Temporary Threshold Shift Research Articles

Nicotinamide riboside protects noise-induced hearing loss by recovering the hair cell ribbon synapses

ObjectiveNicotinamide riboside (NR) has been proved to protect the hearing. To achieve animal models of temporary threshold shift (TTS) and permanent threshold shift (PTS) respectively, evaluate the dynamic change of ribbon synapse before and after NR administration. MethodsMice were divided into control group, noise exposure (NE) group and NR group. The noise was exposed to NE and NR group, and NR was injected before noise exposure. Auditory brainstem response (ABR), ribbon synapse count and cochlear morphology were tested, as well as the concentration of hydrogen peroxide (H2O2) and ATP. ResultsRibbon synapse count decrease with the intensity of noise exposure, and the cochlear morphology remains stable during TTS and was damaged during PTS. NR promotes the oxidation resistance to protect the synapse and the inner ear morphology. ConclusionOur findings suggest that TTS mice are more vulnerable to noise, and NR can promote the recovery of the synapse count to protect the animals’ hearing.

Noise-induced hearing loss in zebrafish: investigating structural and functional inner ear damage and recovery

Exposure to continuous moderate noise levels is known to impair the auditory system leading to Noise-Induced Hearing Loss (NIHL) in animals including humans. The mechanism underlying noise-dependent auditory Temporary Threshold Shifts (TTS) is not fully understood. In fact, only limited information is available on vertebrates such as fishes, which share homologous inner ear structures to mammals and have the ability to regenerate hair cells. The zebrafish Danio rerio is a well-established model in hearing research providing an unmatched opportunity to investigate the molecular and physiological mechanisms of NIHL at the sensory receptor level. Here we investigated for the first time the effects of noise exposure on TTS and functional recovery in zebrafish, as well as the associated morphological damage and regeneration of the inner ear saccular hair cells.Adult specimens were exposed for 24h to white noise at various amplitudes (130, 140 and 150 dB re. 1 μPa) and their auditory sensitivity was subsequently measured with the Auditory Evoked Potential (AEP) recording technique. Sensory recovery was tested at different times post-treatment (after 3, 7 and 14 days) and compared to individuals kept under quiet lab conditions. Results revealed noise level-dependent TTS up to 33 dB and increase in response latency. Recovery of hearing function occurred within 7 days for fish exposed to 130 and 140 dB noise levels, while fish subject to 150 dB only returned to baseline thresholds after 14 days. Hearing impairment was accompanied by significant loss of hair cells only at the highest noise treatment. Full regeneration of the sensory tissue (number of hair cell receptors) occurred within 7 days, which was prior to functional recovery.We provide first baseline data of NIHL in zebrafish and validate this species as an effective vertebrate model to investigate the impact of noise exposure on the structure and function of the adult inner ear and its recovery process.

Temporary Hearing Threshold Shift in Harbor Porpoises (Phocoena phocoena) Due to One-Sixth-Octave Noise Bands at 63 kHz

Temporary Hearing Threshold Shift in Harbor Porpoises (Phocoena phocoena) Due to One-Sixth-Octave Noise Bands at 63 kHz

Temporary hearing threshold shift in harbor seals (Phoca vitulina) due to a one-sixth-octave noise band centered at 32 kHz.

Two female harbor seals were exposed for 60 min to a continuous one-sixth-octave noise band centered at 32 kHz at sound pressure levels of 92 to 152 dB re 1 μPa, resulting in sound exposure levels (SELs) of 128 to 188 dB re 1 μPa2s. This was part of a larger project determining frequency-dependent susceptibility to temporary threshold shift (TTS) in harbor seals over their entire hearing range. After exposure, TTSs were quantified at 32, 45, and 63 kHz with a psychoacoustic technique. At 32 kHz, only small TTSs (up to 5.9 dB) were measured 1-4 min (TTS1-4) after exposure, and recovery was within 1 h. The higher the SEL, the higher the TTS induced at 45 kHz. Below ∼176 dB re 1 μPa2s, the maximum TTS1-4 was at 32 kHz; above ∼176 dB re 1 μPa2s, the maximum TTS1-4 (up to 33.8 dB) was at 45 kHz. During one particular session, a seal was inadvertently exposed to an SEL of ∼191 dB re 1 μPa2s and at 45 kHz, her TTS1-4 was >45 dB; her hearing recovered over 4 days. Harbor seals appear to be equally susceptible to TTS caused by sounds in the 2.5-32 kHz range.

Temporary hearing threshold shift in harbor seals (Phoca vitulina) due to a one-sixth-octave noise band centered at 40 kHz.

As part of a series of studies to determine frequency-dependent susceptibility to temporary hearing threshold shifts (TTS), two female harbor seals (F01 and F02) were exposed for 60 min to a one-sixth-octave noise band centered at 40 kHz at mean sound pressure levels ranging from 126 to 153 dB re 1 μPa [mean received sound exposure level (SEL) range: 162-189 dB re 1 μPa2s]. TTSs were quantified at 40, 50, and 63 kHz within 1-4 min of the exposure for F02 and within 12-16 min of the exposure for F01. In F02, significant TTS1-4 (1-4 min post exposure) occurred at 40 kHz with SELs of ≥183 dB re 1 μPa2s and at 50 kHz with SELs of ≥174 dB re 1 μPa2s. At 63 kHz, TTS1-4 occurred with SELs ≥186 dB re 1 μPa2s. In F01, significant TTS12-16 (12-16 min post exposure) occurred only at 50 kHz with SELs of ≥177 dB re 1 μPa2s. The highest TTSs (27.5 dB in F02, 29.8 dB in F01) occurred at 50 kHz, one-third of an octave above the fatiguing sound's center frequency (SEL = 189 dB re 1 μPa2s); recovery took 2 days in F02 and 4 days in F01. In most other cases, recovery was within 1 h. The seals have a similar susceptibility to TTS from 4 to 40 kHz.

Effects of multiple exposures to pile driving noise on harbor porpoise hearing during simulated flights—An evaluation tool

Exploitation of renewable energy from offshore wind farms is substantially increasing worldwide. The majority of wind turbines are bottom mounted, causing high levels of impulsive noise during construction. To prevent temporary threshold shifts (TTS) in harbor porpoise hearing, single strike sound exposure levels (SELSS) are restricted in Germany by law to a maximum of 160 dB re 1 μPa2s at a distance of 750 m from the sound source. Underwater recordings of pile driving strikes, recorded during the construction of an offshore wind farm in the German North Sea, were analyzed. Using a simulation approach, it was tested whether a TTS can still be induced under current protective regulations by multiple exposures. The evaluation tool presented here can be easily adjusted for different sound propagation, acoustic signals, or species and enables one to calculate a minimum deterrence distance. Based on this simulation approach, only the combination of SELSS regulation, previous deterrence, and soft start allow harbor porpoises to avoid a TTS from multiple exposures. However, deterrence efficiency has to be monitored.

Repeated Moderate Sound Exposure Causes Accumulated Trauma to Cochlear Ribbon Synapses in Mice

Repeated induction of a temporary threshold shift (TTS) may result in a permanent threshold shift (PTS) and is thought to be associated with early onset of age-related hearing loss (ARHL). The possibility that a PTS might be induced by administration of repeated TTS-inducing noise exposures (NEs) over a short period during early adulthood has not been formally investigated. We aimed to investigate possible cumulative acoustic overstimulation effects that permanently shift the auditory threshold. Young adult C57BL/6J mice were exposed twice to moderate white noise in an experimental design that minimized the effects of aging. The first exposure resulted in a reversible noise-induced hearing loss (NIHL) measured as recoverable alterations in auditory brainstem response (ABR) thresholds, waveform amplitudes, and numbers of ribbon synapses. The second NE with the same parameters caused persistent threshold shifts, wave I amplitude reductions, wave IV/I ratio enhancements, and synaptic losses, even though recovery time sufficient for a TTS had been provided. The pattern of PTS resembled NIHL since the observed impairments tonotopically followed the power spectrum of the noise insult, rather than ARHL, which distributes at higher frequencies. No significant changes were observed in the control group as the mice aged. To conclude, our results demonstrate a cumulative effect of repetitive TTS-inducing NE on hearing function and synaptic plasticity that does not cause premature ARHL, thereby providing insight into the pathophysiological mechanisms underlying NIHL and ARHL.

The Development of a Tympanic Membrane Model and Probabilistic Dose-Response Risk Assessment of Rupture Because of Blast.

There is no dose-response model available for the assessment of the risk of tympanic membrane rupture (TMR), commonly known as eardrum rupture, from exposures to blast from nonlethal flashbangs, which can occur concurrently with temporary threshold shift. Therefore, the objective of this work was to develop a fast-running, lumped parameter model of the tympanic membrane (TM) with probabilistic dose-dependent prediction of injury risk. The lumped parameter model was first benchmarked with a finite element model of the middle ear. To develop the dose-response curves, TMR data from a historic cadaver study were utilized. From these data, the binary probability response was constructed and logistic regression was applied to generate the respective dose-response curves at moderate and severe eardrum rupture severity. Hosmer-Lemeshow statistical and receiver operation characteristic analyses showed that maximum stored TM energy was the overall best dose metric or injury correlate when compared with total work and peak TM pressure. Dose-response curves are needed for probabilistic risk assessments of unintended effects like TMR. For increased functionality, the lumped parameter model was packaged as a software library that predicts eardrum rupture for a given blast loading condition.

Social Noise Exposure in a Sample of Slovak University Students.

Purpose: Social noise exposure is currently an emerging problem in adolescents and young adults. Various leisure time activities may be responsible for hearing impairment (temporary or permanent hearing threshold shift or hearing loss). The study aimed to quantify environmental noise from various sources—voluntary (social) noise (personal music players (PMPs), high-intensity noise exposure events), and road traffic noise and to detect hearing disorders in relation to individual listening to PMPs in the sample of young adults living and studying in Bratislava, the capital city of Slovakia. Methods: The study included 1003 university students (306 men and 697 women, average age 23.1 ± 2) living in Bratislava for 4 or more years; 347 lived in the student housing facility exposed to road traffic noise (LAeq = 67.6 dB) and 656 in the control one (LAeq = 53.4 dB). Respondents completed a validated ICBEN 5-grade scale “noise annoyance questionnaire”. In the exposed group a significant source of annoyance was road traffic noise (p < 0.001), noise from entertainment facilities (p < 0.001), industrial noise (p < 0.001), and noise from neighboring flats (p = 0.003). The exposure to PMPs was objectified by the conversion of the subjective evaluation of the volume setting and duration. With the cooperation of the Ear, Nose and Throat (ENT)specialist, we arranged audiometric examinations on the pilot sample of 41 volunteers. Results: From the total sample of respondents, 79.2% reported the use of a PMP in the course of the last week, and the average time was 285 min. There was a significant difference in PMP use between the road traffic noise-exposed (85.6%) and the control group (75.8%) (p = 0.01). Among PMP users 30.7% exceeded the lower action value (LAV) for industry (LAeq,8h = 80 dB). On a pilot sample of volunteers (n = 41), audiometry testing was performed indicating a hearing threshold shift at higher frequencies in 22% of subjects. Conclusions: The results of the study on a sample of young healthy individuals showed the importance of exposure to social noise as well as to road traffic noise and the need for prevention and intervention.

Noise-induced Cochlear Synaptopathy with and Without Sensory Cell Loss

Prior work has provided extensive documentation of threshold sensitivity and sensory hair cell losses after noise exposure. It is now clear, however, that cochlear synaptic loss precedes such losses, at least at low-moderate noise doses, silencing affected neurons. To address questions of whether, and how, cochlear synaptopathy and underlying mechanisms change as noise dose is varied, we assessed cochlear physiologic and histologic consequences of a range of exposures varied in duration from 15 min to 8 h and in level from 85 to 112 dB SPL. Exposures delivered to adult CBA/CaJ mice produced acute elevations in hair cell- and neural-based response thresholds ranging from trivial (∼5 dB) to large (∼50 dB), followed by varying degrees of recovery. Males appeared more noise vulnerable for some conditions of exposure. There was little to no inner hair cell (IHC) loss, but outer hair cell (OHC) loss could be substantial at highest frequencies for highest noise doses. Synapse loss was an early manifestation of noise injury and did not scale directly with either temporary or permanent threshold shift. With increasing noise dose, synapse loss grew to ∼50%, then declined for exposures yielding permanent hair cell injury/loss. All synaptopathic, but no non-synaptopathic exposures produced persistent neural response amplitude declines; those additionally yielding permanent OHC injury/loss also produced persistent reductions in OHC-based responses and exaggerated neural amplitude declines. Findings show that widespread cochlear synaptopathy can be present with and without noise-induced sensory cell loss and that differing patterns of cellular injury influence synaptopathic outcomes.

The use of seal scarers as a protective mitigation measure can induce hearing impairment in harbour porpoises.

Acoustic deterrent devices (ADDs) are used to deter seals from aquacultures but exposure of harbour porpoises (Phocoena phocoena) occurs as a side-effect. At construction sites, by contrast, ADDs are used to deter harbour porpoises from the zone in which pile driving noise can induce temporary threshold shifts (TTSs). ADDs emit such high pressure levels that there is concern that ADDs themselves may induce a TTS. A harbour porpoise in human care was exposed to an artificial ADD signal with a peak frequency of 14 kHz. A significant TTS was found, measured by auditory evoked potentials, with an onset of 142 dB re 1 μPa2s at 20 kHz and 147 dB re 1 μPa2s at 28 kHz. The authors therefore strongly recommend to gradually increase and down regulate source levels of ADDs to the desired deterrence range. However, further research is needed to develop a reliable relationship between received levels and deterrence.

Acoustic trauma from continuous noise: Minimum exposures, issues in clinical trial design, and comments on magnetic resonance imaging exposures.

Acoustic trauma (AT) is permanent hearing loss after a single noise exposure. A few human cases resulting from continuous, i.e., nonimpulsive noise, have been reported as reviewed by Ward [(1991). "Hearing loss from noise and music," presented at Audio Engineering Society, New York, October 4-8]. This paper updates that review by examining 11 cases in nine reports, from 1950 to 2006, with the intention of determining minimum exposures that may cause AT, including the potential risk of exposure to noise from magnetic resonance imaging machines. Diffuse-field related levels above 120 dBA for 10 s or more, or above 130 dBA for 2-3 s (values well above OSHA's unprotected exposure limits), can lead to AT. These cases appear to represent a susceptible fraction of the population, because much more intense exposures (e.g., 130 dBA for 32 min) have been tolerated by groups of volunteers who suffered only temporary threshold shifts. AT from continuous noise is unlikely to occur in OSHA-compliant hearing conservation programs, and probably rare enough in the general civilian population that clinical trials of drugs aimed at treating it are unlikely to be practical. AT from impulse noise, such as gunfire, which is specifically not the topic of the current work, is more amenable to clinical trials, especially in military settings.

Temporary hearing threshold shift in harbor seals (Phoca vitulina) due to a one-sixth-octave noise band centered at 16 kHz.

Temporary hearing threshold shifts (TTSs) were investigated in two adult female harbor seals after exposure for 60 min to a continuous one-sixth-octave noise band centered at 16 kHz (the fatiguing sound) at sound pressure levels of 128-149 dB re 1 μPa, resulting in sound exposure levels (SELs) of 164-185 dB re 1 μPa2s. TTSs were quantified at the center frequency of the fatiguing sound (16 kHz) and at half an octave above that frequency (22.4 kHz) by means of a psychoacoustic hearing test method. Susceptibility to TTS was similar in both animals when measured 8-12 and 12-16 min after cessation of the fatiguing sound. TTS increased with increasing SEL at both frequencies, but above an SEL of 174 dB re 1 μPa2s, TTS was greater at 22.4 kHz than at 16 kHz for the same SELs. Recovery was rapid: the greatest TTS, measured at 22.4 kHz 1-4 min after cessation of the sound, was 17 dB, but dropped to 3 dB in 1 h, and hearing recovered fully within 2 h. The affected hearing frequency should be considered when estimating ecological impacts of anthropogenic sound on seals. Between 2.5 and 16 kHz the species appears equally susceptible to TTS.

The chinchilla animal model for hearing science and noise-induced hearing loss.

The chinchilla animal model for noise-induced hearing loss has an extensive history spanning more than 50 years. Many behavioral, anatomical, and physiological characteristics of the chinchilla make it a valuable animal model for hearing science. These include similarities with human hearing frequency and intensity sensitivity, the ability to be trained behaviorally with acoustic stimuli relevant to human hearing, a docile nature that allows many physiological measures to be made in an awake state, physiological robustness that allows for data to be collected from all levels of the auditory system, and the ability to model various types of conductive and sensorineural hearing losses that mimic pathologies observed in humans. Given these attributes, chinchillas have been used repeatedly to study anatomical, physiological, and behavioral effects of continuous and impulse noise exposures that produce either temporary or permanent threshold shifts. Based on the mechanistic insights from noise-exposure studies, chinchillas have also been used in pre-clinical drug studies for the prevention and rescue of noise-induced hearing loss. This review paper highlights the role of the chinchilla model in hearing science, its important contributions, and its advantages and limitations.

The rat as a model for studying noise injury and otoprotection.

A major challenge for those studying noise-induced injury pre-clinically is the selection of an animal model. Noise injury models are particularly relevant in an age when people are constantly bombarded by loud noise due to occupation and/or recreation. The rat has been widely used for noise-related morphological, physiological, biochemical, and molecular assessment. Noise exposure resulting in a temporary (TTS) or permanent threshold shift (PTS) yields trauma in peripheral and central auditory related pathways. While the precise nature of noise-related injuries continues to be delineated, both PTS and TTS (with or without hidden hearing loss) result in homeostatic changes implicated in conditions such as tinnitus and hyperacusis. Compared to mice, rats generally tolerate exposure to loud sounds reasonably well, often without exhibiting other physical non-inner ear related symptoms such as death, loss of consciousness, or seizures [Skradski, Clark, Jiang, White, Fu, and Ptacek (2001). Neuron 31, 537-544; Faingold (2002). Hear. Res. 168, 223-237; Firstova, Abaimov, Surina, Poletaeva, Fedotova, and Kovalev (2012). Bull Exp. Biol. Med. 154, 196-198; De Sarro, Russo, Citraro, and Meldrum (2017). Epilepsy Behav. 71, 165-173]. This ability of the rat to thrive following noise exposure permits study of long-term effects. Like the mouse, the rat also offers a well-characterized genome allowing genetic manipulations (i.e., knock-out, viral-based gene expression modulation, and optogenetics). Rat models of noise-related injury also provide valuable information for understanding mechanistic changes to identify therapeutic targets for treatment. This article provides a framework for selection of the rat as a model for noise injury studies.

The temporary hearing thresholds shifts in fitness instructors

Noise in the entertainment industry often reaches high sound pressure levels. The aim of this study was to analyze the temporary threshold shifts (TTSs) of hearing among fitness instructors. The study comprised a total of 30 fitness instructors working in fitness clubs. The noise dosimeters were used to determine individual noise exposure during exercises conducted by the instructors. To assess the TTS values, the pure tone audiometry tests were performed before and just after the exercises. The observed TTSs were compared with the predicted TTSs according to the computational model developed by Melnick (1991). Typical fitness exercises lasted from 1 to 2 h and A-weighted equivalent-continuous sound pressure level ranged from 75 to 96 dB. Temporary threshold shifts after the sound exposure were statistically significant. The actual values of TTS fitted well with the values predicted with the TTS computational model. The results show that the computational TTS model gives results consistent with the TTS observed in the study group. Fitness instructors constitute a population at an increased risk of the hearing loss. Raising awareness of this fact and implementing hearing protection programs in this group of workers are urgently needed.

Long-term evidence of noise-induced permanent threshold shift in a harbor seal (Phoca vitulina).

In psychophysical studies of noise-induced hearing loss with marine mammals, exposure conditions are often titrated from levels of no effect to those that induce significant but recoverable loss of auditory sensitivity [temporary threshold shift (TTS)]. To examine TTS from mid-frequency noise, a harbor seal was exposed to a 4.1-kHz underwater tone that was incrementally increased in sound pressure level (SPL) and duration. The seal's hearing was evaluated at the exposure frequency and one-half octave higher (5.8 kHz) to identify the noise parameters associated with TTS onset. No reliable TTS was measured with increasing sound exposure level until the second exposure to a 60-s fatiguing tone of 181 dB re 1 μPa SPL (sound exposure level 199 dB re 1 μPa2s), after which an unexpectedly large threshold shift (>47 dB) was observed. While hearing at 4.1 kHz recovered within 48 h, there was a permanent threshold shift of at least 8 dB at 5.8 kHz. This hearing loss was evident for more than ten years. Furthermore, a residual threshold shift of 11 dB was detected one octave above the tonal exposure, at 8.2 kHz. This hearing loss persisted for more than two years prior to full recovery.

Temporary Hearing Threshold Shift in Harbor Porpoises (Phocoena phocoena) Due to One-Sixth-Octave Noise Band at 32 kHz

Temporary hearing threshold shift (TTS) caused by fatiguing sounds in the 1.5 to 16 kHz range has been documented in harbor porpoises (Phocoena phocoena). To assess impacts of anthropogenic noise on porpoise hearing, TTS needs to be investigated for other frequencies, as susceptibility appears to depend on the frequency of the fatiguing sound. TTS was quantified after two porpoises (Porpoises F05 and M06) were exposed for 1 hour to a continuous one-sixth-octave noise band centered at 32 kHz, at average received sound pressure levels of 118 to 148 dB re 1 µPa, and at a sound exposure level (SEL) range of 154 to 184 dB re 1 µPa2s. Hearing thresholds for 32, 44.8, and 63 kHz tonal signals were determined before and after exposure to quantify initial TTS and recovery. Porpoise M06’s hearing was tested 1 to 4 min after exposure. At 32 kHz, the lowest SEL that resulted in significant TTS1-4 (3.4 dB) was 166 dB re 1 µPa2s. At 44.8 kHz, the lowest SEL that resulted in significant TTS1-4 (5.2 dB) was 178 dB re 1 µPa2s. The highest TTS1-4 (18.3 dB) occurred at 44.8 kHz after exposure to 184 dB SEL. Porpoise F05’s hearing was tested 12 to 16 min after exposure. At 32 kHz, the lowest SEL that resulted in significant TTS12-16 (3.5 dB) was 184 dB re 1 µPa2s. At 44.8 kHz, the lowest SEL that resulted in significant TTS12-16 (1.2 dB) was 178 dB re 1 µPa2s. The highest TTS12-16 (8.2 dB) occurred in Porpoise F05 at 44.8 kHz after exposure to 184 dB SEL. At 63 kHz, no TTS could be elicited in either animal. Considering that Porpoise F05 had more time than Porpoise M06 for recovery, the susceptibility of the two porpoises to TTS after exposure to sounds of 32 kHz was similar. In the range investigated so far (1.5 to 32 kHz), susceptibility to TTS appears to increase with increasing frequency below ~6.5 kHz, and to decrease with increasing frequency above ~6.5 kHz.

Axonal sprouting in the dorsal cochlear nucleus affects gap‑prepulse inhibition following noise exposure.

One of the primary theories of the pathogenesis of tinnitus involves maladaptive auditory-somatosensory plasticity in the dorsal cochlear nucleus (DCN), which is assumed to be due to axonal sprouting. Although a disrupted balance between auditory and somatosensory inputs may occur following hearing damage and may induce tinnitus, examination of this phenomenon employed a model of hearing damage that does not account for the causal relationship between these changes and tinnitus. The present study aimed to investigate changes in auditory-somatosensory innervation and the role that axonal sprouting serves in this process by comparing results between animals with and without tinnitus. Rats were exposed to a noise-inducing temporary threshold shift and were subsequently divided into tinnitus and non-tinnitus groups based on the results of gap prepulse inhibition of the acoustic startle reflex. DCNs were collected from rats divided into three sub-groups according to the number of weeks (1, 2 or 3) following noise exposure, and the protein levels of vesicular glutamate transporter 1 (VGLUT1), which is associated with auditory input to the DCN, and VGLUT2, which is in turn primarily associated with somatosensory inputs, were assessed. In addition, factors related to axonal sprouting, including growth-associated protein 43 (GAP43), postsynaptic density protein 95, synaptophysin, α-thalassemia/mental retardation syndrome X-linked homolog (ATRX), growth differentiation factor 10 (GDF10), and leucine-rich repeat and immunoglobulin domain-containing 1, were measured by western blot analyses. Compared to the non-tinnitus group, the tinnitus group exhibited a significant decrease in VGLUT1 at 1 week and a significant increase in VGLUT2 at 3 weeks post-exposure. In addition, rats in the tinnitus group exhibited significant increases in GAP43 and GDF10 protein expression levels in their DCN at 3 weeks following noise exposure. Results from the present study provided further evidence that changes in the neural input distribution to the DCN may cause tinnitus and that axonal sprouting underlies these alterations.

Repeated temporary threshold shift and changes in cochlear and neural function

A robust temporary threshold shift (TTS) can create significant primary damage to the auditory synapse, termed cochlear synaptopathy (CS). The common model applied to examination of this pathology is a single noise exposure or extended duration exposures at relatively high noise dosages. It is unclear if a single noise exposure that does not produce physiological changes consistent with CS (such as suppressed suprathreshold responses) can create evidence consistent with the pathology induced by repeated exposures. Here, we exposed 16-week (wk) old Sprague-Dawley rats to repeated noise exposures (4 consecutive days, 8–16 kHz octave-band of noise, 97 dB SPL for 2 h) and examined measures of cochlear function (distortion product otoacoustic emissions) and auditory neural integrity (auditory brainstem response, wave 1 amplitude). Our results demonstrated a mean maximal threshold shift of 16 dB at 24 h post the initial noise exposure. Subsequent daily repeated exposures (4 consecutive days) resulted in diminished threshold shift at 24 h post repeated TTS. In addition to recovered thresholds, no sustained reduction in suprathreshold responses was observed. The findings are consistent with conditioning literature suggesting diminished TTS with repeated exposures. Repeated TTS that was not individually synaptopathic did not produce physiological evidence consistent with acute CS.