electron microscopy. As expected, hair cells in the basilar papilla of BWCs were abnormal. As for the vestibular parenchyma, abnormal hair cells were detected in only one structure: the sacculus. Morphological abnormalities of the cochlea and sacculus are pathognomonic signs of Scheibe's dysplasia, the most common inner ear defect associated with congenital hearing loss. Our results suggest that BWCs are afflicted by this genetic disorder.

Recent reports of elevated auditory thresholds in canaries of the Belgian Waterslager strain have shown that this strain has an inherited auditory deficit in which absolute auditory thresholds at high frequencies (i.e. above 2.0 kHz) are as much as 40 dB less sensitive than the thresholds of mixed-breed canaries and those of other strains. The measurement of CAP audiograms showed that the hearing deficit is already present at the level of the auditory nerve (Gleich and Dooling, 1992). Here we show gross abnormalities in the anatomy of the basilar papilla of Belgian Waterslager canaries at the level of the hair cell. The extent of these abnormalities was correlated with the amount of hearing deficit as measured behaviorally.

Newly hatched chicks were exposed to a 900-Hz tone at 120 dB SPL for 48 hours, then sacrificed, along with unexposed controls, at intervals of 0-15 days following exposure. Examination of the basilar papilla by scanning electron microscopy demonstrated a 32% loss of hair cells within the lesion area with substantial shrinkage of the apical surfaces of the survivors. Within days, the papilla returned to a nearly normal appearance, and new hair cells were seen, but the number of new cells was only a fraction--approximately 22%--of the number lost. Expansion of the apical surfaces of the surviving cells to larger than normal size was a major factor in the recovery of the papilla.

Intense noise stimulation (142 dB, 1/3-octave-band noise centred at 1 kHz for 1 h) causes damage mainly in the second turn of the cochlea. Several hours (3-5) after the noise exposure, the endocochlear potential (EP) was found to be very low (5.7 +/- 6.0 mV). Similarly, the K+ concentration in the endolymph (Ke+) had decreased to low values (18.9 +/- 9.5 mM). The return of EP and Ke+ to normal values took 5-20 days. In contrast to the Ke+ changes, the perilymph K+ concentration (Kp+) increased slightly after the noise exposure to 4.5 +/- 1.7 mM and returned to normal values one day after the exposure. Differences were found in the time course of the EP, Ke+ and Kp+ changes after the arrest of ventilat ion when animals with acoustic trauma were com,ared with normal healthy individuals. The anoxic EP in noise-exposed animals never decreased to values more negative than -20 mV. The results imply that the inner ear mechanisms maintaining positive EP, Ke+ and Kp+ are severely damaged after acoustic trauma and that their function is restored in 5-20 days. With respect to some parameters (decrease of the EP during anoxia, the value of anoxic negative EP, EP overshoot after reventilation) the inner ear mechanisms are, however, still abnormal.

Two groups of guinea pigs were exposed to 1/3 octave band noise centered at 4 kHz, 113-118 dB SPL, for 2 h. The animals of the first group were treated with ascorbic acid (AA), 0.5 mg per 1 g of body mass injected intraperitoneally before noise exposure. The second group (control) was exposed without being treated. By means of the surface specimen method and consequent assessment of numerical atrophy of cochlear hair cells it was found that application of ascorbic acid before the noise exposure resulted in a lower or no loss of hair cells especially within the respective frequency segment of the basilar membrane. Possible protective effect of AA and/or the negative effect of hypovitaminosis "C" are discussed.

Five groups of 10-day-old chicks were continuously exposed to either 500 or 1500 Hz pure tone at 125 dB for 4 or 12 h and killed 10 days later. The basilar papillae were fixed, embedded in plastic, sectioned, and hair cells were counted according to type: tall or short. Short hair cells were found to be more susceptible to acoustic overstimulation than tall hair cells. Further, the position of maximum short hair cell loss varied along the length of the basilar papilla as a function of the exposure frequency while the position of tall hair cell loss did not. Similarities between morphological response of short hair cells in avians after acoustic trauma and outer hair cells in mammals are discussed.

The relation between hearing loss and loss of hair cells after prolonged exposure to a simulated industrial noise environment was determined in normotensive albino rats. Hearing loss was assessed behaviorally by a conditioned suppression technique and electrophysiologically by auditory brainstem response to pulses of 1/3 octave filtered full cycle sine waves. The ears were analyzed in surface preparations and the hair cells counted. Sixty-two ears from 46 animals were analyzed after 1, 3, 7, and 15 months of exposure. A hearing loss of up to approximately 30 dB was consistently found with minimal loss of hair cells. Between 30 and 60 dB hearing loss there was a fair correspondence between loss of function and loss of hair cells. After 15 months exposure a relatively larger loss of hair cells was observed than expected from decrease of threshold sensitivity. The results indicate the existence of a systematic although not directly proportional relation between hair cell loss and loss of sensitivity during prolonged noise exposure. It is suggested that the correlation between hearing loss and hair cell loss is influenced, e.g., by duration and level of exposure, degree of hearing loss, and location along the basilar membrane.