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• African mole-rats have only low-frequency hearing; an acoustic fovea is known in one species. • It has been claimed that, uniquely among mammals, certain mole-rats lack evoked otoacoustic emissions and hair-cell active processes. • We describe robust evoked emissions (DPOAE and SFOAE), with highest amplitudes at the frequencies of the acoustic fovea. • In the past, the narrow and strongly curved ear canals of African mole-rats might have complicated successful recording. African mole-rats display highly derived hearing that is characterized by low sensitivity and a narrow auditory range restricted to low frequencies < 10 kHz. Recently, it has been suggested that two species of these rodents do not exhibit distortion product otoacoustic emissions (DPOAE), which was interpreted as evidence for a lack of cochlear amplification. If true, this would make them unique among mammals. However, both theoretical considerations on the generation of DPOAE as well as previously published experimental evidence challenge this assumption. We measured DPOAE and stimulus-frequency otoacoustic emissions (SFOAE) in three species of African mole-rats (Ansell's mole-rat - Fukomys anselli ; Mashona mole-rat - Fukomys darlingi ; naked mole-rat - Heterocephalus glaber) and found unexceptional otoacoustic emission values. Measurements were complicated by the remarkably long, narrow and curved external ear canals of these animals, for which we provide a morphological description. Both DPOAE and SFOAE displayed the highest amplitudes near 1 kHz, which corresponds to the region of best hearing in all tested species, as well as to the frequency region of the low-frequency acoustic fovea previously described in Ansell's mole-rat. Thus, the cochlea in African mole-rats shares the ability to generate evoked otoacoustic emission with other mammals. [Display omitted] [ABSTRACT FROM AUTHOR]

• Mutations in connexin proteins cause congenital nonsyndromic and syndromic hearing loss. • The roles of connexins in age-related hearing loss (ARHL) are largely unexplored. • We found that Cx30 and Cx43 decrease expressions with age in the CBA/CaJ mouse cochlea. • We discovered that aldosterone treatment provides protective effects for Cx30and Cx43. • These results indicate that connexin protein declines are likely mechanisms of ARHL. Age-related hearing loss (ARHL), also known as presbycusis, is the number one communication disorder for aging adults. Connexin proteins are essential for intercellular communication throughout the human body, including the cochlea. Mutations in connexin genes have been linked to human syndromic and nonsyndromic deafness; thus, we hypothesize that changes in connexin gene and protein expression with age are involved in the etiology of ARHL. Here, connexin gene and protein expression changes for CBA/CaJ mice at different ages were examined, and correlations were analyzed between the changes in expression levels and functional hearing measures, such as ABRs and DPOAEs. Moreover, we investigated potential treatment options for ARHL. Results showed significant downregulation of Cx30 and Cx43 gene expression and significant correlations between the degree of hearing loss and the changes in gene expression for both genes. Moreover, dose-dependent treatments utilizing cochlear cell lines showed that aldosterone hormone therapy significantly increased Cx expression. In vivo mouse treatments with aldosterone also showed protective effects on connexin expression in aging mice. Based on these functionally relevant findings, next steps can include more investigations of the mechanisms related to connexin family gap junction protein expression changes during ARHL; and expand knowledge of clinically-relevant treatment options by knowing what specific members of the Cx family and related inter-cellular proteins should be targeted therapeutically. [ABSTRACT FROM AUTHOR]

Abstract Background Bone conduction (BC) is an alternative to air conduction (AC) for stimulation of the inner ear. Stimulation for BC can occur directly on the skull bone, on the skin covering the skull bone, or on soft tissue (i.e., eye, dura). All of these stimuli can elicit otoacoustic emissions (OAE). This study aims to compare OAEs generated by different combinations of stimuli in live humans, including direct stimulation of the intracranial contents via the dura, measured intraoperatively. Methods Measurements were performed in five normal-hearing ears of subjects undergoing a neurosurgical intervention with craniotomy in general anesthesia. Distortion product OAEs (DPOAEs) were measured for f 2 at 0.7, 1, 2, 3, 4, and 6 kHz with a constant ratio of the primary frequencies (f 2 /f 1) of 1.22. Sound pressure L 1 was held constant at 65 dB SPL, while L 2 was decreased in 10 dB steps from 70 to 30 dB SPL. A DPOAE was considered significant when its level was ≥6 dB above the noise floor. Emissions were generated sequentially with different modes of stimulation: 1) pre-operatively in the awake subject by two air-conducted tones (AC-AC); 2) within the same session preoperatively by one air- and one bone-conducted tone on the skin-covered temporal bone as in audiometry (AC-BC); 3) intra-operatively by one air-conducted tone and one bone-vibrator tone applied directly on the dura (AC-DC). A modified bone vibrator (Bonebridge; MED-EL, Innsbruck, Austria) was used for BC stimulation on the dura or skin-covered mastoid. Its equivalent perceived SPL was calibrated preoperatively for each individual by psychoacoustically comparing the level of a BC tone presented to the temporal region to an AC tone at the same frequency. Simultaneously with the DPOAEs, vibrations at the teeth were measured with an accelerometer attached using a custom-made holder. Results It was possible to record DPOAEs for all three stimulation modes. For AC-DC, DPOAEs were not detected above the noise floor below 2 kHz but were detectable at the higher frequencies. The best response was measured at or above 2 kHz with L 2 = 60 dB SPL. The acceleration measured at the teeth for stimulation on the dura was lower than that for stimulation on the bone, especially below 3 kHz. Conclusion We demonstrate a proof-of-concept comparison of DPOAEs and teeth acceleration levels elicited by a bone vibrator placed either against the skin-covered temporal bone, as in audiometry, or directly against the dura mater in patients undergoing a craniotomy. It was demonstrated that DPOAEs could be elicited via non-osseous pathways within the skull contents and that the required measurements could be performed intra-operatively. Highlights • Direct vibratory stimulation on the dura activates the outer hair cells, indicated by DPOAE. • At 70 dB, stimulation on dura and on the skin-covered temple induce a comparable DPOAE amplitude ≥2 kHz. • Below 70 dB, stimulation on dura induces lower amplitudes compared to stimulation on the skin-covered mastoid ≥2 kHz. • Direct stimulation on the dura induces skull vibrations, measurable at the teeth. [ABSTRACT FROM AUTHOR]

Evaluation of cervical evoked myogenic potentials (c-VEMP) is commonly applied in clinical investigations of patients with suspected neurotological symptoms. Short intense acoustic stimulation of peak levels close to 130 dB SPL is required to elicit the responses. A recent publication on bilateral significant sensorineural hearing loss related to extensive VEMP stimulation motivates evaluations of immediate effects on hearing acuity related to the intense acoustic stimulation required to elicit c-VEMP responses. The aim of the current study was to investigate changes in DPOAE-levels and hearing thresholds in relation to c-VEMP testing in humans. More specifically, the current focus is on immediate changes in hearing thresholds and changes in DPOAE-levels at frequencies 0.5 octaves above the acoustic stimulation when applying shorter tone bursts than previously used. Hearing acuity before and immediately after exposure to c-VEMP stimulation was examined in 24 patients with normal hearing referred for neurotologic testing. The stimulation consisted of 192 tonebursts of 6 ms and was presented at 500 Hz and 130 dB peSPL. Békésy thresholds at 0.125–8 kHz and DPOAE I/O growth functions with stimulation at 0.75 and 3 kHz were used to assess c-VEMP related changes in hearing status. No significant deterioration in Békésy thresholds was detected. Significant reduction in DPOAE levels at 0.75 (0.5–1.35 dB) and 3 kHz (1.6–2.1 dB) was observed after c-VEMP stimulation without concomitant changes in cochlear compression. The results indicated that there was no immediate audiometric loss related to c-VEMP stimulation in the current group of patients. The significant reduction of DPOAE levels at a wider frequency range than previously described after the c-VEMP test could be related to the stimulation with shorter tone bursts. The results show that c-VEMP stimulation causes reduction in DPOAE-levels at several frequencies that corresponds to half the reductions in DPOAE levels reported after exposure to the maximally allowed occupational noise for an 8 h working day. Consequently, extended stimuli intensity or stimulation repetition with c-VEMP testing should be avoided to reduce the risk for noise-induced cochlear injury. [ABSTRACT FROM AUTHOR]

Efferent auditory feedback on cochlear hair cells is well studied regarding olivocochlear brainstem mechanisms. Less is known about how the descending corticofugal system may shape efferent feedback and modulate cochlear mechanics. Distortion-product otoacoustic emissions (DPOAEs) are a suitable tool to assess outer hair cell function, as they are by-products of the nonlinear cochlear amplification process. The present project investigates the effects of cortical activity on cubic and quadratic DPOAEs in mongolian gerbils, Meriones unguiculatus , through cortical deactivation using the sodium-channel blocker lidocaine. Contralateral cortical microinjections of lidocaine can lead to either an increase or decrease of median DPOAE levels of up to 10.95 dB. The effects are reversible and comparable at all tested frequencies (0.5–40 kHz). They are not restricted to the preferred frequency of the cortical site of injection. Recovery times are between 20 and 120 min depending on stimulation levels and emission type. When the injection is performed in the ipsilateral hemisphere, DPOAE level shifts are lower in amplitude compared to those after injection in the contralateral hemisphere. No significant changes in DPOAE levels are obtained after saline microinjections. Results indicate that deactivation of auditory cortex activity through lidocaine has a considerable impact on peripheral auditory responses in form of DPOAEs, probably through cortico-olivocochlear pathways. [ABSTRACT FROM AUTHOR]

2,3,7,8-tetrachorodibenzo-p-dioxin (TCDD), a ubiquitous and persistent environmental contaminant, is a potent teratogen. Whereas developmental TCDD toxicity is mediated by the aryl hydrocarbon receptor (AhR), the normal function of the AhR is poorly understood. We tested whether dioxin exposure during a critical period of hair cell development disrupts cochlear function in three mouse strains, (C57BL6, BalbC, and CBA) that contain high affinity AhR-b alleles. C57BL/6, BalbC, and CBA dams were exposed to 500 ng/kg TCDD or olive oil (vehicle) on embryonic day 12 by gavage. Cochlear function was analyzed at 1.5 months of age by measuring 1) auditory brainstem response (ABRs) to tone pips from 5.6 to 30 kHz, and 2) distortion-product otoacoustic emissions (DPOAEs) evoked by primaries with f 2 at the same frequency values. Cochlear threshold sensitivity following TCDD exposure was significantly elevated in both female and male mice in the C57BL/6 strain, carrying the Ahb-1 allele, but not significantly elevated in the BalbC or CBA strains, carrying the Ahb-2 allele. These ABR threshold deficits in mice carrying the Ahb-1 allele parallels the cleft palate incidence to higher TCDD exposures, suggesting that ABR testing could serve as a sensitive indicator of TCDD toxicity in at-risk children. Moreover, DPOAEs were not affected following TCDD exposure in any of the mouse strains, suggesting that following TCDD exposure mice with the Ahb-1 allele exhibit a mild auditory neuropathy. The causes of many auditory neuropathies are unknown, yet a developmental exposure to dioxin may be a risk factor for this condition. [ABSTRACT FROM AUTHOR]

Distortion product otoacoustic emissions (DPOAE) in newborns and adults were evoked by sweeping primaries up and down in frequency at 1 s/octave. Sweeping up and down in frequency resulted in changes in the amplitude vs. frequency functions of the composite DPOAE and its two major components. In addition, DPOAE component phases differed slightly between the up- and down-swept conditions. The changes in amplitude vs. frequency functions were quantified using a covariate correlation technique, yielding single-valued estimates of the magnitude of the frequency changes. Separate analyses were performed for the entire DPOAE frequency range and split into low and high frequency ranges. There were consistent changes in newborn and adult composite DPOAEs and reflection components, but not generator components. Adults had significant frequency changes in the composite DPOAE for all frequency ranges and in the reflection component for the entire frequency range. Newborns had significant frequency change in the reflection component for all frequency ranges. Differences in frequency change between adults and newborns may stem from developmental changes in cochlear processing. Alignment of the component phase differences between the up- and down-swept conditions resulted in elimination of frequency-change in reconstructed composite DPOAEs. [ABSTRACT FROM AUTHOR]

Abstract: Exposure to harsh environment induces stress reactions that increase probability of survival. Stress influences the endocrine, nervous and immune systems and affects the functioning of a variety of organs. Numerous researchers demonstrated that a 24-h exposure to an acoustic rodent repellent provokes stress reaction in exposed animals. In addition to the activated hypothalamic–pituitary–adrenal (HPA) axis, exposed animals had pathological reactions in the reproductive organs, bronchia and skin. Here, we examined the effect of above stress model on the auditory system of Wistar rats. We found that 24-h stress decreases the thresholds and increases the amplitudes of auditory brainstem responses and distortion product otoacoustic emissions. Resultant auditory hypersensitivity was transient and most pronounced between 3 and 6h post-stress, returning to control levels one week later. The concentration of corticosterone and tumor necrosis factor alpha was systemically elevated in stressed animals between 3 and 6h post-stress, confirming the activation of the HPA axis. In addition, expression of the HPA-axis-associated genes: glucocorticoid receptor (GR) and hypoxia-inducible factor 1 alpha (Hif1a) was modulated in the auditory tissues. In detail, in the inferior colliculus, we found an up-regulation of GR mRNA 3h post-stress and continuous up-regulation of Hif1a up to 24h post-stress. In the spiral ganglion, we found no differences in gene expression between stressed and control animals. In the organ of Corti, expression of GR mRNA remained stable, whereas that of Hif1a was significantly down-regulated one week after stress. In addition, the expression of an outer hair cell marker prestin was significantly up-regulated 6h post-stress. We conclude that 24-h stress induces transient hypersensitivity of the auditory system and modulates gene expression in a tissue-specific manner. Stress-induced auditory hypersensitivity could have evolutionary consequence by giving animals an advantage of hearing better under stress conditions. [Copyright &y& Elsevier]

Abstract: Contralateral acoustic stimulation is known to activate the medial olivocochlear system which is capable of modulating the amplification process in the outer hair cells of the inner ear. We investigated the influence of different levels of contralateral broadband noise on distortion product otoacoustic emissions in humans, with a particular focus on the quadratic distortion product at f2–f1. The primary stimulus frequency ratio was optimized to yield maximum f2–f1 level. While the cubic distortion product at 2f1–f2 was not significantly affected during contralateral noise stimulation, the level of f2–f1 was reduced by up to 4.8dB on average (maximum: 10.1dB), with significant suppression occurring for noise levels as low as 40dB SPL. In addition, a significant phase lead was observed. Quadratic distortions are minimal at a symmetrical position of the transfer function of the cochlear amplifier. The observed sensitivity of f2–f1 to contralateral noise stimulation could hence be resulting from a shift of the operating state and/or a change in the gain of the cochlear amplification due to contralateral induced efferent modulation of the outer hair cell properties. [Copyright &y& Elsevier]

Abstract: Distortion-product otoacoustic emissions (DPOAEs) were measured in a New World primate, the common marmoset (Callithrix jacchus). We determined the optimal primary-tone frequency ratio (f 2/f 1) to generate DPOAEs of maximal amplitude between 3 and 24kHz. The optimal f 2/f 1, determined by varying f 2/f 1 from 1.02 to 1.40 using equilevel primary tones, decreased with increasing f 2 frequency between 3 and 17kHz, and increased at 24kHz. The optimal f 2/f 1 ratio increased with increasing primary-tone levels from 50 to 74dB SPL. When all stimulus parameters were considered, the mean optimal f 2/f 1 was 1.224–1.226. Additionally, we determined the effect of reducing L 2 below L 1. Decreasing L 2 below L 1 by 0, 5, and 10dB (f 2/f 1 =1.21) minimally affected DPOAE strength. DPOAE levels were stronger in females than males and stronger in the right ear than the left, just as in humans. This study is the first to measure OAEs in the marmoset, and the results indicate that the effect of varying the frequency ratio and primary-tone level difference on marmoset DPOAEs is similar to the reported effects in humans and Old World primates. [Copyright &y& Elsevier]

Abstract: The Mongolian gerbil (Meriones unguiculatus) is one of the animal models in auditory research that has been used in several studies on age-related hearing loss. The standard laboratory strain is domesticated as it was bred in captivity for more than 70 years. We compared properties of distortion product otoacoustic emissions (DPOAEs) in domesticated gerbils with wild-type gerbils from F6–F7 generations of a strain originating from animals trapped in Central Asia in 1995. Up to an age of 9months, DPOAE thresholds were comparable between both strains and were below 10dB SPL for f2 frequencies between 4 and 44kHz. In older domesticated animals, the thresholds were increased by up to 12dB. Significant increases were found at stimulus frequencies of 2kHz, 12–20kHz, and 56–60kHz. The best frequency ratio f2/f1 to evoke maximum DPOAE amplitude was larger in domesticated animals at the age of 9 months or older. While these data show that there is a deterioration of cochlear sensitivity due to domestication, the magnitude of the described changes is small. Thus, the general suitability of domesticated gerbils for auditory research seems not to be affected. [Copyright &y& Elsevier]

Abstract: Infrasound (i.e., <20Hz for humans; <100Hz for chinchillas) is not audible, but exposure to high-levels of infrasound will produce large movements of cochlear fluids. We speculated that high-level infrasound might bias the basilar membrane and perhaps be able to minimize noise-induced hearing loss. Chinchillas were simultaneously exposed to a 30Hz tone at 100dB SPL and a 4kHz OBN at either 108dB SPL for 1.75h or 86dB SPL for 24h. For each animal, the tympanic membrane (TM) in one ear was perforated (∼1mm2) prior to exposure to attenuate infrasound transmission to that cochlea by about 50dB SPL. Controls included animals that were exposed to the infrasound only or the 4kHz OBN only. ABR threshold shifts (TSs) and DPOAE level shifts (LSs) were determined pre- and post-TM-perforation and immediately post-exposure, just before cochlear fixation. The cochleae were dehydrated, embedded in plastic, and dissected into flat preparations of the organ of Corti (OC). Each dissected segment was evaluated for losses of inner hair cells (IHCs) and outer hair cells (OHCs). For each chinchilla, the magnitude and pattern of functional and hair cell losses were compared between their right and left cochleae. The TM perforation produced no ABR TS across frequency but did produce a 10–21dB DPOAE LS from 0.6 to 2kHz. The infrasound exposure alone resulted in a 10–20dB ABR TS at and below 2kHz, no DPOAE LS and no IHC or OHC losses. Exposure to the 4kHz OBN alone at 108dB produced a 10–50dB ABR TS for 0.5–12kHz, a 10–60dB DPOAE LS for 0.6–16kHz and severe OHC loss in the middle of the first turn. When infrasound was present during exposure to the 4kHz OBN at 108dB, the functional losses and OHC losses extended much further toward the apical and basal tips of the OC than in cochleae exposed to the 4kHz OBN alone. Exposure to only the 4kHz OBN at 86dB produces a 10–40dB ABR TS for 3–12kHz and 10–30dB DPOAE LS for 3–8kHz but little or no OHC loss in the middle of the first turn. No differences were found in the functional and hair-cell losses from exposure to the 4kHz OBN at 86dB in the presence or absence of infrasound. We hypothesize that exposure to infrasound and an intense 4kHz OBN increases cochlear damage because the large fluid movements from infrasound cause more intermixing of cochlear fluids through the damaged reticular lamina. Simultaneous infrasound and a moderate 4kHz OBN did not increase cochlear damage because the reticular lamina rarely breaks down during this moderate level exposure. [Copyright &y& Elsevier]

Abstract: The influence of the sympathetic efferent fibers on cochlear susceptibility to noise-induced hearing loss is still an open question. In the current study, we explore the effects of unilateral and bilateral Superior Cervical Ganglion (SCG) ablation in the chinchilla on hearing loss from noise exposure, as measured with inferior colliculus (IC) evoked potentials, distortion product otoacoustic emissions (DPOAE), and outer hair cell (OHC) loss. The SCG was isolated at the level of the bifurcation of the carotid artery and removed unilaterally in 15 chinchillas. Another eight chinchillas underwent bilateral ablation. Twelve animals were employed as sham controls. Noise exposure was a 4kHz octave band noise for 1h at 110dB SPL. Results showed improved recovery of DPOAE amplitudes after noise exposure in ears that underwent SCGectomy, as well as lower evoked potential threshold shifts relative to sham controls. Effects of SCGectomy on OHC loss were small. Results of the study suggest that sympathetic fibers do exert some influence on susceptibility to noise, but the influence may not be a major one. [Copyright &y& Elsevier]

Abstract: The adaptive properties of distortion product otoacoustic emissions (DPOAEs) at 2f 1 − f 2 were investigated in 12 ears of normally hearing adults aged 18–30 years using long-lasting 1-s primary-tone on-times. In this manner, DPOAE adaptation at a single f 2 of 1.55kHz (f 2/f 1 =1.21) was evaluated as a function of the levels of the primary tones in a matrix of L 1,L 2 settings, which varied from 45 to 80dB SPL, in 5-dB steps. DPOAEs were elicited under both monaural and binaural stimulus-presentation conditions. Adaptation was defined as the difference in DPOAE levels between the initial 92-ms baseline measure using a standard protocol and one obtained during the final 92ms of the prolonged 1-s primary-tones. These differences were averaged across subjects to create contour plots of mean adaptation in the L 1,L 2 space. The 2f 1 − f 2 DPOAE revealed consistent regions of suppression (⩽−0.5dB difference) or enhancement (⩾+0.5dB difference) with respect to baseline measures within the L 1,L 2 matrix for both acoustic-stimulation conditions. Specifically, 2f 1 − f 2 DPOAE suppressions of 1–2dB occurred for both monaural and binaural presentations, typically at level combinations in which L 1 > L 2. In contrast, larger 2f 1 − f 2 DPOAE enhancements of 3–4dB occurred for only the binaural condition, at primary-tone level combinations where L 1 < L 2. Although adaptation activity was also evaluated for the DPOAEs at f 2 − f 1, 2f 2 − f 1, and 3f 1 −2f 2, these emissions were either immeasurable (e.g., f 2 − f 1) or only present in a subset of subjects over a narrow range of primary-tone frequencies and levels that did not support a systematic analysis. In summary, the 2f 1 − f 2 results suggest that a potentially important area for adaptation measures exists in the L 1,L 2 space, when L 1 is lower than L 2. This combination of primary-tone levels can lead to large DPOAE adaptation effects that may be related to a notch in the DPOAE response/growth or input/output (I/O) function. [Copyright &y& Elsevier]

Abstract: Inbred C57BL/6J mice carry two copies of an age-related hearing loss gene (Ahl). It has been shown that these mice begin losing high-frequency hearing at two months. Several functional studies have reported that the Ahl gene renders mice more susceptible to noise-induced hearing loss (NIHL) than strains which do not carry this gene [e.g., Hear. Res. 93 (1996) 181; Hear. Res. 155 (2001) 82; J. Assoc. Res. Otolaryngol. 2 (2001) 233]. Johnson et al. [Hear. Res. 114 (1997) 83] developed a congenic B6.CAST-+ Ahl mouse which carries the wild-type allele from Mus musculus castaneus at the Ahl locus. Five each of young C57BL/6J males and females, and B6.CAST-+ Ahl males were exposed to a 4-kHz octave band of noise at 108 dB SPL for 4h. Non-noise-exposed mice of the same strains and age served as controls. The noise-exposed mice were functionally tested for ABR thresholds and DPOAE levels pre-exposure and three times post-exposure: 0 days to determine the magnitude of temporary threshold shift (TTS); 6 days to determine rate of recovery; and 20 days to determine the magnitude of permanent threshold shift (PTS). At 20 days post-exposure, the animals underwent cardiac perfusion to fix their cochleae. The isolated cochleae were embedded in plastic and dissected into flat preparations. By phase-contrast microscopy, each cochlea was evaluated from apex to base to quantify the losses of hair cells, nerve fibers and stria vascularis and to localize stereocilia damage. Functional data from each mouse were aligned with the cytocochleogram using the frequency–place map of Ou et al. [Hear. Res. 145 (2000) 111; Hear. Res. 145 (2000) 123]. Sizable variation in the magnitude of TTS, PTS and hair-cell loss was found among mice of the same genetic strain. The congenic B6.CAST-+ Ahl male mice had significantly less TTS immediately post-exposure than C57BL/6J males or females but not less PTS or hair-cell losses at 20 days post-exposure. These results indicate that, at one month of age, mice carrying two copies of the Ahl gene have an increased susceptibility to TTS from a low-frequency noise before they have any indication of age-related hearing or hair-cell loss. However, this appeared not to be the case for PTS. The Ahl gene appears to play a role in susceptibility to NIHL but, other genes as well as systemic and local factors must also be involved. [Copyright &y& Elsevier]

Abstract: For the causal evaluation of occupational hearing damage it is important to identify definitely the noise source. Here we tested, whether recordings of distortion product otoacoustic emissions (DPOAEs) in awake guinea pigs can distinguish the effects of different industrial noises. Six groups of 12 animals each were investigated before and over four months after a single 2 h exposure to specific, played-back industrial noise as well as before and for 2 months after impulse noise exposure. We compared broadband noise (buzz saw, bottle washing machine), low frequency noise (drawing press), and mid-frequency noise (bottle filling machine). All animals had stable DPOAE levels before noise exposure. Frequency specific decreases in DPOAEs were found after exposure to the different noises. Broadband noise diminished mostly all frequencies tested, whereas low- or mid-frequency noise had a greater effect on DPOAE evoked by middle and higher frequencies, respectively. DPOAE evoked by middle and higher frequencies were obliterated after impulse noise. Morphological analysis of the cochleae confirmed these alterations. OHC loss was found in the middle turns of the cochleae corresponding to the diminution of DPOAE. We conclude that different kinds of industrial noise tend to produce typical changes in DPOAE levels. [Copyright &y& Elsevier]

Abstract: Rapid efferent adaptation of the distortion product otoacoustic emission (DPOAE) predicts susceptibility to noise-induced damage, and is linked to the concentration of the efferent receptor (α9). Maximum adaptation occurs at intense primary levels, rapidly switching from positive to negative orientation in a very narrow (2 dB) range of F1 and F2 levels. Aminoglycosides are commonly used antibiotics, with the undesirable side-effect of ototoxicity. Susceptibility to hair cell damage from the aminoglycoside gentamicin can be quite variable, even within a single strain and species of animal. Since one of gentamicin’s first sites of action in the outer hair cell (OHC) is at the efferent receptor, it is possible that efferent activity could be a predictor of susceptibility to gentamicin induced damage. Significant sex-related differences were found in two strains of guinea pigs when treated with gentamicin. Female guinea pigs were more susceptible both to systemic effects and to specific ototoxic effects. Efferent-mediated DPOAE adaptation served as a predictor of sensitivity to aminoglycoside damage, predicting both number of days before onset of deafness in male animals, and predicting final threshold shifts from gentamicin doses which produced variable results. [Copyright &y& Elsevier]

Abstract: Objective:: Tinnitus is one of the most common and distressing otological symptoms. Although numerous therapeutic modalities have been tried, there is no consensus regarding effective therapeutic agents up to now. The effects of lidocaine on tinnitus have been reported in literature using either subjective or audiologic tests. Nevertheless, the otoacoustic emissions (OAEs) have not been utilized to demonstrate lidocaine’s effect on the cochlea in the English literature. The aim of this study was to evaluate the effect of lidocaine on tinnitus by considering the alterations with tinnitus, it induces on OAEs and subjective symptoms. Methods:: This study was performed in 30 patients with tinnitus. Twenty-eight of the patients had normal hearing and two of them evidenced mild sensorineural hearing loss. To determine the severity of tinnitus, the patients were required to fill out a tinnitus scoring scale before lidocaine infusion on the same day. Then, lidocaine was administered intravenously to each patient at a dose of 1.5 mg/kg body weight over a period of 30 min. Spontaneous otoacoustic emissions (SOAEs) and distortion product otoacoustic emissions (DPOAEs) were measured three times; namely before lidocaine injection, at 25 min after injection and on the next day. The severity of tinnitus was scored again 1 d, 1 wk and 1 mo after lidocaine administration. Results:: Immediately after infusion, four patients (13.3%) declared total suppression of tinnitus, whereas three patients (10%) reported only partial relief in tinnitus subjectively. The patients, who had a subjective improved response (group 1) were compared with the patients, who had no response (group 2). Statistically significant changes (p<0.05) in DPOAE response/growth or input/output (I/O) functions were observed at 1, 2, 3, 4 and 6 kHz frequencies in lidocaine responders and at 1, 2, 3, 4 and 5 kHz frequencies in no responders at different primary stimulus levels. Statistically significant changes (p<0.05) were seen at 2 kHz for 53 dB and at 3 kHz for 62 dB SPL primaries in both groups. When the significant results of these two groups were compared with each other, differences were found insignificant. Conclusion:: Systematic OAE measurements revealed that no changes occurred in SOAE and DPOAE levels in that alterations disappeared the next day. Subjective relief from tinnitus was stated in some of the patients and lasted for 4 wk at longest. [Copyright &y& Elsevier]

In cases of sudden, reversible hearing loss where perilymphatic fistulas are thought to be the cause, a multitude of causes have been postulated. These include perilymphatic pressure changes, Simmons’ double-break theory, perilymphatic hemorrhage, pneumolabyrinth, and others. This study was proposed to explore the role pneumolabyrinth may have in this pathology. Guinea pigs were fitted with cochlear perfusion pumps pumping artificial perilymph into the left scala tympani. One group of animals received a bubble (∼1.5–2 μl) introduced into the scala tympani while the other group of animals received continuous infusion of artificial perilymph. The animals’ cochlear function was monitored using distortion product otoacoustic emissions (DPOAEs) while the animals’ behavior was assessed to evaluate for vestibular dysfunction. While unaffected by pump surgery, animals that received air into the scala tympani had their DPOAEs eliminated by day 2 after pump placement. On day 6, positional changes in the DPOAEs were observed where the left lateral decubitus position showed a sharp demarcation at 4 kHz, where lower DPOAE frequencies were abolished and higher ones minimally affected, with DPOAEs normal in the prone position. By days 8 and 20, DPOAEs recovered to normal amplitudes. Vestibular dysfunction was never detected in any animal that received a pneumolabyrinth. All control animals receiving a continuous perilymph infusion exhibited no loss of cochlear function throughout the testing period. The reversible nature of pneumolabyrinth induced hearing loss and the pneumolabyrinth’s sole presence (without other possible causes of hearing loss, such as pressure differentials or round window membrane perforations) are powerful indicators of the role of air in the pathology of perilymphatic fistulas. In addition, the fluctuation of the hearing loss with positional changes supports the use of positional audiometry when evaluating perilymphatic fistulas. [Copyright &y& Elsevier]

• Auditory sensitivity was measured before/after blasts in CBA/CaJ mice. • Sensitivity measured by behavioral and physiological tests decreased. • Thresholds, but not threshold shifts, were different across methods. • Longitudinal changes to hearing after a blast reflect damage to auditory periphery. Blast trauma is a common acoustic/physical insult occurring in modern warfare. Twenty percent of active duty military come into close proximity to explosions and experience mild to severe sensory deficits. The prevalence of such injuries is high but correlating auditory sensitivity changes with the initial insult is difficult because injury and evaluations are often separated by long time periods. Here, auditory sensitivity was measured before and after a traumatic blast in adult CBA/CaJ mice using auditory brainstem responses, distortion production otoacoustic emissions, and behavioral detection of pure tones. These measurements included baseline auditory sensitivity prior to injury in all mice, and again at 3, 30, and 90 days after the blast in the two physiological groups, and daily for up to 90 days in the behavioral group. Mice in all groups experienced an initial deterioration in auditory sensitivity, though physiological measurements showed evidence of recovery that behavioral measurements did not. Amplitudes and latencies of ABR waves may reflect additional changes beyond the peripheral damage shown by the threshold changes and should be explored further. The present work addresses a major gap in the current acoustic trauma literature both in terms of comparing physiological and behavioral methods, as well as measuring the time course of recovery. [ABSTRACT FROM AUTHOR]