Sound damage and gentamicin treatment produce different patterns of damage to the efferent innervation of the chick cochlea

Both sound exposure and gentamicin treatment cause damage to sensory hair cells in the peripheral chick auditory organ, the basilar papilla. This induces a regeneration response which replaces hair cells and restores auditory function. Since functional recovery requires the re-establishment of connections between regenerated hair cells and the central nervous system, we have investigated the effects of sound damage and gentamicin treatment on the neuronal elements within the cochlea. Whole-mount preparations of basilar papillae were labeled with phalloidin to label the actin cytoskeleton and antibodies to neurofilaments, choline acetyltransferase, and synapsin to label neurons; and examined by confocal laser scanning microscopy. When chicks are treated with gentamicin or exposed to acoustic overstimulation, the transverse nerve fibers show no changes from normal cochleae assayed in parallel. Efferent nerve terminals, however, disappear from areas depleted of hair cells following acoustic trauma. In contrast, efferent nerve endings are still present in the areas of hair cell loss following gentamicin treatment, although their morphological appearance is greatly altered. These differences in the response of efferent nerve terminals to sound exposure versus gentamicin treatment may account, at least in part, for the discrepancies reported in the time of recovery of auditory function.     

High-frequency auditory feedback is not required for adult song maintenance in Bengalese finches

Male Bengalese finches do not normally change their vocal patterns in adulthood; song is stereotyped and stable over time. Adult song maintenance requires auditory feedback. If adults are deafened, song will degrade within 1 week. We tested whether feedback of all sound frequencies is required for song maintenance. The avian basilar papilla is tonotopically organized; hair cells in the basal region encode high frequencies, and low frequencies are encoded in progressively apical regions. We restricted the spectral range of feedback available to a bird by killing either auditory hair cells encoding higher frequencies or those encoding both high and low frequencies and documented resultant changes in song. Birds were treated with either Amikacin alone to kill high-frequency hair cells or Amikacin and sound exposure to target hair cells across the entire papilla. During treatment, song was recorded from all birds weekly. After treatment and song recording, evoked-potential audiograms were evaluated on each bird, and papillas were evaluated by scanning electron microscopy. Results showed that hair cell damage over 46-63% of the basal papilla and the corresponding high-frequency hearing loss had no effect on song structure. In birds with hair cell damage extending further into the apical region of the papilla and corresponding low-frequency and high-frequency hearing loss, song degradation occurred within 1 week of beginning treatment and was comparable with degradation after surgical deafening. We conclude that either low-frequency spectral cues or temporal cues via feedback of the song amplitude envelope are sufficient for song maintenance in adult Bengalese finches.     

Are aminoglycoside antibiotics excitotoxic?

Guinea pigs received gentamicin to induce a profound hearing loss (61 dB auditory threshold shift at 18 kHz). Concomitant administration of maleic or tartaric acid dissolved in dimethyl sulfoxide (DMSO) significantly reduced the threshold shift to < 40 dB. The results have several important implications. First, they support the hypothesis of a free-radical mechanism of gentamicin toxicity since the protective compounds are metal chelators and scavengers. Second, they caution against these and similar chemicals, commonly found in drug preparations, as vehicles in tests of aminoglycoside toxicity. For example, a recent study by others describing attenuation of aminoglycoside ototoxicity by NMDA antagonists may have been influenced by the presence of maleate, tartrate and DMSO. Third, they suggest simple antioxidants as a potentially efficient and inexpensive clinical prophylaxis of aminoglycoside-induced hearing loss.     

R-phenylisopropyladenosine attenuates noise-induced hearing loss in the chinchilla

Reactive oxygen species, which are cytotoxic to living tissues, are thought to be partly responsible for noise-induced hearing loss. In this study R-phenylisopropyladenosine (R-PIA), a stable non-hydrolyzable adenosine analogue which has been found effective in upregulating antioxidant enzyme activity levels, was topologically applied to the round window of the right ears of chinchillas. Physiological saline was applied to the round window of the left ears (control). The animals were then exposed to a 4 kHz octave band noise at 105 dB SPL for 4 h. Inferior colliculus evoked potential thresholds and distortion product otoacoustic emissions (DPOAE) were measured and hair cell damage was documented. The mean threshold shifts immediately after the noise exposure were 70-90 dB at frequencies between 2 and 16 kHz. There were no significant differences in threshold shifts at this point between the R-PIA-treated and control ears. By 4 days after noise exposure, however, the R-PIA-treated ears showed 20-30 dB more recovery than saline-treated ears at frequencies between 4 and 16 kHz. More importantly, threshold measurements made 20 days after noise exposure showed 10-15 dB less permanent threshold shifts in R-PIA-treated ears. The amplitudes of DPOAE also recovered to a greater extent and outer hair cell losses were less severe in the R-PIA-treated ears. The results suggest that administration of R-PIA facilitates the recovery process of the outer hair cell after noise exposure.     

Attenuation of neomycin ototoxicity by iron chelation

Increasing evidence suggests that aminoglycoside ototoxicity is mediated by the formation of an aminoglycoside-iron complex and that the creation of this complex is a preliminary step in generation of free radical species and subsequent hair cell death. In this study we have assessed the ability of the iron chelator deferoxamine to attenuate the hearing loss induced by an ototoxic dose of the aminoglycoside neomycin (100 mg/kg per day for 14 days). Experiments were carried out on pigmented guinea pigs weighing 250 to 300 g. Changes in auditory sensitivity were characterized by monitoring shifts in compound action potential (CAP) thresholds, recorded through indwelling electrodes implanted at the round window, vertex, and contralateral mastoid. Results show that animals receiving neomycin alone suffered a mean threshold shift exceeding 35 dB at all test frequencies (2.0, 4.0, and 8.0 kHz) 30 days after initiation of treatment. In comparison, all animals receiving cotherapy of neomycin and deferoxamine (150 mg/kg twice daily for 14 days) maintained their CAP threshold, suggesting significant protection from neomycin ototoxicity. A statistical comparison of treatment groups showed that in the animals receiving cotherapy with neomycin and deferoxamine, deferoxamine produced a significant protective effect against neomycin-induced ototoxicity (P < 0.001). These results provide further evidence of the intrinsic role of iron in aminoglycoside ototoxicity and suggest that deferoxamine may have a therapeutic role in attenuating the cytotoxic action of aminoglycoside antibiotics.     

Regulation of proteoglycan and hyaluronan synthesis by elevated level of intracellular cyclic adenosine monophosphate in peritubular cells from immature rat testis

The morphology of the basilar papilla of the emu was investigated quantitatively with light and scanning electron microscopical techniques. The emu is a member of the Paleognathae, a group of flightless birds that represent the most primitive living avian species. The comparison of the emu papilla with that of other, more advanced birds provides insights into the evolution of the avian papilla. The morphology of the emu papilla is that of an unspecialised bird, but shows the full range of features previously shown to be typical for the avian basilar papilla. For example, the orientation of the hair cells' sensitive axes varied in characteristic fashion both along and across the papilla. Many of the quantitative details correlate well with the representation of predominantly low frequencies along the papilla. The most distinctive features were an unusually high density of hair cells and an unusual tallness of the hair-cell bodies. This suggests that the evolution of morphologically very short hair cells, which are a hallmark of avian papillae, is a recent development in evolution. The small degree of differentiation in hair-cell size contrasts with the observation that a significant number of hair cells in the emu lack afferent innervation. It is therefore suggested that the development of functionally different hair-cell types in birds preceded the differentiation into morphologically tall and short hair cells.     

Cost of illness: an inextricable maze or an aid in decision making? The case of schizophrenia

Distortion-product otoacoustic emissions (DPOAEs) are still undergoing evaluation for clinical use. Although the effects of ageing on otoacoustic emissions have been studied quite extensively in the past, DPOAE response-growth or input-output (I-O) measures, which are well suited as an objective method for monitoring cochlear function at specific frequencies, have been less thoroughly examined. The aim of the present study was to assess the 2f1-f2 DPOAEs in a clinical setting in order to examine the response of 20 normally hearing middle-aged adults and to compare the results with those of 20 people of the same age with ears of sensorineural high-frequency hearing loss (HL). The experiment consisted of two stages. First, the DPOAE-gram was recorded in 1-4-octave steps at a stimulus level of 70 dB SPL over a frequency range of the f2 primary tone which extended from 1.001 to 6.299 kHz. Secondly, in order to elicit DPOAE I-O functions, the two primary stimuli were presented at equilevel intensities ranging from 20 to 71 dB SPL. The stimulus-level step size was 3 dB. The I-O functions were recorded at five separate DPOAE frequencies, with the f2 frequency most closely related to the clinical audiogram (f2 = 1.0, 1.5, 2.0, 4.0 and 6.0 kHz). Two clearly separated portions in the form of the I-O function for normally hearing ears were found. The first portion, in response to primary levels of 60 dB SPL and below, showed a plateau (saturating) behaviour. If primary levels exceeded 60 dB SPL, I-O functions became more linear. The attenuation of the saturation portion of the I-O function in ears with high-frequency HL across the frequency-test range is difficult to explain because elevated behavioural thresholds were observed only for frequencies > 1.5 kHz. Thus, the more linear I-Os associated with the hearing-loss frequencies may indicate deficiencies in the active properties of outer hair cells (OHCs), whereas those for I-Os < 1.5 kHz, where hearing was normal, may indicate a beginning of damage to active OHC micromechanical processes prior to their clinical manifestation. DPOAE recordings from people with high-frequency HL, possibly age-related, supplement recordings of TEOAEs and give complementary information on degenerative changes in the outer hair-cells. DPOAE I-O functions may reveal discrete pathological alterations both in the active cochlear signal processing and in the passive mechanisms of the cochlea prior to their detection by clinical audiometric tests.     

Regeneration of cochlear efferent nerve terminals after gentamycin damage

Chickens recover auditory function after hair cell loss caused by ototoxic drug damage or acoustic overstimulation, indicating that mechanisms exist to reestablish appropriate neuronal connections to regenerated hair cells. However, despite similar hair cell regeneration times, hearing recovery takes substantially longer after aminoglycoside than after sound damage. We have therefore begun examining damage and regeneration of efferent nerve terminals by immunolabeling whole-mount cochleae for differentially localized synaptic proteins and by visualizing the distribution of label with confocal microscopy. In undamaged cochleae, the synaptic proteins synapsin and syntaxin show similar distribution patterns corresponding to the large cup-like terminals on short hair cells. After gentamycin administration, these terminals are disrupted as hair cells are lost, leaving smaller, more numerous synapsin-reactive structures in the sensory epithelium. Syntaxin reactivity remains associated with the extruded hair cells, indicating that the presynaptic membrane is still attached to the postsynaptic site. In contrast, after sound damage, both synapsin and syntaxin reactivity are lost from the epithelium with extruded hair cells. As regenerated hair cells differentiate after gentamycin treatment, the synapsin labeling associated with cup-like efferent endings reappears but is not completely restored even after 60 d of recovery. Thus, efferent terminals are reestablished much more slowly than after sound damage (), consistent with the prolonged loss of hearing function. This in vivo model system allows comparison of axonal reconnection after either complete loss (sound damage) or partial disruption (gentamycin treatment) of axon terminals. Elucidating the differences in recovery between these injuries can provide insights into reinnervation mechanisms.     

A dynamic model of outer hair cell motility including intracellular and extracellular fluid viscosity

The deformation response of a guinea pig outer hair cell is modeled for mechanical and electrical stimulation up to 25 kHz. The analysis uses a Fourier series technique for a finite length cell surrounded internally and externally by a much larger continuum of viscous fluid. The analytical solution predicts that outer hair cell length changes occur due to applied mechanical or electrical stimulation without significant resonance, characteristic of a highly damped system. The deformation is found to have little attenuation up to a corner frequency of about 2 kHz for long cells and 10 kHz for short cells, in agreement with published experimental results. For electrical loading of 1 mV across the lateral cell wall, deformation for short cells is calculated to be greater than 1 nm for frequencies up to 20 kHz. These results support the proposition that in vivo the outer hair cell modifies the character of basilar membrane deformation on a cycle-by-cycle basis. An estimate of the capability of the cell to supply energy to the basilar membrane is given based on published values of outer hair cell material properties.     

Expression of novel potassium channels in the chick basilar papilla

Ionic currents are critical for the functioning of the inner ear auditory sensory epithelium. We set out to identify and molecularly clone the genes encoding the channels responsible for several currents in the chick basilar papilla. Here we describe an inward-rectifying K+ channel, cKir2.3, present in both hair cells and support cells in the apical end of the chick basilar papilla. The biophysical properties of the human ortholog, hKir2.3, are similar to those of an inward-rectifying channel found in the apical end of the chick basilar papilla, suggesting that this channel may contribute to the corresponding current. Additionally, we describe two new members of the Kv6 subfamily of putative regulatory voltage-gated K channels, cKv6.2 and cKv6.3. Both are expressed in hair cells in the apical end of the chick basilar papilla; cKv6.2 is also strongly expressed in support cells and in the brain.     

Sound and vibration sensitivity of VIIIth nerve fibers in the frogs Leptodactylus albilabris and Rana pipiens pipiens

1. Responses of 73 fibers to dorso-ventral vibration were recorded in the saccular and utricular branchlets of Rana pipiens pipiens using a ventral approach. The saccular branchlet contained nearly exclusively vibration-sensitive fibers (33 out of 36) with best frequencies (BFs) between 10 and 70 Hz, whereas none of the 37 fibers encountered in the utricular branchlet responded to dorso-ventral vibrations. 2. Using a dorsal approach we recorded from the VIIIth nerve near its entry in the brainstem and analyzed responses to both sound and vibration stimuli for 65 fibers in R. pipiens pipiens and 25 fibers in Leptodactylus albilabris. The fibers were classified as amphibian papilla (AP), basilar papilla (BP), saccular or vestibular fibers based on their location in the nerve. Only AP and saccular fibers responded to vibrations. The AP-fibers responded to vibrations from 0.01 cm/s2 and to sound from 40 dB SPL by increasing their spike rate. Best frequencies (BFs) ranged from 60 to 900 Hz, and only fibers with BFs below 500 Hz responded to vibrations. The fibers had identical BF's for sound and vibration. The saccular fibers had BFs ranging from 10 to 80 Hz with 22 fibers having BFs at 40-50 Hz. The fibers responded to sound from 70 dB SPL and to vibrations from 0.01 cm/s2. 3. No differences in sensitivity, tuning or phase-locking were found between the two species, except that most BP-fibers in R. pipiens pipiens had BFs from 1.2 to 1.4 kHz, whereas those in L. albilabris had BFs from 2.0 to 2.2 kHz (matching the energy peak of L. albilabris' mating call). 4. The finding that the low-frequency amphibian papilla fibers are extremely sensitive to vibrations raises questions regarding their function in the behaving animal. They may be substrate vibration receptors, respond to sound-induced vibrations or bone-conducted sound.     

Ultrastructural, physiological, and molecular defects in the inner ear of a gene-knockout mouse model for autosomal Alport syndrome

It is well documented that damage to the chick cochlea caused by acoustic overstimulation or ototoxic drugs is reversible. Second-order auditory neurons in nucleus magnocellularis (NM) are sensitive to changes in input from the cochlea. However, few experiments studying changes in NM during cochlear hair cell loss and regeneration have been reported. Chicks were given a single systemic dose of gentamicin, which results in maximal hair cell loss in the base of the cochlea after 5 days. Many new hair cells are present by 9 days. These new hair cells are mature but not completely recovered in organization by 70 days. We counted neurons in Nissl-stained sections of the brainstem within specific tonotopic regions of NM, comparing absolute cell number between gentamicin- and saline-treated animals at both short and long survival times. Our data suggest that neuronal number in rostral NM parallels hair cell number in the base of the cochlea. That is, after a single dose of gentamicin, we see a loss of both cochlear hair cells and NM neurons early, followed by a recovery of both cochlear hair cells and NM neurons later. These results suggest that neurons, like cochlear hair cells, can recover following gentamicin-induced damage.     

Basilar papilla explants: a model to study hair cell regeneration-repair and protection

Explants of basilar papillae from 6-7 days posthatch chicks were cultured in growth medium for a period of 1-8 days. Hair cells were counted following staining of stereocilia bundles with FITC-phalloidin, and the percentage of hair cell survival was determined by comparison to control (i.e. uncultured) specimens. Hair cell integrity was evaluated by scanning electron microscopy. Although previous studies have utilized organotypic culture of the basilar papilla to assess cell proliferation and ototoxicity, viability and integrity of hair cells was documented for periods of up to only 2 3 days. Our results demonstrate substantive auditory hair cell viability for a period of 7 days in vitro. We describe a pattern of natural hair cell loss in organotypic culture that progresses along a proximal-distal, abneural-neural gradient, mimicking the pattern of hair cell loss that occurs following ototoxic insult to the chick basilar papilla in vivo and the pattern we observed during a 48-h period of exposure of basilar papilla explants to an ototoxic dose of neomycin. Our results provide an important quantitative step for the use of organotypic culture of the chick basilar papilla as a purposeful model to investigate the process of hair cell regeneration-repair in the avian auditory system.     

Homozygous and frequent deletion of proximal 8p sequences in human prostate cancers: identification of a potential tumor suppressor gene site

The mechanisms for hair cell recovery were investigated after intraortic application of 50 microg gentamicin into the perilymphatic space of the superior semicircular canal of the chinchilla. Histologic evaluation of one normal group and four posttreatment groups (7, 14, 28, and 56 days) was made with light and transmission electron microscopic techniques. The numeric changes of hair cells and supporting cells was quantified with the dissector technique. At 7 and 14 days after treatment, no type I hair cells were present, and 85% and 88% of type II hair cells were lost. Supporting cells decreased to 76% at 7 days, but they recovered to 91% at 14 days. Recovery of the epithelia was evident 28 days after treatment; 83% were type II hair cells, and 3% were type I hair cells. The supporting cell number remained close to normal (86%). Between 14 and 28 days after treatment, there was an increase of 1758 of type II hair cells, representing approximately 125 new hair cells per day. At the same time interval the number of supporting cells remained near normal. These results suggest that new hair cells might be the result of supporting cell mitotic division and differentiation.     

Interleukin 8 can affect inner ear function

The chemokine interleukin 8 (IL-8) was instilled into the round window niche of rats through a small perforation in the tympanic membrane in order to study its effect on inner ear function by electrophysiological and morphological techniques. The frequency-specific auditory brainstem response (ABR) was recorded at the frequencies 4, 8, 10, 12, 16 and 20 kHz just before and 1, 2, 5 and 14 days after instilling IL-8 to ascertain the hearing level during each interval. Morphological examination by light microscopy was performed during the same interval following the instillation of IL-8. On day 1, the rise in ABR threshold was within 5 dB SPL (non-significant elevation). However, a significant threshold elevation (above 5 dB SPL) occurred in high-frequency areas (16 and 20 kHz) on day 2, and in middle frequency areas (10 and 12 kHz) on day 5 with sensorineural hearing loss type intensity-latency curves. By day 14, the elevated thresholds had returned to pre-instillation levels. In the lowest areas (4 and 8 kHz), no significant threshold elevation was detected at any time during the observation period. By light microscopy, on day 1, clusters of inflammatory cells (predominantly neutrophils) were observed just outside the round window membrane (RWM), while only a few neutrophils were detected in the cochlea. These cells were still present outside the RWM on day 2. The neutrophils had disappeared by day 5 and only macrophages were present on the middle ear side of the RWM. However, throughout the observation period, the organ of Corti and stria vascularis appeared to be intact. These results suggest that IL-8 in the middle ear cavity is able to influence inner ear function.     

Functional mapping of the U3 small nucleolar RNA from the yeast Saccharomyces cerevisiae

The 2 f1-f2 distortion product otoacoustic emission (DP) was measured in 20 normal hearing subjects and 15 patients with moderate cochlear hearing loss and compared to the pure-tone hearing threshold, measured with the same probe system at the f2 frequencies. DPs were elicited over a wide primary tone level range between L2 = 20 and 65 dB SPL. With decreasing L2, the L1-L2 primary tone level difference was continuously increased according to L1 = 0.4L2 + 39 dB, to account for differences of the primary tone responses at the f2 place. Above 1.5 kHz, DPs were measurable with that paradigm on average within 10 dB of the average hearing threshold in both subject groups. The growth of the DP was compressive in normal hearing subjects, with strong saturation at moderate primary tone levels. In cases of cochlear impairment, reductions of the DP level were greatest at lowest, but smallest at highest stimulus levels, such that the growth of the DP became linearized. The correlation of the DP level to the hearing threshold was found to depend on the stimulus level. Maximal correlations were found in impaired ears at moderate primary tone levels around L2 = 45 dB SPL, but at lowest stimulus levels in normal hearing (L2 = 25 dB SPL). At these levels, 17/20 impaired ears and 14/15 normally hearing ears showed statistically significant correlations. It is concluded that for a clinical application and prediction of the hearing threshold, DPs should be measured not only at high, but also at lower primary tone levels.     

Time course of nerve-fiber regeneration in the noise-damaged mammalian cochlea

The time course of events which are essential for nerve-fiber regeneration in the mammalian cochlea was determined using a group of chinchillas that had been exposed for 3.5 hr to an octave band of noise with a center frequency of 4 kHz and a sound pressure level of 108 dB. The animals recovered from 40 min (0 days) to 100 days at which times their inner ears were fixed and the organs of Corti prepared for phase-contrast and bright-field microscopy as plastic-embedded flat preparations. Selected areas identified in the flat preparations were semi-thick and thin sectioned at radial or tangential angles for examination by bright-field and transmission electron microscopy. The following time-ordered events appeared critical for nerve-fiber regeneration: (1) The area of the basilar membrane in which regeneration had a possibility of occurring showed signs of severe injury. Outer hair cells degenerated first followed by outer pillars, inner pillars, inner hair cells and other supporting cells; (2) Myelinated nerve fibers in the osseous spiral lamina became fragmented, starting at the distal ends of the fibers. This degeneration gradually extended back to Rosenthal's canal; (3) Fibrous processes, originating from Schwann-like cells in the osseous spiral lamina, extended laterally on the basilar membrane; (4) Schwann cells lined up medial to the habenulae perforata in the areas of severest damage, apparently ready to migrate through the habenulae onto the basilar membrane; (5) Schwann-cell nuclei appeared on the basilar membrane beneath the developing layer of squamous epithelium which was in the process of replacing the degenerated portion of the organ of Corti; (6) Regenerated nerve fibers with thin myelin sheaths or a simple investment of Schwann cell cytoplasm appeared in areas of total loss of the organ of Corti; and (7) The myelin sheaths on the regenerated nerve fibers gradually became thicker.     

Acoustic startle threshold of the albino rat (Rattus norvegicus).

The startle threshold of the albino Sprague-Dawley rat runs parallel to the curve of the hearing threshold. The difference between the startle and hearing threshold is 87 dB (SPL) at a background noise level of 75 dB (SPL). At 110 dB (SPL), the threshold has a range from 2 kHz to 50 kHz with a minimum at 10 kHz and a second minimum at 40 kHz. Amplitude and latency of the startle response are not only dependent on the sensation level of the acoustic stimulus but also on the frequency. At threshold, only the head movement component of the startle response is elicited. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Postnatal development of the organ of Corti in cats: a light microscopic morphometric study

This study quantitatively characterizes the development of the major morphological features of the organ of Corti during the first 2 weeks postnatal, the period when the cat auditory system makes the transition from being essentially non-functional to having nearly adult-like responses. Four groups of kittens (n = 3) were studied at one day postnatal (P1), P5, P10, P15, and compared to adults. Measurements were made of the organ of Corti at 3 cochlear locations: 20%, 60% and 85% of basilar membrane length from the base cochlear locations which in the adult correspond to best frequencies of approximately 20 kHz, 2 kHz and 500 Hz, respectively. In addition, measurements of basilar membrane length and opening of the tunnel of Corti were made in 20 cochlear specimens from kittens aged P0-P6. Results indicate that: (i) at P0 the basilar membrane has attained adult length, and the tunnel of Corti is open over approximately the basal one-half of the cochlea; (ii) the initial opening of the tunnel of Corti occurs at a site about 4 mm from the cochlear base (best frequency of approximately 25 kHz in the adult cochlea); (iii) the thickness of the tympanic cell layer decreases markedly at the basal 20-kHz location; (iv) the areas of the tunnel of Corti and space of Nuel and the angulation of the inner hair cells (IHC) relative to the basilar membrane all show marked postnatal increases at both the middle and apical locations; (v) IHC are nearly adult-like in length and shape at birth, whereas the OHC (at 2-kHz and 500-Hz locations) undergo marked postnatal changes; (vi) disappearance of the marginal pillars and maturation of the supporting cells are not yet complete by P15.     

Hair bundle morphology on surviving hair cells of the chick basilar papilla exposed to intense sound

Exposure to intense sound produces a well-defined "patch" lesion on the chick basilar papilla in which 30-35% of the short hair cells are lost. The present study compares various aspects of sensory hair bundle morphology on surviving hair cells in the patch lesion with hair bundles from matched locations on nonexposed control papilla immediately after removal from the exposure and 12-days post exposure. The height and thickness of the hairs, the total number of hairs in the bundle, the width of the bundle, and the area and perimeter of the apical surface of the hair cell were quantified from scanning electron microscope photomicrographs. An attempt was also made to determine if there was a consistent microstructure to the pattern of hair cell loss within the lesion area. Similar observations in 12-day recovered ears are also presented. The results indicated that stereocilia height increased and width decreased on surviving hair cells in the exposed ear. The width of the hair bundle, the hair cell surface area, and perimeter also decreased. However, the number of hairs per cell remained unchanged, and there was no evidence of any consistent organization to the hair cell loss within the patch across a number of specimens. These observations indicated that the hair bundles on short hair cells underwent changes as a consequence of intense sound exposure. The results after 12 days of recovery were complicated by developmental changes on the papilla and incomplete maturation of the newly regenerated hair cells. It remains to be seen whether these changes were the result of cell sampling in the sound-damaged ear or were due to true structural alterations within the sensory hairs themselves.