Pure Tone Exposure Research Articles

Effects of 90 dB pure tone exposure on auditory and cardio-cerebral system functions in macaque monkeys

Excessive noise exposure presents significant health risks to humans, affecting not just the auditory system but also the cardiovascular and central nervous systems. This study focused on three male macaque monkeys as subjects. 90 dB sound pressure level (SPL) pure tone exposure (frequency: 500Hz, repetition rate: 40Hz, 1 min per day, continuously exposed for 5 days) was administered. Assessments were performed before exposure, during exposure, immediately after exposure, and at 7-, 14-, and 28-days post-exposure, employing auditory brainstem response (ABR) tests, electrocardiograms (ECG), and electroencephalograms (EEG). The study found that the average threshold for the Ⅴ wave in the right ear increased by around 30 dB SPL right after exposure (P < 0.01) compared to pre-exposure. This elevation returned to normal within 7 days. The ECG results indicated that one of the macaque monkeys exhibited an RS-type QRS wave, and inverted T waves from immediately after exposure to 14 days, which normalized at 28 days. The other two monkeys showed no significant changes in their ECG parameters. Changes in EEG parameters demonstrated that main brain regions exhibited significant activation at 40Hz during noise exposure. After noise exposure, the power spectral density (PSD) in main brain regions, particularly those represented by the temporal lobe, exhibited a decreasing trend across all frequency bands, with no clear recovery over time. In summary, exposure to 90 dB SPL noise results in impaired auditory systems, aberrant brain functionality, and abnormal electrocardiographic indicators, albeit with individual variations. It has implications for establishing noise protection standards, although the precise mechanisms require further exploration by integrating pathological and behavioral indicators.

Bottlenose dolphin (Tursiops truncatus) temporary threshold shift in response to frequency-modulated and pure-tone exposures centered at 28 kHz

There is a scarcity of marine mammal temporary threshold shift (TTS) data for noise exposures representative of naval continuous active sonar (CAS). In this study, bottlenose dolphin (n = 2) TTS was measured following exposure to frequency-modulated (FM) tones with temporal characteristics representative of CAS, but frequencies shifted to the dolphins' region of best hearing sensitivity (20–40 kHz). Exposures were conducted at multiple sound pressure levels and durations ranging from 2 to 60 min. Additional exposures to 28-kHz pure tones at matched cumulative sound exposure levels examined the effect of exposure bandwidth on TTS. Hearing thresholds were measured using behavioral methods and supplemented by electrophysiological auditory brainstem response and auditory steady-state response methods. Larger TTS magnitudes were observed for the FM versus the pure-tone exposures in both dolphins. A consistent pattern of TTS was not observed using either electrophysiological method, contrary to what has been noted in some previous studies. Future testing will evaluate TTS following exposure to simulated CAS centered near 3 kHz, at the lower-frequencyend of the bottlenose dolphin’s hearing range but representative of the actual frequencies of naval CAS. [Work funded by US Navy Living Marine Resources.]

Ephrin-A3 is required for tonotopic map precision and auditory functions in the mouse auditory brainstem.

Tonotopy is a prominent feature of the vertebrate auditory system and forms the basis for sound discrimination, but the molecular mechanism that underlies its formation remains largely elusive. Ephrin/Eph signaling is known to play important roles in axon guidance during topographic mapping in other sensory systems, so we investigated its possible role in the establishment of tonotopy in the mouse cochlear nucleus. We found that ephrin-A3 molecules are differentially expressed along the tonotopic axis in the cochlear nucleus during innervation. Ephrin-A3 forward signaling is sufficient to repel auditory nerve fibers in a developmental stage-dependent manner. In mice lacking ephrin-A3, the tonotopic map is degraded and isofrequency bands of neuronal activation upon pure tone exposure become imprecise in the anteroventral cochlear nucleus. Ephrin-A3 mutant mice also exhibit a delayed second wave in auditory brainstem responses upon sound stimuli and impaired detection of sound frequency changes. Our findings establish an essential role for ephrin-A3 in forming precise tonotopy in the auditory brainstem to ensure accurate sound discrimination.

The sense of hearing in the Pacific oyster, Magallana gigas.

There is an increasing concern that anthropogenic noise could have a significant impact on the marine environment, but there is still insufficient data for most invertebrates. What do they perceive? We investigated this question in oysters Magallana gigas (Crassostrea gigas) using pure tone exposures, accelerometer fixed on the oyster shell and hydrophone in the water column. Groups of 16 oysters were exposed to quantifiable waterborne sinusoidal sounds in the range of 10 Hz to 20 kHz at various acoustic energies. The experiment was conducted in running seawater using an experimental flume equipped with suspended loudspeakers. The sensitivity of the oysters was measured by recording their valve movements by high-frequency noninvasive valvometry. The tests were 3 min tone exposures including a 70 sec fade-in period. Three endpoints were analysed: the ratio of responding individuals in the group, the resulting changes of valve opening amplitude and the response latency. At high enough acoustic energy, oysters transiently closed their valves in response to frequencies in the range of 10 to <1000 Hz, with maximum sensitivity from 10 to 200 Hz. The minimum acoustic energy required to elicit a response was 0.02 m∙s-2 at 122 dBrms re 1 μPa for frequencies ranging from 10 to 80 Hz. As a partial valve closure cannot be differentiated from a nociceptive response, it is very likely that oysters detect sounds at lower acoustic energy. The mechanism involved in sound detection and the ecological consequences are discussed.

Manipulation of BDNF Signaling Modifies the Experience-Dependent Plasticity Induced by Pure Tone Exposure during the Critical Period in the Primary Auditory Cortex

Sensory experience powerfully shapes cortical sensory representations during an early developmental “critical period” of plasticity. In the rat primary auditory cortex (A1), the experience-dependent plasticity is exemplified by significant, long-lasting distortions in frequency representation after mere exposure to repetitive frequencies during the second week of life. In the visual system, the normal unfolding of critical period plasticity is strongly dependent on the elaboration of brain-derived neurotrophic factor (BDNF), which promotes the establishment of inhibition. Here, we tested the hypothesis that BDNF signaling plays a role in the experience-dependent plasticity induced by pure tone exposure during the critical period in the primary auditory cortex. Elvax resin implants filled with either a blocking antibody against BDNF or the BDNF protein were placed on the A1 of rat pups throughout the critical period window. These pups were then exposed to 7 kHz pure tone for 7 consecutive days and their frequency representations were mapped. BDNF blockade completely prevented the shaping of cortical tuning by experience and resulted in poor overall frequency tuning in A1. By contrast, BDNF infusion on the developing A1 amplified the effect of 7 kHz tone exposure compared to control. These results indicate that BDNF signaling participates in the experience-dependent plasticity induced by pure tone exposure during the critical period in A1.

Critical period for acoustic preference in mice

Preference behaviors are often established during early life, but the underlying neural circuit mechanisms remain unknown. Adapting a unique nesting behavior assay, we confirmed a "critical period" for developing music preference in C57BL/6 mice. Early music exposure between postnatal days 15 and 24 reversed their innate bias for silent shelter, which typically could not be altered in adulthood. Instead, exposing adult mice treated acutely with valproic acid or carrying a targeted deletion of the Nogo receptor (NgR(-/-)) unmasked a strong plasticity of preference consistent with a reopening of the critical period as seen in other systems. Imaging of cFos expression revealed a prominent neuronal activation in response to the exposed music in the prelimbic and infralimbic medial prefrontal cortex only under conditions of open plasticity. Neither behavioral changes nor selective medial prefrontal cortex activation was observed in response to pure tone exposure, indicating a music-specific effect. Open-field center crossings were increased concomitant with shifts in music preference, suggesting a potential anxiolytic effect. Thus, music may offer both a unique window into the emotional state of mice and a potentially efficient assay for molecular "brakes" on critical period plasticity common to sensory and higher order brain areas.

Time and Frequency Characteristics of Temporary Threshold Shifts Caused by Pure Tone Exposures

The time-frequency characteristics of Temporary Threshold Shifts (TTS) caused by pure tones were determined using the Békésy audiometric method with narrow-band noise of short duration as the probe stimuli. Two experiments were done using exposures of 3 min at 100 dB above threshold. In the first experiment, the frequency dependent characteristics of TTS produced by a 500-Hz tone were assessed. Thresholds were determined from 0.25 to 2 kHz in 1/2-octave steps for up to 20 min after the exposure. The results showed that the maximum affected frequency was 1/2 octave above the exposure frequency. In the second experiment, the TTS recovery curve produced by a 1-kHz pure tone exposure was assessed at 1.5 kHz, at approximately 15 s intervals for the first 5 min and at regularly increasing intervals up to 45 min after the exposure. The results showed a maximum in the recovery around 2 min after the exposure. The data gathered in these experiments were used to construct a mathematical model of TTS recovery. The model describes both the 1/2-octave shift and the 2-min bounce and it can be used in the comparison of temporary changes in the auditory function, assessed at different times and frequencies.

Critical Period Window for Spectral Tuning Defined in the Primary Auditory Cortex (A1) in the Rat

Experience-dependent plasticity during development results in the emergence of highly adapted representations of the external world in the adult brain. Previous studies have convincingly shown that the primary auditory cortex (A1) of the rat possesses a postnatal period of sensory input-driven plasticity but its precise timing (onset, duration, end) has not been defined. In the present study, we examined the effects of pure-tone exposure on the auditory cortex of developing rat pups at different postnatal ages with a high temporal resolution. We found that pure-tone exposure resulted in profound, persistent alterations in sound representations in A1 only if the exposure occurred during a brief period extending from postnatal day 11 (P11) to P13. We also found that postnatal sound exposure in this epoch led to striking alterations in the cortical representation of sound intensity.

Do click-evoked otoacoustic emissions have frequency specificity?

Whether click-evoked otoacoustic emissions (CEOAEs) have frequency specificity is an issue still subject to debate. In order to resolve this issue, changes in the frequency components of the CEOAE power spectrum, together with changes in compound action potential (CAP) thresholds before and after pure-tone exposure in guinea pigs, were examined. Changes in CAP thresholds immediately before and 1 h after exposure were compared with changes in the frequency components in the CEOAE power spectrum before and 1 h after exposure. The ILO 88 was used for measurement of CEOAEs. Total echo energy in the CEOAE power spectrum was converted into frequency bands of 1000 Hz. Shifts in filtered echo power (FEP) levels correlated maximally with those in CAP thresholds at 0.5 kHz above the same frequency. Stepwise regression indicated that only one step could be entered in a linear regression model using the variable of CAP threshold shifts at 0.5 kHz above the same frequency for all FEP shifts except FEP4.5. The remaining variables played a negligible role, since variance no longer changed when they were included in the regression equation. From these results, it was concluded that CEOAEs display frequency specificity. Influence on CEOAEs from higher frequencies is negligible.

聴覚障害におけるグルタミン酸の役割

L-Glutamate is believed to be a neurotransmitter in the first auditory synapse between the inner hair cells and the dendrites of spiral ganglion type I cells. It is released by a variety of mechanisms, such as anoxia, acoustic trauma and some ototoxic drugs. Although excessive release of glutamate is supposed to be toxic to the surrounding neurons, the exact mechanism of action in the cochlea remains unclear. In the first experiment, we investigated the effects of glutamate on hearing by the administration of AMPA, an agonist of glutamate, to the cochlea of guinea pigs. AMPA caused a reversible increase in the threshold of the compound action potential (CAP). Secondly, we studied the glutamate excitotoxicity induced by transient cochlear anoxia by means of occlusion of the bilateral vertebral arteries in gerbils. Five minutes of occlusion caused a drastic increase in the CAP threshold, which recovered after recirculation. The threshold returned to preischemic levels on the 3rd day, but in some animals it increased again after the 5th day, suggesting delayed neuronal death. Glutamate concentration in the perilymph increased following ischemic insult. Histological studies revealed that ischemic pathological changes were severe in the dendrites of the primary afferent auditory nerve, composing the synapse with the inner hair cell. In the 3rd experiment, the effects of noise exposure on hearing were studied in mice lacking the glutamate transporter GLAST (mutant mice). Continuous 4kHz pure tone exposure of 105dB for 30 minutes caused an increase in the CAP threshold in both mutant and wild mice. However, the increase was more severe and the recovery was later in mutant than in wild mice. Glutamate concentration in the perilymph was consistently higher in the former than in the latter. These results suggested that excessive glutamate released in the cochlea as a consequence of anoxia or acoustic trauma caused damage to the surrounding neurons, especially to the dendrites of the primary afferent auditory nerve. Glutamate excitotoxicity is, therefore, thought to underlie sensory hearing loss attributed to a variety of causes.

Changes in evoked otoacoustic emissions in the guinea pig after pure-tone acoustic overstimulation.

To test if click-evoked otoacoustic emissions (CEOAEs) have frequency specificity, continuous changes in CEOAEs (especially frequency components of the CEOAE power spectrum) after pure-tone exposure in guinea pigs were examined. Pure-tone stimuli (0.5 kHz, 120 dB SPL; 2 kHz, 115 dB SPL; 4 kHz, 110 dB SPL) were given in a closed system for 3 min. After exposure, the frequency components in the CEOAE power spectrum decreased maximally at one-half octave or more above the overstimulation frequency. They partially recovered 2 h after exposure. The time course of compound action potential (CAP) thresholds after exposure was similar to that of the frequency components of the CEOAE power spectrum. It was concluded that some local damage caused by outer hair-cell dysfunction in the guinea pig cochlea can be detected by measuring shifts in frequency components in the CEOAE power spectrum.

Effects of a dopaminergic agonist in the guinea pig cochlea

This study investigates the role of dopamine, a putative lateral efferent neurotransmitter/modulator, in cochlear physiology and physiopathology. Cochlear potentials were recorded in guinea pigs after intracochlear perfusion of increasing doses (0.1–1 mM) of piribedil, an agonist of the D2/D3 receptors. A dose-dependent reduction in the amplitude of auditory nerve compound action potential (CAP) was observed, predominantly at high-intensity tone-burst stimulations, and without significant effect on CAP threshold. There was no variation of cochlear microphonic and summating potential. When 1 mM piribedil was perfused into the cochlea during continuous 130 dB SPL pure tone exposure (6 kHz, 15 min), CAP threshold shifts were significantly less than in control animals with artificial perilymph-perfused cochleas. No dendritic damage was observed, although there was evident hair cell damage. Similarly, radial dendrites were clearly protected against ischemia-induced damage when 1 mM piribedil was applied prior to a 10-min ischemia. These results suggests that dopamine modulates the activity of radial afferent fibers via D2/D3 receptors. The protective effect of piribedil during acoustic trauman or ischemia suggests that this modulation corresponds to a prevention of excitotoxicity due to dysfunction of inner hair cell neurotransmission.

Recovery of thresholds and temporal integration in adult chickens after high-level 525-Hz pure-tone exposure

Three adult, female chickens, previously trained to detect pure tones using a positive reinforcement paradigm, were exposed to pure tones at 525 Hz at 120-dB sound-pressure level for 48 h. Immediately after exposure, pure-tone thresholds were elevated between 10 and 56 dB compared to pre-exposure values. The configuration of the initial hearing loss was essentially flat between 500 and 2000 Hz, with slightly less loss at lower and higher frequencies. Over the course of 100 to 600 h, depending on subject and test frequency, thresholds returned to preexposure levels. The slopes of the threshold-duration functions measured shortly after exposure were shallower than normal, but returned to the normal slope of approximately 3 dB per doubling of duration as hearing loss resolved to less than 15 to 20 dB. The cochleas from additional chickens examined by scanning electron microscopy (SEM) and fluorescence microscopy between 0 and 1512 h post-exposure showed extensive damage to the tectorial membrane over the middle two-thirds of the cochlea, with mild to moderate hair cell loss in the region of the cochlea associated with the exposure frequency.

Recovery of auditory function and structure in the chick after two intense pure tone exposures

Groups of neonatal chicks were examined in three experimental conditions that differed in the age and number of times they were exposed to a pure tone of 0.9 kHz at 120 dB SPL for 48 h. Several animals were exposed once at 2 or 16 days of age. while others were subjected twice to the above stimulus, first at 2 days and then at 16 days. Evoked potential measures of threshold shift, obtained at 0, 12 or 26 days post-exposure, were used to determine the degree of hearing loss and recovery. The average threshold loss in the mid-range frequencies was about 57 dB at 0 days for all three conditions. This level was reduced to about 15 dB in all three groups at 12 days of recovery, while in birds exposed once at 2 days, but allowed 26 days to recover, the post-exposure thresholds returned to pre-exposure levels. Scanning electron microscopic analysis of cochlear structure was conducted in groups of similarly exposed and recovered animals. Twelve days post-exposure, the structural analysis revealed regeneration of a single honeycomb-like tectorial membrane layer in both the once and twice-exposed cochleae. However, damage to, and repair of, the tectorial membrane after the second exposure revealed the production of a second honeycomb layer in about half the animals examined. The results indicated that chicks retain the capacity to repair receptor epithelium damage and recover considerably from hearing loss after multiple exposures to intense sound.

Distortion-product emissions in rabbit: II. Prediction of chronic-noise effects by brief pure-tone exposures

In an attempt to predict the susceptibility of the cochlea to the harmful influences of excessive sound, the effects of initially exposing the same rabbits to brief pure-tones were related to the subsequent effects of octave-band noise (OBN) exposure using measures of distortion-product otoacoustic emissions (DPOAEs). The pure-tone exposure paradigm consisted of determining the rate at which a 100-dB SPL, low-frequency tone reduced the amplitude of a 1.5-kHz DPOAE, elicited by 50-dB SPL primaries. To establish the stability of the rate-reduction index, the tonal-exposure protocol was repeated on three separate occasions for each subject. Subsequently, the same rabbits were exposed chronically to a 95-dB SPL OBN, centered at 1-kHz, until DPOAE amplitudes between 1–5 kHz were diminished to noise-floor levels, i.e., by 10–30 dB, in response to 45-dB SPL primaries. The results revealed a visually apparent relation between the slope of the tonal-induced DPOAE-loss functions and the number of days required to reach the criterion decrement in emission level during chronic exposure to noise. Analysis of the frequency extent of the noise-induced changes revealed significant correlations between the previously measured rate of pure-tone induced reductions of DPOAE amplitude and the subsequent amount of decrement produced by OBN exposure. Thus, rabbits exhibiting slow rates of tonal-induced decrements in low-frequency DPOAEs were resistant to the amplitude-reducing effects of a subsequent chronic OBN exposure in that it typically took more than four days to achieve the targeted amount of DPOAE loss. In contrast, animals showing rapid rates of tonal-induced DPOAE reduction tended to require only two to four days of noise exposure to attain the requisite decrease in the amplitudes of low-frequency DPOAEs.

Distortion-product emissions in rabbit: I. Altered susceptibility to repeated pure-tone exposures

An important issue in understanding the development of noise-induced hearing loss is whether prior acoustic overstimulation alters the susceptibility of the cochlea to further damage. The present work was designed to establish a model of activity-dependent changes in the susceptibility of the cochlea to acoustic overstimulation by regularly exposing the ear to a low-frequency pure tone. As a quantitative index of cochlear function, 2ƒ 1−ƒ 2 distortion-product otoacoustic emissions (DPOAEs) were monitored systematically over time in three groups of rabbits, with each group experiencing a unique paradigm that incorporated repeated exposure to the low-frequency tone. Common to each rabbit's exposure protocol was that a given experimental session consisted of two exposure episodes, separated by a 40-min period. Experimental sessions were repeated three times, with 2- to 3-day recovery periods interposed between sessions. The rate of decrement in DPOAE amplitude over a prescribed time period was utilized as a measure of susceptibility to the acoustic trauma. The overall results indicated that ears were more susceptible to exposure 40 mins after the first exposure of a session than they were initially. A series of control experiments indicated that the robustness of the acoustic middle-ear reflex (AMR) did not change between the exposure episodes. Consequently, changes in the AMR could not account for the increased susceptibility seen following the first exposure. However, in awake rabbits with stronger AMRs, higher pure-tone exposure levels were needed to produce increased susceptibility to the second exposure. After 2–3 days of intersession recovery, susceptibility to the effects of excessive sound returned close to its original baseline level. The outcome of these studies demonstrated a reduced capacity for the ear to resist the harmful effects of exposure to a moderately intense tone, which was repeated twice over a brief 40-min period, but little change in susceptibility when identical exposures were repeated over longer intersession intervals of several days.

Some effects of tonal fatiguing on spontaneous and distortion-product otoacoustic emissions.

Auditory fatiguing can be considered a suitable test to assess some cochlear mechanisms and diseases otherwise not easily detectable. Since spontaneous otoacoustic emissions (SOAEs) originate from active sources within the cochlea they show sensitive and early vulnerability to noise, displaying informative time-courses after overstimulation in the short (0-6 s) and in the long term (1-10 min) depending on the frequency of the fatiguing stimulus. Distortion product otoacoustic emissions too, in subjects with SOAEs, show interesting modifications after pure-tone exposure, detectable either on distortion product audiograms or in the growth functions. The modifications take place within a period of 5-7 minutes and strongly depend on the frequency of the fatiguing stimulus and on the closeness between SOAE and distortion product place. The data suggest that not only the interaction place between f1 and f2 has to be considered from a biomechanical and clinical point of view, but also the specific distortion product place on the cochlear partition.

Hair cell damage after continuous and interrupted pure tone overstimulation: A scanning electron microscopic study in the guinea pig

In our earlier investigations [Fredelius et al., Hear. Res. 30, 157–167 (1987)] acoustic trauma was studied after continuous 3.85-kHz pure tone exposures of different intensities and durations. In the present investigation, the importance of the introduction of a break during longer 3.85-kHz pure tone exposures was studied. Female pigmented guinea pigs wereexposed to 108, 114, or 120 dB SPL for 6 h with or without a 1-h break after the first 3 h. Four weeks after exposure the cochleas were prepared for scanning electron microscopy and the resulting hair cell damage was evaluated according to a 4-grade damage scale. Significant differences could be demonstrated in the hair cell damage in the animals exposed to continuous acoustic overstimulation and those exposed to intermittent overstimulation. The importance of rest periods to decrease hair cell damage during long periods of acoustic overstimulation was clearly demonstrated.

Additivity of threshold losses produced by acute acoustic trauma

We have previously [Patuzzi and Rajan, Hear. Res. 60, 165–177, 1992] formulated a model to describe how the threshold elevations produced by a variety of independent, short-term cochlear manipulations add when the manipulations are combined. The manipulations were presumed to affect only the ‘active process’ in the cochlea. The present report applied this model to the effects observed after acute acoustic trauma in normal-hearing guinea pigs and in guinea pigs with idiopathic threshold losses. Successive loud pure-tone exposures were presented to the normal-hearing guinea pigs, while only a single exposure was presented to the guinea pigs with idiopathic hearing losses. Various parameters of exposure and inter-exposure delays were used to create a variety of threshold elevations, and the total hearing losses observed in the various groups were compared to the total hearing losses predicted by the model. In most cases a statistically-valid 1:1 relationship was obtained between the predicted values and the observed values. In cases where the model's predictions were found not to fit the data, this appeared to be due to inclusion of data previously defined to be outside the scope of the model. When such data were excluded, there was good agreement between the model's predictions and the observed data. The model was further tested by comparing its predictions with data obtained in studies of acute noise trauma in chinchillas and humans by other researchers. The model's predictions were found to agree with these data as well. Thus, across a number of different types and conditions of exposures, the model appears to provide a very good description of the additivity of threshold losses produced by acute acoustic trauma. The generality of and constraints on the model are discussed.

The structural and functional aspects of hair cell regeneration in the chick as a result of exposure to intense sound

This paper summarizes the structural and functional damage caused by intense sound exposure in neonatal chicks. Scanning electron microscopy has been used to follow the structural changes to the papilla and their subsequent repair. Pure-tone exposures produced a localized lesion consisting of tectorial membrane destruction, changes in surface organization of the papilla, and hair cell loss. The papilla underwent significant repair following the exposure and new hair cells could be identified on the sensory surface after 4 days of recovery. In addition, various evoked-potential methods provided an objective assessment of auditory function and demonstrated that the peripheral ear was severely impaired by overstimulation. Auditory function returned to near normal levels within 3 days postexposure. The inescapable conclusion from these observations was that hair cell regeneration had little to do with the functional recovery observed during the first 3 days. Tectorial membrane regeneration and the restoration of cochlear micromechanics were combined to form a hypothesis to account for the restoration of auditory function.