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Funder: Calico Life Sciences, LLC, The naked mole‐rat (Heterocephalus glaber) has fascinated zoologists for at least half a century. It has also generated considerable biomedical interest not only because of its extraordinary longevity, but also because of unusual protective features (e.g. its tolerance of variable oxygen availability), which may be pertinent to several human disease states, including ischemia/reperfusion injury and neurodegeneration. A recent article entitled ‘Surprisingly long survival of premature conclusions about naked mole‐rat biology’ described 28 ‘myths’ which, those authors claimed, are a ‘perpetuation of beautiful, but falsified, hypotheses’ and impede our understanding of this enigmatic mammal. Here, we re‐examine each of these ‘myths’ based on evidence published in the scientific literature. Following Braude et al., we argue that these ‘myths’ fall into four main categories: (i) ‘myths’ that would be better described as oversimplifications, some of which persist solely in the popular press; (ii) ‘myths’ that are based on incomplete understanding, where more evidence is clearly needed; (iii) ‘myths’ where the accumulation of evidence over the years has led to a revision in interpretation, but where there is no significant disagreement among scientists currently working in the field; ( iv ) ‘myths’ where there is a genuine difference in opinion among active researchers, based on alternative interpretations of the available evidence. The term ‘myth’ is particularly inappropriate when applied to competing, evidence‐based hypotheses, which form part of the normal evolution of scientific knowledge. Here, we provide a comprehensive critical review of naked mole‐rat biology and attempt to clarify some of these misconceptions.

Age-related hearing loss (ARHL) is a public health problem that has been associated with negative health outcomes ranging from increased frailty to an elevated risk of developing dementia. Significant gaps remain in our knowledge of the underlying central neural mechanisms, especially those related to the efferent auditory pathways. Thus, the aim of this study was to quantify and compare age-related alterations in the cholinergic olivocochlear efferent auditory neurons. We assessed, in young-adult and aged CBA mice, the number of cholinergic olivocochlear neurons, auditory brainstem response (ABR) thresholds in silence and in presence of background noise, and the expression of excitatory and inhibitory proteins in the ventral nucleus of the trapezoid body (VNTB) and in the lateral superior olive (LSO). In association with aging, we found a significant decrease in the number of medial olivocochlear (MOC) cholinergic neurons together with changes in the ratio of excitatory and inhibitory proteins in the VNTB. Furthermore, in old mice we identified a correlation between the number of MOC neurons and ABR thresholds in the presence of background noise. In contrast, the alterations observed in the lateral olivocochlear (LOC) system were less significant. The decrease in the number of LOC cells associated with aging was 2.7-fold lower than in MOC and in the absence of changes in the expression of excitatory and inhibitory proteins in the LSO. These differences suggest that aging alters the medial and lateral olivocochlear efferent pathways in a differential manner and that the changes observed may account for some of the symptoms seen in ARHL.

BackgroundMelanin pigmentation is present within the auditory and vestibular systems of the mammalian inner ear and may play a role in maintaining auditory and vestibular function. Melanocytes within the stria vascularis (SV) are necessary for the generation of the endocochlear potential (EP) and decreased EP has been linked to age-related hearing loss. Melanocytes and pigment-containing “dark cells” are present within the vestibular system, but have a less well-defined role. African–American individuals have increased pigmentation within the SV and vestibular system, which is hypothesized to be related to lower rates of age-related hearing loss and vestibular dysfunction. It remains unclear if increased pigmentation confers lifelong protection against hearing loss and vestibular dysfunction.MethodsMouse temporal bones were collected from juvenile (3–4 week) and aged (20–32 months) CBA/CaJ mice. Pediatric and adult human temporal bones from Caucasian or African–American individuals were examined from the Johns Hopkins Temporal Bone Collection. Information regarding Fitzpatrick skin type were unavailable, and self-identified race/ethnicity was used as a proxy. Images were taken using light microscopy at 20× magnification. ImageJ software (v1.53) was used to measure pigment within the SV and vestibular system.ResultsIn mouse temporal bones pigmentation within the SV increased with age, but pigmentation within the vestibular system did not increase with age. In human temporal bones pigmentation within the SV increased with age and pigmentation within the vestibular system increased within the wall of the utricle, but not other regions of the vestibular system. African–American individuals had higher amounts of pigment within the SV and vestibular system, among both pediatric and adult populations.ConclusionStria vascularis pigmentation increases with age in mouse and human temporal bones. Pigmentation within the vestibular system did not increase with age in mouse specimens and only increased within the utricular wall with age in human specimens. Individuals who identified as African–American had higher pigment content within the SV and vestibular system, both as children and as adults. These results highlight how similar age-related pigmentary changes occur in the auditory and vestibular systems across species and underscore the importance of racial/ethnic diversity in human temporal bone studies.

Naked mole-rats are highly vocal, eusocial, subterranean rodents with, counterintuitively, poor hearing. The causes underlying their altered hearing are unknown. Moreover, whether altered hearing is degenerate or adaptive to their unique lifestyles is controversial. We used various methods to identify the factors contributing to altered hearing in naked and the related Damaraland mole-rats and to examine whether these alterations result from relaxed or adaptive selection. Remarkably, we found that cochlear amplification was absent from both species despite normal prestin function in outer hair cells isolated from naked mole-rats. Instead, loss of cochlear amplification appears to result from abnormal hair bundle morphologies observed in both species. By exploiting a well-curated deafness phenotype-genotype database, we identified amino acid substitutions consistent with abnormal hair bundle morphology and reduced hearing sensitivity. Amino acid substitutions were found in unique groups of six hair bundle link proteins. Molecular evolutionary analyses revealed shifts in selection pressure at both the gene and the codon level for five of these six hair bundle link proteins. Substitutions in three of these proteins are associated exclusively with altered hearing. Altogether, our findings identify the likely mechanism of altered hearing in African mole-rats, making them the only identified mammals naturally lacking cochlear amplification. Moreover, our findings suggest that altered hearing in African mole-rats is adaptive, perhaps tailoring hearing to eusocial and subterranean lifestyles. Finally, our work reveals multiple, unique evolutionary trajectories in African mole-rat hearing and establishes species members as naturally occurring disease models to investigate human hearing loss.

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.

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.

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.

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.

Fast excitatory synaptic transmission in central synapses is mediated primarily by AMPA receptors (AMPARs), which are heteromeric assemblies of four subunits, GluA1-4. Among these subunits, rapidly gating GluA3/4 appears to be the most abundantly expressed to enable neurotransmission with submillisecond precision at fast rates in subsets of central synapses. However, neither definitive identification of the molecular substrate for native AMPARs in these neurons, nor their hypothesized functional roles in vivo has been unequivocally demonstrated, largely due to lack of specific antagonists. Using GluA3 or GluA4 knockout (KO) mice, we investigated these issues at the calyx of Held synapse, which is known as a high-fidelity synapse involved in sound localization. Patch-clamp recordings from postsynaptic neurons showed that deletion of GluA4 significantly slowed the time course of both evoked and miniature AMPAR-mediated excitatory postsynaptic currents (AMPAR-EPSCs), reduced their amplitude, and exacerbated AMPAR desensitization and short-term depression (STD). Surprisingly, presynaptic release probability was also elevated, contributing to severe STD at GluA4-KO synapses. In contrast, only marginal changes in AMPAR-EPSCs were found in GluA3-KO mice. Furthermore, independent of changes in intrinsic excitability of postsynaptic neurons, deletion of GluA4 markedly reduced synaptic drive and increased action potential failures during high-frequency activity, leading to profound deficits in specific components of the auditory brainstem responses associated with synchronized spiking in the calyx of Held synapse and other related neurons in vivo. These observations identify GluA4 as the main determinant for fast synaptic response, indispensable for driving high-fidelity neurotransmission and conveying precise temporal information.

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.

SUMMARY Plasticity of thalamocortical (TC) synapses is robust during early development and becomes limited in the adult brain. We previously reported that a short duration of deafening strengthens TC synapses in the primary visual cortex (V1) of adult mice. Here, we demonstrate that deafening restores NMDA receptor (NMDAR)-dependent long-term potentiation (LTP) of TC synapses onto principal neurons in V1 layer 4 (L4), which is accompanied by an increase in NMDAR function. In contrast, deafening did not recover long-term depression (LTD) at TC synapses. Potentiation of TC synapses by deafening is absent in parvalbumin-positive (PV+) interneurons, resulting in an increase in feedforward excitation to inhibition (E/I) ratio. Furthermore, we found that a brief duration of deafening adult mice recovers rapid ocular dominance plasticity (ODP) mainly by accelerating potentiation of the open-eye responses. Our results suggest that cross-modal sensory deprivation promotes adult cortical plasticity by specifically recovering TC-LTP and increasing the E/I ratio., In Brief Plasticity of thalamocortical (TC) synapses is limited in adults. Rodríguez et al. demonstrate that a brief period of deafening adults recovers LTP at TC synapses in visual cortex and accelerates ocular dominance plasticity. These results suggest that cross-modal sensory deprivation may be an effective way to promote adult cortical plasticity., Graphical Abstract

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...

Spherical and globular bushy cells of the AVCN receive huge auditory nerve endings specialized for high fidelity neural transmission in response to acoustic events. Recent studies in mice and other rodent species suggest that the distinction between bushy cell subtypes is not always straightforward. We conducted a systematic investigation of mouse bushy cells along the rostral-caudal axis in an effort to understand the morphological variation that gives rise to reported response properties in mice. We combined quantitative light and electron microscopy to investigate variations in cell morphology, immunostaining, and the distribution of primary and non-primary synaptic inputs along the rostral-caudal axis. Overall, large regional differences in bushy cell characteristics were not found; however, rostral bushy cells received a different complement of axosomatic input compared to caudal bushy cells. The percentage of primary auditory nerve terminals was larger in caudal AVCN, whereas non-primary excitatory and inhibitory inputs were more common in rostral AVCN. Other ultrastructural characteristics of primary auditory nerve inputs were similar across the rostral and caudal AVCN. Cross sectional area, postsynaptic density length and curvature, and mitochondrial volume fraction were similar for axosomatic auditory nerve terminals, although rostral auditory nerve terminals contained a greater concentration of synaptic vesicles near the postsynaptic densities. These data demonstrate regional differences in synaptic organization of inputs to mouse bushy cells rather than the morphological characteristic of the cells themselves.

Efferent innervation of the cochlea undergoes extensive modification early in development, but it is unclear if efferent synapses are modified by age, hearing loss, or both. Structural alterations in the cochlea affecting information transfer from the auditory periphery to the brain may contribute to age-related hearing deficits. We investigated changes to efferent innervation in the vicinity of inner hair cells (IHCs) in young and old C57BL/6 mice using transmission electron microscopy to reveal increased efferent innervation of IHCs in older animals. Efferent contacts on IHCs contained focal presynaptic accumulations of small vesicles. Synaptic vesicle size and shape were heterogeneous. Postsynaptic cisterns were occasionally observed. Increased IHC efferent innervation was associated with a smaller number of afferent synapses per IHC, increased outer hair cell loss, and elevated auditory brainstem response thresholds. Efferent axons also formed synapses on afferent dendrites but with a reduced prevalence in older animals. Age-related reduction of afferent activity may engage signaling pathways that support the return to an immature state of efferent innervation of the cochlea.

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.

Mice missing the alpha9 nicotinic acetylcholine receptor subunit (A9KO) show a lack of classic efferent effects on cochlear activity; however, behavioral and physiological studies in these mice have failed to support common hypotheses about the role of efferent feedback in auditory function. A9KO mice do not show deficits detecting or discriminating tones in noise. These mice also do not appear to be more susceptible to age-related hearing loss, and they do not show increased auditory brainstem response thresholds when chronically exposed to moderate-level noise. A9KO mice do show increased susceptibility to temporal processing deficits, especially when exposed to environmental noise. Furthermore, A9KO mice show extremely variable, and sometimes poor, performance when discriminating changes in the location of broadband sounds in the horizontal plane. Temporal and spatial processing deficits may be attributable to abnormal or poorly optimized representation of acoustic cues in the central auditory pathways...

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.]

Canaries have been domesticated for well over 100 years. They have been bred for specific characteristics such as song, plumage, or body shape. Here we measured audiograms in several canary strains using both behavioral (operant conditioning) and physiological (auditory brainstem responses) methods. Overall, there was a good correspondence between behavioral and ABR audiograms, but there were differences in audiogram shape and sensitivity between strains. Belgian Waterslager canaries bred for low‐pitched song had elevated high frequency thresholds, while Spanish Timbrado canaries bred for high‐pitched song had slightly better high frequency thresholds than canaries that were not bred for song. Other strains showed intermediate sensitivity. These results suggest there can be more variability in hearing within a species than previously thought and that these differences are correlated with other behavioral or morphological traits. [Work supported by DC00198, DC001372, DC04664‐01A2, and DC005450.]

Belgian Waterslager canaries (BWS) are bred for their low‐frequency song and have been shown to have hair cell abnormalities in the inner ear that result in elevated thresholds at higher frequencies. Previous results show that resolution of temporal fine structure, or the ability to resolve rapidly occurring changes in complex sounds, is enhanced in BWS canaries. In a continuing effort to assess the effects of the BWS inner ear pathology on hearing, we here investigate the ability to integrate acoustic information over longer periods of time. Absolute thresholds for 1.0‐, 2.0‐, and 4.0‐kHz pure tones were measured in BWS and normal‐hearing nonBWS canary strains for durations ranging from 5 to 480 ms using operant conditioning methods. NonBWS canaries showed a decrease in threshold of approximately 10–15 dB with increasing tone duration for all frequencies. In contrast, BWS showed almost no change in threshold across the range of durations tested for all frequencies. The reduced temporal integration in BWS...

Many studies have examined frequency discrimination in birds, but there has not been as complete a description of avian intensity discrimination abilities. Birds appear to be slightly less sensitive to changes in intensity than humans and other mammals; however, few studies have systematically looked at the effects of both frequency and presentation level on intensity discrimination in birds. Here we describe intensity discrimination as a function of frequency and sensation level in two small songbird species, the canary (Serinus canarius), the zebra finch (Taeniopygia guttata), and a nonsongbird species, the budgerigar (Melopsittacus undulatus). Intensity difference limens (DLIs) for pure tones were obtained from birds using standard operant conditioning procedures and the Method of Constant Stimuli. DLIs ranged from approximately 2–6 dB, which are slightly larger than the DLIs reported in mammals. For all three species, DLIs become smaller with increasing presentation level, but show little effect across frequency for a given level. These results are consistent with previous reports in other species. [Work supported by NIH DC01372 to RJD and DC05450 to AML.]

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.]