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Age-related hearing loss is a very common sensory disability, affecting one in three older adults. Establishing a link between anatomical, physiological, and behavioral markers of presbycusis in a mouse model can improve the understanding of this disorder in humans. We measured age-related hearing loss for a variety of acoustic signals in quiet and noisy environments using an operant conditioning procedure and investigated the status of peripheral structures in CBA/CaJ mice. Mice showed the greatest degree of hearing loss in the last third of their lifespan, with higher thresholds in noisy than in quiet conditions. Changes in auditory brainstem response thresholds and waveform morphology preceded behavioral hearing loss onset. Loss of hair cells, auditory nerve fibers, and signs of stria vascularis degeneration were observed in old mice. The present work underscores the difficulty in ascribing the primary cause of age-related hearing loss to any particular type of cellular degeneration. Revealing these complex structure-function relationships is critical for establishing successful intervention strategies to restore hearing or prevent presbycusis.

Bats are long-lived animals that show presumed resistance to noise-induced and age-related hearing loss, which has been attributed to their dependence on sound processing for survival. Echolocation and basic auditory functions have been studied extensively in the big brown bat (Eptesicus fuscus), an insectivorous microchiropteran species. We conducted hearing tests and analysis of cochlear sensory cells in a group of big brown bats that exhibited anomalies in behavioral sonar tracking experiments and/or lacked neural responses to acoustic stimulation in subcortical auditory nuclei. We show for the first time the presence of profound deafness and extensive cochlear damage in an echolocating bat species. Auditory brainstem responses were abnormal or absent in these bats, and histological analyses of their cochleae revealed extensive loss of hair cells, supporting cells, and spiral ganglion neurons. The underlying cause of deafness is unknown.

Acoustic startle response (ASR) modification procedures, especially prepulse inhibition (PPI), are increasingly used as behavioral measures of auditory processing and sensorimotor gating in rodents due to their perceived ease of implementation and short testing times. In practice, ASR and PPI procedures are extremely variable across animals, experimental setups, and studies, and the interpretation of results is subject to numerous caveats and confounding influences. We review considerations for modification of the ASR using acoustic stimuli, and we compare the sensitivity of PPI procedures to more traditional operant psychoacoustic techniques. We also discuss non-auditory variables that must be considered. We conclude that ASR and PPI measures cannot substitute for traditional operant techniques due to their low sensitivity. Additionally, a substantial amount of pilot testing must be performed to properly optimize an ASR modification experiment, negating any time benefit over operant conditioning. Nevertheless, there are some circumstances where ASR measures may be the only option for assessing auditory behavior, such as when testing mouse strains with early-onset hearing loss or learning impairments.

Introduction It is estimated over 466 million people worldwide have disabling hearing loss, and untreated hearing loss is associated with poorer health outcomes. The influence of sex as a biological variable on hearing loss is not well understood, especially for differences in underlying mechanisms which are typically elucidated through non-clinical research. Although the inclusion of sex as a biological variable in clinical studies has been required since 1993, sex reporting has only been recently mandated in National Institutes of Health funded non-clinical studies. Objective This article reviews the literature on recent non-clinical and clinical research concerning sex-based differences in hearing loss primarily since 1993, and discusses implications for knowledge gaps in the translation from non-clinical to clinical realms. Conclusions The disparity between sex-based requirements for non-clinical versus clinical research may inhibit a comprehensive understanding of sex-based mechanistic differences. Such disparities may play a role in understanding and explaining clinically significant sex differences and are likely necessary for developing robust clinical treatment options.

The effects of traumatic noise-exposure and deafening on auditory system function have received a great deal of attention. However, lower levels of noise as well as temporary conductive hearing loss also have consequences on auditory physiology and hearing. Here we review how abnormal acoustic experience at early ages affects the ascending and descending auditory pathways, as well as hearing behavior.

Individuals who have sustained a traumatic brain injury (TBI) often report auditory dysfunction including changes to their hearing sensitivity, tinnitus, and hyperacusis. One factor that may have a significant contribution to a person’s post-injury outcomes is whether the TBI occurred in combination with a high intensity noise exposure (e.g., as in the case of a car accident). To date, no study has examined the combined effects of a brain injury and high intensity noise exposure to evaluate whether this would lead to worse overall auditory outcomes than either trauma in isolation. In this study we tested the auditory sensitivity of male and female CBA/CaJ laboratory mice before and 3, 7, 14, 30, 60, and 90 days after acoustic (noise exposure), physical (controlled cortical impact), and combined acoustic and physical injuries. Following completion of the experiment, cochlear and brain tissue was fixed with paraformaldehyde and central and peripheral auditory structures were examined for damage. Our preliminary results show that physical injuries alone cause damage to the auditory sensitivity of mice measured using the auditory brainstem response, reduced acoustic startle responses in quiet and noise, yet hair cells remain intact. Long-term consequences on auditory perception are being tracked in these mice.

Sound localization and directional hearing are fundamental for rodents to successfully navigate their environment, detect predators and prey, and locate conspecifics. In this chapter, the cues available to rodents for localizing and discriminating sounds in space are reviewed, including interaural level and timing differences and spectral cues. The neural circuits supporting sound localization are also introduced. Sound localization acuity and directional hearing behavior in azimuth and elevation that have been measured in terrestrial and subterranean rodent species are compared. Due to the limited scope of behavioral testing performed in most rodent species to date, binaural evoked potential studies that have been used to probe directional hearing in rodents are also considered as an alternative to labor-intensive behavioral measures. Finally, the trends observed across species are summarized and areas for future study are suggested.

Perceptual performance in persons with hearing loss, especially those using devices to restore hearing, is not fully predicted by traditional audiometric measurements designed to evaluate the status of peripheral function. The integrity of auditory brainstem synapses may vary with different forms of hearing loss, and differential effects on the auditory nerve-brain interface may have particularly profound consequences for the transfer of sound from ear to brain. Loss of auditory nerve synapses in ventral cochlear nucleus (VCN) has been reported after acoustic trauma, ablation of the organ of Corti, and administration of ototoxic compounds. The effects of gradually acquired forms deafness on these synapses are less well understood. We investigated VCN gross morphology and auditory nerve synapse integrity in DBA/2J mice with early-onset progressive sensorineural hearing loss. Hearing status was confirmed using auditory brainstem response audiometry and acoustic startle responses. We found no change in VCN volume, number of macroneurons, or number of VGLUT1-positive auditory nerve terminals between young adult and older, deaf DBA/2J. Cell-type specific analysis revealed no difference in the number of VGLUT1 puncta contacting bushy and multipolar cell body profiles, but the terminals were smaller in deaf DBA/2J mice. Transmission electron microscopy confirmed the presence of numerous healthy, vesicle-filled auditory nerve synapses in older, deaf DBA/2J mice. The present results suggest that synapses can be preserved over a relatively long time-course in gradually acquired deafness. Elucidating the mechanisms supporting survival of central auditory nerve synapses in models of acquired deafness may reveal new opportunities for therapeutic intervention.

Sound processing in the cochlea is modulated by cholinergic efferent axons arising from medial olivocochlear neurons in the brainstem. These axons contact outer hair cells in the mature cochlea and inner hair cells during development and activate nicotinic acetylcholine receptors composed of α9 and α10 subunits. The α9 subunit is necessary for mediating the effects of acetylcholine on hair cells as genetic deletion of the α9 subunit results in functional cholinergic de-efferentation of the cochlea. Cholinergic modulation of spontaneous cochlear activity before hearing onset is important for the maturation of central auditory circuits. In α9KO mice, the developmental refinement of inhibitory afferents to the lateral superior olive is disturbed, resulting in decreased tonotopic organization of this sound localization nucleus. In this study, we used behavioral tests to investigate whether the circuit anomalies in α9KO mice correlate with sound localization or sound frequency processing. Using a conditioned lick suppression task to measure sound localization, we found that three out of four α9KO mice showed impaired minimum audible angles. Using a prepulse inhibition of the acoustic startle response paradigm, we found that the ability of α9KO mice to detect sound frequency changes was impaired, whereas their ability to detect sound intensity changes was not. These results demonstrate that cholinergic, nicotinic α9 subunit mediate, transmission in the developing cochlear plays an important role in the maturation of hearing.

Studies have suggested a role of weakened medial olivocochlear (OC) efferent feedback in accelerated hearing loss and increased susceptibility to noise. The present study investigated the progression of hearing loss with age and exposure to a noisy environment in medial OC-deficient mice. Alpha9 nicotinic acetylcholine receptor knockout (α9KO) and wild types were screened for hearing loss using auditory brainstem responses. α9KO mice housed in a quiet environment did not show increased hearing loss compared to wild types in young adulthood and middle age. Challenging the medial OC system by housing in a noisy environment did not increase hearing loss in α9KO mice compared to wild types. ABR wave 1 amplitudes also did not show differences between α9KO mice and wild types. These data suggest that deficient medial OC feedback does not result in early onset of hearing loss.

Zellweger spectrum disorder (ZSD) is a disease continuum that results from inherited defects in PEX genes essential for normal peroxisome assembly. These autosomal recessive disorders impact brain development and also cause postnatal liver, adrenal, and kidney dysfunction, as well as loss of vision and hearing. The hypomorphic PEX1-G843D missense allele, observed in approximately 30% of ZSD patients, is associated with milder clinical and biochemical phenotypes, with some homozygous individuals surviving into early adulthood. Nonetheless, affected children with the PEX1-G843D allele have intellectual disability, failure to thrive, and significant sensory deficits. To enhance our ability to test candidate therapies that improve human PEX1-G843D function, we created the novel Pex1-G844D knock-in mouse model that represents the murine equivalent of the common human mutation. We show that Pex1-G844D homozygous mice recapitulate many classic features of mild ZSD cases, including growth retardation and fatty livers with cholestasis. In addition, electrophysiology, histology, and gene expression studies provide evidence that these animals develop a retinopathy similar to that observed in human patients, with evidence of cone photoreceptor cell death. Similar to skin fibroblasts obtained from ZSD patients with a PEX1-G843D allele, we demonstrate that murine cells homozygous for the Pex1-G844D allele respond to chaperone-like compounds, which normalizes peroxisomal β-oxidation. Thus, the Pex1-G844D mouse provides a powerful model system for testing candidate therapies that address the most common genetic cause of ZSD. In addition, this murine model will enhance studies focused on mechanisms of pathogenesis.

Exposure to high intensity sound can lead to temporary or permanent threshold shifts. Noise exposures that do not cause long-term hearing deficits, however, can induce extensive afferent ribbon synapse loss, while hair cells and spiral ganglion neurons remain mostly intact (Kujawa and Liberman, 2009). This loss of synapses despite normal hearing thresholds is referred to as hidden hearing loss (HHL). We examined the development of HHL in laboratory mice using operant conditioning with positive reinforcement. After exposing mice to 8–16 kHz narrowband noise at 100 dB SPL for 2 h, hearing thresholds temporarily shifted for both pure tone and ultrasonic vocalization stimuli; however, post-exposure thresholds and threshold shifts varied by sex and age. Immunohistochemistry and transmission electron microscopy were conducted to quantify peripheral damage and central synaptic reorganization once behavioral testing was complete. Brains were collected, sectioned, and labeled against VGLUT1 or GAD65 and labeling was quantified in the ventral cochlear nucleus. Cochleas were also collected, dissected, and labeled for myosin6 to label hair cells and either CTBP2 or SV2 to identify afferent or efferent terminals, respectively. Our findings show that mice are able to behaviorally recover hearing following non-traumatic noise exposure despite changes in peripheral and central auditory structures.

Accurate quantification of cell populations is essential in assessing and evaluating neural survival and degeneration in experimental groups. Estimates obtained through traditional two-dimensional counting methods are heavily biased by the counting parameters in relation to the size and shape of the neurons to be counted, resulting in a large range of inaccurate counts. In contrast, counting every cell in a population can be extremely labor-intensive. The present study hypothesizes that design-based stereology provides estimates of the total number of cochlear spiral ganglion neurons (SGNs) in mice that are comparable to those obtained by other accurate cell-counting methods, such as a serial reconstruction, while being a more efficient method. SGNs are indispensable for relaying auditory information from hair cells to the auditory brainstem, and investigating factors affecting their degeneration provides insight into the physiological basis for the progression of hearing dysfunction. Stereological quantification techniques offer the benefits of efficient sampling that is independent of the size and shape of the SGNs. Population estimates of SGNs in cochleae from young C57 mice with normal-hearing and C57 mice with age-related hearing loss were obtained using the optical fractionator probe and traditional two-dimensional counting methods. The average estimated population of SGNs in normal-hearing mice was 7009, whereas the average estimated population in mice with age-related hearing loss was 5096. The estimated population of SGNs in normal-hearing mice fell within the range of values previously reported in the literature. The reduction in the SGN population in animals with age-related hearing loss was statistically significant. Stereological measurements required less time per section compared to two-dimensional methods while optimizing the amount of cochlear tissue analyzed. These findings demonstrate that design-based stereology provides a practical alternative to other counting methods such as the Abercrombie correction method, which has been shown to notably underestimate cell populations, and labor-intensive protocols that account for every cell individually.

Increased prevalence of emotional distress is associated with tinnitus and hearing loss. The underlying mechanisms of the negative emotional response to tinnitus and hearing loss remain poorly understood, and it is challenging to disentangle the emotional consequences of hearing loss from those specific to tinnitus in listeners experiencing both. We addressed these questions in laboratory rats using three common rodent anxiety screening assays: elevated plus maze, open field test, and social interaction test. Open arm activity in the elevated plus maze decreased substantially after one trial in controls, indicating its limited utility for comparing pre- and post-treatment behavior. Open field exploration and social interaction behavior were consistent across multiple sessions in control animals. Individual sound-exposed and salicylate-treated rats showed a range of phenotypes in the open field, including reduced entries into the center in some subjects and reduced locomotion overall. In rats screened for tinnitus, less locomotion was associated with higher tinnitus scores. In salicylate-treated animals, locomotion was correlated with age. Sound-exposed and salicylate-treated rats also showed reduced social interaction. These results suggest that open field exploratory activity is a selective measure for identifying tinnitus distress in individual animals, whereas social interaction reflects the general effects of hearing loss. This animal model will facilitate future studies of the structural and functional changes in the brain pathways underlying emotional distress associated with hearing dysfunction, as well as development of novel interventions to ameliorate or prevent negative emotional responses.

Purpose: To assess possible damage to the hearing of experimental and companion animal subjects of magnetic resonance imaging (MRI) scans. Materials and Methods: Using animal hearing threshold data and sound level measurements from typical MRI pulse sequences, we estimated “equivalent loudness” experienced by several experimental and companion animals commonly subjects of MRI scans. We compared the equivalent loudness and exam duration to safe noise standards set by the National Institute for Occupational Safety and Health (NIOSH). Results: Monkeys, dogs, cats, pigs, and rabbits are frequently exposed to equivalent loudness levels during MRI scans beyond what is considered safe for human exposure. The sensitive frequency ranges for rats and mice are shifted substantially upward and their equivalent loudness levels fall within the NIOSH safe zone. Conclusion: MRI exposes many animals to levels of noise and duration that would exceed NIOSH human exposure limits. Researchers and veterinarians should use hearing protection for animals during MRI scans. Experimental research animals used in MRI studies are frequently kept and reimaged, and hearing loss could result in changed behavior. Damage to companion animals' hearing could make them less sensitive to commands and generally worsen interactions with family members. Much quieter MRI scanners would help decrease stress and potential harm to scanned animals, normalize physiology during MRI, and enable MRI of awake animals. J. Magn. Reson. Imaging 2012;36:743–747. © 2012 Wiley Periodicals, Inc.

Auditory neuropathy spectrum disorder (ANSD) describes a prevalent hearing disorder that is characterized by normal cochlear outer hair cell (OHC) function and abnormal auditory nerve function (1). Minimum diagnostic criteria include normal otoacoustic emissions (OAEs) and missing or aberrant auditory brainstem responses (ABRs). Changes in the ABR are assumed to arise from a dys-synchronization of sound-driven activity in the auditory nerve. The loss of temporal processing can impair speech, sound localization, and listening in noise. The impact of ANSD on speech has encouraged neonatal screening programs for early diagnosis of the disorder. These programs have revealed a higher incidence of ANSD among infants who have been treated in neonatal intensive care units (NICUs)(2,3). Although the health concerns that necessitate early hospitalization are varied, a constant factor in NICU treatments is the noise exposure that is generated by equipment, procedures, and staff (4,5). Several surveys have reported NICU noise levels consistently above the recommendations of the American Academy of Pediatrics (AAP) for both sustained (Leq) and maximum transient exposures (Lmax) (6). At present, significant ambiguities remain on what constitutes an acceptable level of noise exposure in human infants. While it is clear that a single loud exposure at a young age can accelerate hearing loss and promote spiral ganglion degeneration (7), the effects of persistent moderate exposures are difficult to estimate because environmental noise exerts pervasive effects on the developing auditory system. The deficits often manifest as perceptual disorders that are independent of overt hearing loss (8,9). Physiological studies of the cochlea and auditory nerve have provided detailed functional analyses of the medial olivocochlear system (MOCS). In normal individuals, the release of acetylcholine by the MOCS hyperpolarizes the membrane potentials of OHCs (10). The resulting decrease in cochlear mechanical sensitivity protects the ear from damaging levels of noise (11) and enhances auditory processing in distracting levels of noise (12,13). Recent clinical evidence suggests that ANSD is more prevalent among MOCS-compromised children (14). One explanation for this increased risk is that synaptic development of the central auditory pathways requires regulated sound-driven activity in the ascending inputs of the auditory nerve (15–17). When young individuals are exposed to environmental noise, MOC feedback may preserve normal synaptic development by regulating potentially disruptive levels of noise-driven activity. To investigate this novel developmental role for the MOCS, the feedback system was silenced in laboratory mice by a genetic modification of cholinergic signaling (18). The mice were reared in background noise, and then screened for ANSD using established diagnostic criteria. The audiological implications of the observed processing deficits were further delineated with a behavioral assay of temporal acuity. The refinement of this animal model allowed us to relate common clinical observations to direct electrophysiological recordings from the post-synaptic targets of the auditory nerve in the ventral cochlear nucleus. These recordings revealed significant functional impairments of the synaptic specializations that dictate the quality of temporal coding in the auditory brainstem.

Tinnitus is a pervasive auditory dysfunction affecting up to 10% of the adult population. The perception of ringing or hissing in the absence of a physical stimulus in one or both ears can be caused by acoustic trauma and other factors. Mice are a commonly used model for auditory disorders in humans, although the behavioral examination of tinnitus in mice has primarily been limited to reflexive measures involving inhibition of the acoustic startle by gaps in noise. Using an identification paradigm, we behaviorally tested whether mice show symptoms of tinnitus following long-term moderate noise exposure. Tinnitus was demonstrated by a shift in categorizing silence as narrowband noise. This experiment demonstrated that tinnitus can be induced in mice using noise exposure, similar to that caused by salicylate. Physiological and anatomical experiments reveal synaptic changes including response facilitation, increased reliability, increased synaptic terminal area, and increased number of release sites in mice ...

Plasticity in the medial and lateral olivocochlear (MOC and LOC) systems in response to chronic exposure to background noise was investigated. Three different age-groups of young mice were exposed to the same chronic moderate noise conditions with either immediate tissue harvest or harvest following restoration to quiet conditions, with age matched controls. Cochleae were dissected and standard immunohistochemistry protocols were used to label hair cells with antibodies against myosin 6 and olivocochlear synaptic terminals with synaptic vesicle protein 2 (SV2). Specimens were imaged using confocal microscopy, and density of SV2 labeling was quantified. There was no statistically significant difference in MOC SV2 density between mice raised in noise and age matched controls for any group. However, there was a statistically significant increase in LOC SV2 density for adult mice raised in noise, particularly at higher frequency regions. This could suggest a protective upregulation of the efferent system against chronic moderate noise exposure. The increase in LOC innervation persisted for juvenile mice raised in noise with subsequent restoration to quiet conditions. These data suggest that the LOC system demonstrates sound-dependent plasticity, but that synaptic morphology may be altered for a substantial time period after exposure to noise ceases.

Animal models offer an opportunity to investigate the consequences of asymmetrical hearing loss with a level of control over extraneous variables that is not possible with human listeners. Experimental manipulations to induce unilateral conductive or sensorineural hearing loss in animal models have demonstrated substantial and diverse changes in physiological function, anatomical reorganization of neural projections, and adverse effects on auditory behaviors. Our experiments in rodents exposed to acoustic trauma with one ear plugged result in asymmetrical hearing loss and abnormal auditory brainstem response waveforms that occur when either the unprotected or protected ear is stimulated. Susceptibility to auditory brainstem response deficits appears to differ between the right and left sides. Asymmetrical hearing loss is associated with increased startle reactivity to loud sounds, suggesting abnormal loudness perception or an increased emotional response to sound. These animals also show abnormal social interaction, and some subjects show reduced exploratory behavior in a novel environment indicative of heightened anxiety. These studies provide a framework for investigating the interplay between the auditory and non-auditory behavioral consequences of hearing loss, as well as the underlying neuropathology.Animal models offer an opportunity to investigate the consequences of asymmetrical hearing loss with a level of control over extraneous variables that is not possible with human listeners. Experimental manipulations to induce unilateral conductive or sensorineural hearing loss in animal models have demonstrated substantial and diverse changes in physiological function, anatomical reorganization of neural projections, and adverse effects on auditory behaviors. Our experiments in rodents exposed to acoustic trauma with one ear plugged result in asymmetrical hearing loss and abnormal auditory brainstem response waveforms that occur when either the unprotected or protected ear is stimulated. Susceptibility to auditory brainstem response deficits appears to differ between the right and left sides. Asymmetrical hearing loss is associated with increased startle reactivity to loud sounds, suggesting abnormal loudness perception or an increased emotional response to sound. These animals also show abnormal social i...

The mechanisms that underlie hyperacusis are poorly understood, due in part to the lack of a behavioral animal model. Traditional self-report methods used to measure loudness and loudness discomfort are not suitable for use with animals because the animals cannot provide subjective responses about the magnitude of an internal psychological perception. Instead, reaction time (RT) measures have been used in animals to estimate loudness perception. In the present study, the authors demonstrate that RTs are shorter at moderate and high sound levels in canaries of a strain with a hereditary high-frequency hearing loss than in normal canaries, indicating increased loudness. As far as we know, this is the first report of hyperacusis in a nonhuman animal and demonstrates that RT is a potentially useful measure in animal models of hyperacusis.

The Belgian Waterslager canary is unique for its loud, low-pitched song which is accompanied by a hereditary pathology involving missing and damaged hair cells in the basal end of the papilla. These birds were been bred for hundreds of years for loud, low-pitched song. Breeders likely selected for high frequency hearing loss. In spite hair cell regeneration, the papillae in these birds never approaches that of normal-hearing canaries. Auditory nerve and brainstem responses are also diminished, and auditory brainstem nuclei show reduced cell size. And these birds show a suite of psychoacoustic deficits consistent with impaired active processing as seen in humans with hearing loss. It is rather remarkable, then, that Belgian Waterslagers are able to learn, discriminate, and produce complex, species-specific sounds with such impaired frequency selectivity and phase processing. This feat, in the presence of severe peripheral auditory damage, underscores the importance of temporal information in the avian auditory perception and vocal learning. The obvious genetic basis of this pathology places the Belgian Waterslager canary in another unique position of being the only nonhuman organism which must navigate through vocal development and vocal learning in the face of an inherited developmental peripheral auditory pathology.The Belgian Waterslager canary is unique for its loud, low-pitched song which is accompanied by a hereditary pathology involving missing and damaged hair cells in the basal end of the papilla. These birds were been bred for hundreds of years for loud, low-pitched song. Breeders likely selected for high frequency hearing loss. In spite hair cell regeneration, the papillae in these birds never approaches that of normal-hearing canaries. Auditory nerve and brainstem responses are also diminished, and auditory brainstem nuclei show reduced cell size. And these birds show a suite of psychoacoustic deficits consistent with impaired active processing as seen in humans with hearing loss. It is rather remarkable, then, that Belgian Waterslagers are able to learn, discriminate, and produce complex, species-specific sounds with such impaired frequency selectivity and phase processing. This feat, in the presence of severe peripheral auditory damage, underscores the importance of temporal information in the avian audi...

Normal-hearing (NH) listeners and hearing-impaired (HI) listeners detected and discriminated time-reversed harmonic complexes constructed of equal-amplitude harmonic components with fundamental frequencies (F0s) ranging from 50 to 800 Hz. Component starting phases were selected according to the positive and negative Schroeder-phase algorithms to produce within-period frequency sweeps with relatively flat temporal envelopes. Detection thresholds were not affected by component starting phases for either group of listeners. At presentation levels of 80 dB SPL, NH listeners could discriminate the two waveforms nearly perfectly when the F0s were less than 300–400 Hz but fell to chance performance for higher F0s. HI listeners performed significantly poorer, with reduced discrimination at several of the F0s. In contrast, at a lower presentation level meant to nearly equate sensation levels for the two groups, NH listeners’ discrimination was poorer than HI listeners at most F0s. Roving presentation levels had little effect on performance by NH listeners but reduced performance by HI listeners. The differential impact of roving level suggests a weaker perception of timbre differences and a greater susceptibility to the detrimental effects of experimental uncertainty in HI listeners.

Noise in animal housing facilities is an environmental variable that can affect hearing, behavior and physiology in mice. The authors measured sound levels in two rodent housing rooms (room 1 and room 2) during several 24-h periods. Room 1, which was subject to heavy personnel traffic, contained ventilated racks and static cages that housed large numbers of mice. Room 2 was accessed by only a few staff members, contained static cages only and housed fewer mice. In both rooms, background sound levels were usually about 80 dB, and transient noises caused sound levels to temporarily rise 30-40 dB above the baseline level; such peaks occurred frequently during work hours (8:30 AM to 4:30 PM) and infrequently during non-work hours. Noise peaks during work hours in room 1 occurred about two times as often as in room 2 (P = 0.01). Use of changing stations located in the rooms caused background noise to increase by about 10 dB. Loud noise and noise variability were attributed mainly to personnel activity. Attempts to reduce noise should concentrate on controlling sounds produced by in-room activities and experimenter traffic; this may reduce the variability of research outcomes and improve animal welfare.

Belgian Waterslager canaries (BWC) are bred to produce a distinctive low-pitched song with energy restricted to a lower range of frequencies than in other types of canaries. Previous studies have shown a high frequency hearing loss primarily above 2000 Hz that is related to hair cell abnormalities in BWC, but little is known about auditory perception in these birds. Here, frequency, duration, and intensity discrimination, temporal integration, gap detection, and discrimination of temporally reversed harmonic complexes in BWC were measured and compared to normal-hearing non-BWC. BWC had excellent frequency discrimination ability at 1000 Hz, but showed poor frequency discrimination compared to non-BWC at frequencies in the region of hearing loss. Duration and intensity discrimination were not adversely affected in BWC. Temporal integration was reduced in BWC, except at 2000 Hz. Gap detection and discrimination of temporally reversed stimuli were somewhat better in BWC than in non-BWC. Those tests that relied primarily on temporal processing were less affected by the cochlear damage in BWC than tests that probably relied more on audibility and spectral analysis. Thus, despite significant high frequency hearing loss and extensive damage along the basilar papilla, BWC retain relatively good hearing abilities under many conditions.

The mammalian medial olivocochlear (MOC) efferent feedback system protects the ear from intense noise exposure, aids in cochlear gain control, and improves responses to signals in noise. Unequivocal behavioral effects of eliminating MOC feedback have been difficult to demonstrate. We used an acoustic startle reflex (ASR) modification paradigm to reveal behavioral effects of eliminating MOC feedback in mice. Mice lacking the alpha9 nicotinic acetylcholine receptor subunit showed increased facilitation of the ASR reflex in the presence of background noise, abnormal responses to brief fluctuations in background noise, and abnormal inhibition of the ASR by changes in the location of noise in azimuth and elevation. Abnormal behavioral responses occurred in the absence of cochlear hearing loss. The behavioral effects of weakened MOC feedback may reflect both direct and indirect effects of abnormal cochlear gain control in the presence of noise. The results provide further evidence for a role of MOC efferent feedback in hearing in noise and demonstrate that noise‐related hearing deficits can occur when hearing thresholds are normal.

Belgian Waterslager canaries (BWS), bred for a distinct low‐pitched song, have an inherited high‐frequency hearing loss related to hair cell abnormalities. Many hair cells are missing or damaged, and many of the remaining hair cells have abnormal stereocilia bundles. To investigate how the hair cell abnormalities affect frequency tuning along the BWS basilar papilla, we measured psychophysical tuning curves (PTCs) in BWS and normal‐hearing non‐BWS canaries using operant conditioning procedures. Non‐BWS canaries showed relatively symmetrical tuning curves that became more narrowly tuned with increasing center frequency. Despite near‐normal hearing at low frequencies, PTCs in BWS were elevated for all center frequencies tested. The sharpness of tuning was normal in BWS for PTCs with a center frequency of 1000 Hz and broader than normal at higher frequencies. The shapes of the PTCs were abnormal in BWS, particularly at higher frequencies. The abnormal tuning properties in the BWS are consistent with changes in the impedance characteristics of the basilar papilla due to structural damage. [Work supported by NIH DC01372 and DC04664.]

Sensorineural hearing loss is associated with reduced frequency selectivity due to the broadening of the auditory filters in mammals. In European starlings, hearing loss caused by the ototoxic drug kanamycin results in the widening of auditory filters at 5 kHz [Marean et al. (1998)]. In the present study, we examine frequency selectivity in a bird with a permanent hereditary hearing impairment, the Belgian Waterslager (BWS) canary. This strain of canary has long been bred for its loud, low‐frequency song, and has been shown to have a hearing loss primarily at higher frequencies (2 kHz and above). Using operant conditioning and the method of constant stimuli, thresholds for detecting pure tones in flat‐spectrum broadband noise were measured in BWS and non‐BWS canaries. Critical ratios were calculated for comparison with other species of birds. At higher frequencies, critical ratios for BWS canaries were much larger than those of non‐BWS canaries and other birds, suggesting reduced frequency selectivity in the region of the birds’ hearing loss. [Work supported by NIDCD R01DC001372 to RJD and Brenda M. Ryals.]