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ARTICLES Table of Contents   
Year : 2000  |  Volume : 3  |  Issue : 9  |  Page : 23-32
Noise-induced hearing loss in rats

1 Hearing Research Laboratories, University Medical Centre, Utrecht; TNO Food and Nutrition Research,Zeist, Netherlands
2 Hearing Research Laboratories, University Medical Centre, Utrecht, Netherlands
3 TNO Food and Nutrition Research,Zeist, Netherlands

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The effect of noise exposure on the auditory system is well known from animal studies. However, most of the studies concern short-term exposure conditions. The purpose of the present research was to find the dose-effect curve for hearing loss in rats following 5 days of noise exposure. Three groups of eight Wag/Rij rats were exposed to broad band noise at levels of 90, 100 and 110 dB SPL for 8 hours/day and 5 consecutive days. An additional group of eight rats served as the control group. Between three and seven weeks after the exposure, hearing was tested by electrocochleography (CAP) and distortion product otoacoustic emissions (DPOAE). Subsequently, the cochlea were morphologically examined. Only the highest two exposure levels affected hearing. The DPOAE growth curves at 4, 8 and 16 kHz and the CAP growth curves at 4, 8, 12, 16 and 24 kHz were affected after the 110 dB SPL broad band noise. After the 100 dB SPL noise, only the 12 kHz CAP growth curve was affected. At the light microscopic level, OHC damage was not detected in this study.

Keywords: rat, noise exposure, distortion product otoacoustic emissions, outer hair cells, electrocochleography, cochlea

How to cite this article:
Cappaert NL, Klis SF, Muijser H, Kulig BM, Smoorenburg GF. Noise-induced hearing loss in rats. Noise Health 2000;3:23-32

How to cite this URL:
Cappaert NL, Klis SF, Muijser H, Kulig BM, Smoorenburg GF. Noise-induced hearing loss in rats. Noise Health [serial online] 2000 [cited 2023 May 30];3:23-32. Available from: https://www.noiseandhealth.org/text.asp?2000/3/9/23/31773

  Introduction Top

Noise-induced hearing loss (NIHL) is a significant occupational health problem in industrialized countries (Alberti, 1998). NIHL has been studied extensively in both humans and animals (see: Saunders et al., 1985; Borg et al., 1995; Salvi et al., 1995 for review). A complex interaction between intensity, duration, spectral energy distribution and temporal patterns of the sound determines the amount of hearing loss, the frequencies at which hearing is affected and reversibility of the hearing loss (see: Borg et al., 1995; Salvi et al., 1995 for review). At present, at least two mechanisms have been proposed for NIHL: mechanical injuries to the receptor cells induced by excessive movement of the cochlear partition (Saunders et al., 1985) and damage due to metabolic exhaustion resulting in distortion of the homeostasis of the organ of Corti (Slepecky, 1986). Probably, these two mechanisms both contribute to NIHL.

Several studies have been performed with rats exposed to noise alone for a period longer than one day. However, these studies used different strains of rats, different exposure paradigms and different types of noise spectra (Borg, 1982a,b; Engstrom, 1984, Johnson et al., 1988; 1990; Lataye and Campo, 1997; Sullivan and Conolly, 1988). The purpose of the present study was to establish the relationship between the level of broad band noise (8 hours/day for 5 consecutive days) and the amount of functional hearing loss together with the accompanying morphological changes in the organ of Corti of the Wag/Rij rat. By means of these data, it is possible to determine a dose-effect curve to quantify the damage.

This dose-effect curve is important with regard to the issue of combined exposure to noise and ototoxic chemicals. Exposure to various chemical compounds, like aminoglycosides, cisplatin, loop diuretics, salicylate and organic solvents have been proven to impair hearing. Moreover, these chemical compounds seem to potentiate NIHL (see Boettcher et al., 1987 for review). To investigate the combined effects of noise and ototoxic compounds, it is important to expose groups of experimental animals both to the noise and the ototoxic compound alone and to the combinations of the two, at moderate levels of the noise and chemicals. Thus, the purpose of this study is 1) to provide a baseline for the effects of noise on hearing in rats, which will be used in ongoing studies on combined exposures in our laboratory, and 2) to add to the rather limited information we have on the effects of noise on hearing in this species.

  Materials and methods Top


Male Wag/Rij rats, with an average weight of 200 g at the beginning of the experiment, were obtained from Charles River (Germany). Animals were group-housed in wire mesh cages (four per cage). Food and water were available ad lobatum. Lights were on from 7:00 a.m. to 7:00 p.m. The animals were weighed weekly. The possible differences in weight-gain between the noise-exposed animals and control animals were tested with t-tests. Care and use of the animals reported on in this paper were approved by the Animal Care and Use Committee of the Faculty of Medicine, Utrecht University, under number DEC-GNK-95011.

Protocol and noise exposure

Rats were assigned at random to the following four groups (eight rats per group): control (exposed to ambient noise of about 65 dB) and N90, N100 and N110 exposed to 90, 100 and 110 dB SPL broad band noise, respectively.

The rats were exposed in wire mesh cages (l: 40 cm; w: 25 cm; h: 15 cm; four rats per cage), with an acoustically transparent mesh floor. The cages were placed in Hazleton cabins (standard whole-body inhalation exposure chambers) with a dimension of approximately 2 x 2 x 2 metre. Noise was generated (precision noise generator type 8075A, Hewlett Packard), amplified (Akai AM-17 or Sony AF470) and presented through four piezo ceramic tweeters (Motorola L054) mounted 0.34 metre above the cages. The resulting sound field was measured, without the rats present, at multiple locations to assess the uniformity of the noise (using a 1/4" Bruel & Kjer microphone (type 4135) and a measuring amplifier (Bruel & Kjer, type 2610) with linear filter settings). Typically, the variation in broad band noise level from location to location was within 1 dB. One-third­ octave-band spectra (50 Hz - 40 kHz) were obtained with a spectrum analyser (Stanford Research Systems, model SR760 FFT). These one third-octave-band spectra of the four conditions are depicted in [Figure - 1]. Ambient noise was below 50 dB SPL over most of the frequency range. At very low frequencies (500 Hz), it was highly variable and could reach levels up to 60 dB SPL, which explains why in [Figure1] the ambient noise level in the 500 Hz band is higher than that of the 90 dB exposure level. Most energy in the noise exposure fell between 2 and 12.5 kHz.

Measurement of 2f 1 -f 2 distortion product otoacoustic emissions, electrocochleography and harvesting of the cochlea took place between 3 to 7 weeks after the noise exposure. Generally, two animals were processed per day. Each day, we obtained animals from an experimental group different from that of the day before, to avoid unwanted bias. The 3 to 7 weeks post-exposure interval was chosen because noise effects that still exist 20 to 30 days after the last exposure, are considered to be permanent (Salvi et al., 1995).

The rats were anesthetized during surgery and during the DPOAE and electrophysiological measurements. The animals were anesthetized with an intramuscular injection of Thalamonal (0.1 ml/100 g body weight; Thalamonal contains 2.5 mg/ml droperidol and 0.05 mg/ml fentanyl). This was followed by ventilation with a gas mixture containing 33% O2, 66% N2O and 1% Halothane through a trachea cannula. Heart frequency was monitored and temperature was kept at 38°C. The rat was placed on its back in an animal holder and the pinnae were resected.

Stimulus generation, distortion product recording and system calibration

Stimulus generation and acquisition of distortion product otoacoustic emissions (DPOAE) were controlled by a host computer, with a signal processing board (AP2) and modular audiometry system (Tucker Davis Technology, Gainesville, USA). This system was controlled by custom-made software. Two primaries (f1 and f 2 ), 240 ms in duration, were generated by the computer and sent to two separate D/A converters. Subsequently, they were fed through low-pass cut-off filters (36 kHz), attenuators and headphone buffers. The resulting stimuli were delivered to the ear canal through an ER-10C probe system (Etymotic Research, Elk Grove Village, USA), incorporating two speakers and one low-noise microphone. The recorded microphone signal was amplified (40 dB) and A/D converted. Data acquisition was started 100 ms after the onset of the primaries, to avoid start-up transients. The primaries and the response were both sampled at a rate of 66.67 kHz. The recorded signals were time-averaged, windowed (Hanning shaped) and transformed by fast Fourier analysis.

To calibrate the microphone of the probe system in dB SPL, a microphone correction table was generated, using the frequency-response of the ER­10C microphone, provided by the manufacturer. At the beginning of each experiment, the probe was positioned in the ear canal and the primaries were adjusted per ear. According to the table, f1 and f 2 were presented at 60 dB SPL and the responses were measured via the ER-10C microphone. If the measured amplitudes of the primaries deviated from the target amplitude, the attenuator settings were adjusted.

Amplitude growth curves of the 2f 1 -f 2 DPOAE were obtained for the primary f 2 frequencies 4, 8, 16 and 22.6 (half an octave above 16) kHz, where the f 2 /f 1 ratio was 1.25. The levels of the primaries were L 2 =L 1 -10 and the intensity of L1 was increased in 5 dB steps from 40 to 80 dB SPL.

Each pair of primaries was presented 8 times. DPOAE growth curves were obtained from both ears.

The level of the noise floor at the location of the DPOAE was measured with the same procedure and using the same recording and stimulus set up, immediately before the 2f 1 -f 2 determination, but with the f1 and f 2 switched off.

Analysis of variance (ANOVA) was performed on the DPOAE growth curves measured after the respective noise exposures, for all tested frequencies and averaged over right and left ears. Noise exposure was a between-subjects factor and frequency and level of stimulation were within­ subjects factors. Post hoc Tukey's HSD test was used to further examine significant differences.


Electrocochleography was performed immediately after the distortion product measurement. Techniques for electrocochleography were described previously (Stengs et al., 1997) and are only summarized here. Auditory evoked responses were recorded differentially with a silver-ball electrode at the apex of the cochlea and a reference electrode in the muscles of the neck. Trains of 8 ms tone bursts of 1, 2, 4, 8, 12, 16 and 24 kHz were presented, with cosine shaped rise and fall time of 1 ms, except at 1 kHz (2 ms) and 2 kHz (1.5 ms). Consecutive tone bursts were presented with alternating polarity. The inter-burst interval was 99 ms. The responses were pre-amplified (100 times), band-pass filtered (-12 dB/octave, -3 dB at 1 Hz and 10 kHz), A/D converted at a sample frequency of 33.3 kHz and averaged. The averaged responses to the opposite polarity tone bursts were saved separately for off-line analysis. The compound action potential (CAP) was obtained by addition of the responses of opposite polarity. The CAP amplitude was defined as the difference between the highest negative peak and the summating potential in the complex waveform. The threshold is defined as the stimulus level that produced a 1 µV CAP response (iso-response level).

The CAP data were logarithmically transformed before analysis to improve homogeneity of variance and to make proportional effects linear. Subsequently, data from left and right ears were averaged for each stimulus condition. ANOVA was performed as for the DPOAE.


Immediately after electrocochleography, the cochlea's of the rats were fixed by trans cardial perfusion with a chilled tri-aldehyde fixative consisting of 3% glutaraldehyde, 2% formaldehyde, 1% acrolein, 2.5% dimethylsulfoxide in 0.1 M sodium cacodylate buffer (pH 7.4), followed by overnight immersion in the same fixative at 4°C. Subsequently, cochlea's were processed according to the routine method used for guinea pigs (De Groot et al., 1987). Semithin (1 µm) mid modiolar sections were cut and stained with 1% methylene blue, 1% azur II in 1% tetraborate. Sections were studied under the light. In a mid modiolar section of the rat cochlea, the organ of Corti was examined at five locations, separated by a half-turn distance. Hair cell counts were performed at each of these five locations in both the left and right cochlea, using 5-6 serial sections. If a hair cell is not seen in these 5-6 serial 1 µm sections, it can be reliably assumed that the cell is not present. Two investigators, independently of one other, in a single-blind fashion performed all OHC counts. Estimates were made of the characteristic frequencies of the locations along the basilar membrane at which the OHCs were counted; the corresponding frequencies were calculated to be 52, 21, 11, 4 and 0.1 kHz, according to a frequency map published by Miller (1991).

The results for the left and right cochlea were pooled and averaged per location. ANOVA was used for statistical evaluation of the OHC counts. Noise exposure was a between-subjects factor, cochlear location a within-subjects factor.

  Results Top

General health

During the experiment, the rats exhibited no overt signs of ill health following the noise exposure. At the end of the treatment period the weight of the exposed rats was not different from that of the control animals (t-test, p = 0.39).

Distortion product otoacoustic emission

DPOAE growth curves for 2f 1 -f 2 amplitude of the four groups are presented in [Figure - 2], for all tested frequencies and averaged for left and right ears per stimulus condition. Obvious deterioration of the DPOAE growth curves for the N110 group was observed at 4, 8 and 16 kHz. At 22.6 kHz, the decrease was less severe. After 90 and 100 dB SPL noise, the DPOAE growth curves resembled that of the control group. However, a trend of enhancement of the growth curves for the N90 and N100 group could be distinguished at 22.6 kHz for the highest primary levels.

ANOVA performed on the whole data set of DPOAE growth curves (all frequencies and stimulus levels included) showed main effects of noise level, frequency and stimulus level and significant interactions. The significant interaction between noise level and frequency was further pursued by ANOVA performed at each frequency separately. A significant effect of noise level was found at 4 kHz (p < 0.01; F(3,27) = 4.9), 8 kHz (p < 0.01; F(3,27) = 49.3) and 16 kHz (p < 0.01; F (3,27) = 8.8). No significant decrease was found at 22.6 kHz after the 110 dB SPL noise, although [Figure - 2] suggested such a trend. Subsequently, post hoc Tukey HSD tests were performed at each frequency. They showed differences in DPOAE growth curves between the control group and that of the N110 group at 4, 8 and 16 kHz (all p < 0.01).


CAP amplitude growth curves are shown in [Figure - 3], for all tested frequencies and averaged over left and right ears. An apparent effect of noise exposure level was observed in the N110 group at 4, 8, 12, 16 and 24 kHz. 100 dB SPL noise only slightly affected the 12 kHz growth curve. The panels for 4, 8, 12 and 16 kHz show steeper growth curves for noise at 110 dB SPL than that for the lower noise levels.

ANOVA, performed on the averaged CAP growth curves of the right and left ears (with all frequencies included), showed significant main effects of noise level, frequency and stimulus level and significant interactions. The interaction between noise level and frequency was further pursued by ANOVA at each stimulus frequency separately. Effects of noise level were detected at 4 kHz (p < 0.01; F(3,28) = 39.9), 8 kHz (p < 0.01; F(3,28) = 228.9), 12 kHz (p < 0.01; F(3,28) = 150.4), 16 kHz (p < 0.01; F(3,28) = 96.2) and 24 kHz (p < 0.01; F(3,28) = 7.9). Significant interactions between noise level and stimulus level were detected at 2 kHz (p < 0.01; F(24,224) = 2.6), 4 kHz (p < 0.01; F(24,224) = 43.9), 8 kHz (p < 0.01; F(24,224) = 28.9), 12 kHz (p < 0.01; F(24,224) = 25.3), 16 kHz (p < 0.01; F(24,224) = 15.6) and 24 kHz (p < 0.01; F(24,224) = 2.3). First, post hoc Tukey HSD performed per frequency, showed differences between the CAP growth curves of the control group and those of the N110 group (all p < 0.01) at 4, 8, 12, 16 and 24 kHz. In addition, at 12 kHz a difference was found between the growth curve of the control group and that of the N100 group (p < 0.01). Second, post hoc Tukey HSD performed per frequency and stimulus level showed, after 110 dB SPL noise, differences in CAP growth curves below stimulus levels of 96, 96, 92, 67 and 53 dB SPL at 4, 8, 12, 16 and 24 kHz, respectively. At higher stimulus levels, the growth curves did not show any difference.


To quantify the effect of noise on the OHC population, the number of OHCs present at each location was counted. All expected OHCs were present at the five examined locations, both in the cochlea of control animals and in the noise­exposed animals. Also, inner hair cell (IHC) loss was not observed.

  Discussion Top

Three groups of eight rats were exposed to broad band noise at levels of 90, 100 and 110 dB SPL for 8 hours/day and 5 consecutive days. An additional group of eight rats (exposed to the ambient noise at 65 dB SPL) served as the control group. Effects on hearing were abundant after the highest noise level: the DPOAE growth curves at 4, 8 and 16 kHz and the CAP growth curves at 4, 8, 12, 16 and 24 kHz were affected. The 100 dB SPL broad band noise only affected the 12 kHz CAP growth curve. The DPOAE results resemble those found for the CAP. The steeper CAP growth curves found with hearing loss are reminiscent of recruitment, which indicates OHC loss (Patuzzi et al., 1989). Both the decrease in DPOAE amplitude after the noise exposure of 110 dB SPL and the steeper CAP growth curves suggest OHC loss in the 4-24 kHz region. However, all OHCs were present, even after 110 dB SPL noise-exposure, and damage to the cells was not apparent at the light-microscopic level. We have to conclude that the OHCs were functionally damaged. Further, we can not exclude additional damage to the IHCs (Engstrom, 1984). Stereociliar pathology or subcellular damage, which is difficult to visualize at the light microscopic level, may have been present in OHCs and IHCs. The relation between functionally evaluated effects and morphological loss is not always straight forward after noise exposure: extensive physiological hearing loss can exist with minor or even undetectable morphological changes (Borg et al., 1995). Engstrom (1984) exposed rats to industrial noise (3-30 kHz, 100 dB L eq (lin), 10 hours/day for one month). Auditory brainstem responses showed permanent threshold shifts at 6 and 12 kHz two weeks after the last exposure day. Yet, hair cell loss was not found anywhere on the basilar membrane. However, using scanning electron microscopy, IHCs in the area 6-8 mm from the apex frequently showed fused stereocilia bundles. Intense sound can also induce excitotoxicity, which is the excessive release of neurotransmitter from the IHCs to the underlying post-synaptic element (see: Eybalin, 1993 for review). However, this cannot explain our results. The dendritic swelling caused by excitotoxicity is reversible (Robertson, 1983; Puel et al., 1998).

We compared our results to all previously published results known to us, obtained with rats exposed to different levels of noise for longer periods (1 week to 15 months). The group at the Karolinska Institute exposed rats to 100 dB L eq (lin) variable broad band noise for 4 weeks (10 hours/day, 7 days/week) and tested hearing with auditory brainstem responses in several studies. Only the noise-alone results will be discussed here. The exposure noise consisted of a noise band, 1680 Hz wide, sweeping from 3 to 30 kHz. Most of the energy fell between 5 and 15 kHz (Borg, 1982a;

Engstrom, 1984; Johnson et al., 1988, 1990). Maximum hearing loss was 50 dB at 12.5 kHz (Johnson et al., 1988), 26 dB at 12.5 kHz (Johnson et al., 1990) and 30 dB between 12 and 20 kHz (Borg, 1982a). Borg (1982b) exposed rats for periods of up to 15 months with the noise protocol described above. Hearing loss kept increasing with exposure duration and reached a maximal of 75 dB at 15 months (37 dB at 1 month, 44 dB at 2 months and 62 dB at 3 months; maximal loss always between 20 and 44 kHz). Sullivan and Connolly (1988) exposed rats to 110 dB broad band noise with peak energy at 0.5 and 20 kHz respectively for 6 hours/day, 5 days/week for 4 weeks. Maximum hearing loss was found around 50 dB between 4 and 8 kHz. Lataye and Campo (1997) exposed rats for 6 hours/day, 5 days/week for 4 weeks to a 92 dB octave band noise centered at 8 kHz. Auditory function was tested by recording brainstem auditory evoked potentials. A 30 dB hearing loss was detected after the exposure at 10­12 kHz. Rats exposed to 95 dB SPL broad band noise (18 hours/day, 5 days/week, 3 weeks; energy peak between 2 and 16 kHz) showed a maximum threshold shift of 25 dB at 8 kHz with reflex modification audiometry (Muijser et al., in press). The maximum loss in this study was 42 dB at 12 kHz, about half an octave above the peak in the energy spectrum of the 110 dB SPL noise.

As a common measure for noise exposition in the various studies, we calculated the total exposure based upon the equal-energy theory. The equal energy theory proposes that the damaging effect of noise on hearing depends directly upon the total sound energy in such a way that there is a trade-off between the level of the exposure and its duration (Vertes et al., 1981; Ward et al., 1981). This principle was formulated to estimate hearing loss in workers who are exposed for many years. We used the following formula to adjust the noise exposures in the various rat studies to an equivalent 8 hours a day, 5 days a week, 1 week exposure (the exposure of our study):

10 . 10 log {(h/8) . (d/5) . w} in which h=hours per day, d=days per week and w=number of weeks of exposure

[Figure - 4] shows the result of this comparison. On the horizontal axis the adjusted exposure levels are presented. On the vertical axis we plotted the maximum hearing loss at any frequency encountered in the various studies, independently of the frequency spectrum of noise or what method was used to evaluate the hearing loss (behavioral, brainstem evoked potentials or electrocochleogra­phy). All hearing loss was expressed in threshold shift (dB). This comparison shows a consistent relation amongst the results from the studies included. The higher the adjusted noise exposure level, the higher the accompanying hearing loss. This relationship is clear, despite the fact that the types of noise, exposure regimens used and method of evaluating hearing loss were variable in the studies included in this comparison. Thus, the equal-energy concept provides a useful descriptor of hearing loss in rats exposed to noise for 6 to 18 hours per day, 5 to 7 days per week over periods of 1 week to 15 months at equivalent levels of 95 to 120 dB re an 8 hour, 5 days a week, one week exposure. [Figure - 4] demonstrated that the results of the present study are well in line with the previous results.

In conclusion, this study (and previous studies) show that it takes 100 to 110 dB SPL noise to cause measurable damage to the rat cochlea in an exposure paradigm representative of industrial situations. This information will be valuable for ongoing experiments into the combined effect of exposure to noise and ototoxic chemicals.

  Acknowledgements Top

This study was supported by grants of NWO-MW (grant-number 9004-63-085) and by the Heinsius­Houbolt Fund. The authors would like to thank J.C.M.J. de Groot, R. Bulder and F. Hendriksen for their histological assistance.[23]

  References Top

1.Alberti P.W. (1988) Noise, the most ubiquitous pollutant. Noise & Health 1: 3-5.  Back to cited text no. 1    
2.Boettcher F.A., Henderson D., Gratton M.A., Danielson R.W., Byrne C.D. (1987) Synergistic interactions of noise and other ototraumic agents. Ear & Hearing 8: 192-212.  Back to cited text no. 2    
3.Borg E. (1982a) Noise-induced hearing loss in rats with renal hypertension. Hear. Res. 8: 93-99.  Back to cited text no. 3    
4.Borg E. (1982b) Noise-induced hearing loss in normotensive and spontaneously hypertensive rats. Hear. Res. 8: 117-130.  Back to cited text no. 4    
5.Borg E., Canlon B., Engstrom B. (1995) Noise induced hearing loss. Literature review and experiments in rabbits. Morphological and electrophysiological features, exposure parameters and temporal factors, variability and interactions. Scand. Audiol. Suppl 40, 1-147.  Back to cited text no. 5    
6.De Groot, J.C.M.J., Veldman, J.E., Huizing, E.H. (1987) An improved fixation method for guinea pig cochlear tissues. Acta Otolaryngol. (Stock.) 104: 234-242.  Back to cited text no. 6    
7.Engstrom B. (1984) Fusion of stereocilia on inner hair cells in man and in rabbit, rat and guinea pig. Scan. Audiol. 13: 87-92.  Back to cited text no. 7    
8.Eybalin E. (1993) Neurotransmitters and neuromodulators of the mammalian cochlea. Physiol. Reviews. 73: 309-373.  Back to cited text no. 8    
9.Johnson A.-C., Juntunen L., Nylen P., Borg, E., Hoglund G. (1988) Effect of interaction between noise and toluene on auditory function in the rat. Acta Otolaryngol. 105: 56­63.  Back to cited text no. 9    
10.Johnson A.-C., Nylen P., Borg, E., Hoglund G. (1990) Sequence of exposure to noise and toluene can determine loss of auditory sensitivity in the rat. Acta Otolaryngol. 109: 43-40.  Back to cited text no. 10    
11.Lataye R., Campo P. (1997) Combined effects of simultaneous exposure to noise and toluene on hearing function. Neurotox. Teratol. 19: 373-382.  Back to cited text no. 11    
12.Muijser H., Lammers J.H.C.M., Kulig B.M. (In press Noise and Health) Effects of exposure to trichloroethylene and noise on hearing in rats.  Back to cited text no. 12    
13.Muller M. (1991) Frequency representation in the rat cochlea. Hear. Res. 51: 247-254.  Back to cited text no. 13    
14.Patuzzi R.B., Yates G.K., Johnstone B.M. (1989) Outer hair cell receptor current and sensorineural hearing loss. Hear. Res. 42: 47-72.  Back to cited text no. 14    
15.Puel J.-L., Ruel J. Gervais d'Alpin C., Pujol R. (1998) Excitotoxicity and repair of cochlear synapses after noise­trauma induced hearing loss. Neuroreport 9: 2109-2114.  Back to cited text no. 15    
16.Robertson D. (1983) Functional significance of dendritic swelling after loud sounds in the guinea pig cochlea. Hear. Res. 9: 263-278.  Back to cited text no. 16    
17.Salvi R.J., Henderson D., Eddins A.C. (1995) Effects of noise exposure on the auditory system. In Handbook of neurotoxicology. Chang L.W. ed. Marcel Dekker Inc, New York, pp 907-961.  Back to cited text no. 17    
18.Saunders J.C., Dear S.P., Schneider M.E. (1985) The anatomical consequences of acoustics injury: A review and tutorial. J. Acoust. Soc. Am. 78: 833-860.  Back to cited text no. 18    
19.Slepecky N. (1986) Overview of mechanical damage to the inner ear: noise as a tool to probe cochlear function. Hear. Res. 22: 307-321.  Back to cited text no. 19    
20.Stengs C.H.M., Klis S.F.L., Huizing E.H., Smoorenburg G.F. (1997) Cisplatin-induced ototoxicity; Electrophysiological evidence of sponteneous recovery in the albino guinea pig. Hear. Res. 111: 103-113.  Back to cited text no. 20    
21.Sullivan M.J., Connoly R.B. (1988) Dose-response hearing loss for white noise in the Sprague-Dawley rat. Fund. Appl. Toxicol. 10: 109-113.  Back to cited text no. 21    
22.Vertes D., Axelsson A., Miller J., Liden G. (1981) Cochlear vascular and electrophysiological effects in the guinea pig to 4 kHz pure tones of different durations and intensities. Acta Otolaryngol. 92: 15-24.  Back to cited text no. 22    
23.Ward W.D., Santi P.A., Duvall A.J., Turner C.W. (1981) Total energy and critical intensity concepts in noise damage. Ann. Otol. 90: 584-590.  Back to cited text no. 23    

Correspondence Address:
Natalie LM Cappaert
Hearing Research Laboratories, University Medical Centre, Room G.02.531, Heidelberglaan 100, NL-3584 CX, Utrecht
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Source of Support: None, Conflict of Interest: None

PMID: 12689440

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  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]