Protection against noise trauma by pre-exposure to a low level acoustic stimulus

Canlon, Barbara; Borg, Erik; Flock, Åke

doi:10.1016/0378-5955(88)90107-4

Cited by 181 publications

(100 citation statements)

References 18 publications

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“…It has been demonstrated in the cat, guinea pig 6) , rabbit 7) , chinchilla 8,9) and human 10) . Noise of 85-100 dB SPL has been proved to be the best intensity for inducing the effect of sound conditioning, and the effect is in proportion to noise intensity in this narrow range [11][12][13] .…”

Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and NoiseExposure: Hongyan ZUO, et al. Department of Occupational Hygiene, Institute of Health and Environmental Medicine of Tianjin, PR ChinaSound conditioning has reduced noise-induced hearing loss in experimental mammalian animals and in clinical observation. Forty guinea pigs were grouped as: A, control; B, conditioning noise exposure group; C, high level noise exposure group; and D, conditioning noise exposure followed by a high level noise exposure group. Auditory brainstem response thresholds were measured. The cochlear sensory epithelia surface was observed microscopically. Calmodulin, F-actin and heat shock protein 70 (HSP70) in hair cells were immunohistochemistrically stained. The intracellular free calcium was stained for confocal microscopy. The ABR threshold shift after noise exposure was higher in group C than D, and showed a quicker and better recovery in group D than C. Stereocilia loss and the disarrangement of outer hair cells were observed, with the greatest changes seen in group C, followed by g r o u p s D a n d B .T h e m o s t i n t e n s i v e immunohistochemical intracellular expressions of calmodulin, F-actin, and HSP70 were found in group D, followed by groups C, B and A. The highest intensity of the fluorescent intracellular free Ca 2+ staining in the isolated outer hair cells was observed in group C. The ABR and morphological studies confirmed the protective effect from noise trauma of sound conditioning. The protective mechanism of hair cells during sound conditioning was enforced through the increase of cellular cytoskeleton proteins and through the relieving of intracellular calcium overloading caused by the traumatic noise. (J Occup Health 2008; 50: 373-379)

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Section: Discussionmentioning

confidence: 99%

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Zuo¹,

Cui²,

She³

et al. 2008

Journal of Occupational Health

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“…We do not know whether targeted stimulation needs to be continued as long as in the present study. Previous studies (Canlon et al, 1988) have suggested a beneficial effect of acoustic stimulation in protecting the auditory system. Moreover, it has been shown that age-related hearing loss is reduced by life-long acoustic stimulation (Willott and Bross, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Thus, noiseinduced hearing loss is assumed to be permanent. In this context, it is well established that sound conditioning before inducing a noise trauma reduces the amount of hearing loss (Canlon et al, 1988;Niu and Canlon, 2002;Niu et al, 2003). More interestingly, one study found that unilateral removal of middle ear ossicles after an acoustic trauma, resulting in an attenuation of environmental sound of ϳ50 dB over a wide frequency band (250 Hz to 8 kHz), is associated with greater hearing loss in that ear compared with that in the opposite ear with intact middle ear (Fukushima et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

Noreña¹,

Eggermont²

2005

J. Neurosci.

297

188

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Exposure to sound of sufficient duration and level causes permanent damage to the peripheral auditory system, which results in the reorganization of the cortical tonotopic map. The changes are such that neurons with pre-exposure tuning to frequencies in the hearing loss range now become tuned to frequencies near the near-normal lower boundary of the hearing loss range, which thus becomes over represented. However, cats exposed to a traumatizing noise and immediately thereafter placed for a few weeks in an enriched acoustic environment presented a much-restricted hearing loss compared with similarly exposed cats that were placed for the same time in a quiet environment. The enriched environment spectrally matched the expected hearing loss range and was ϳ40 dB above the level of the expected hearing loss. The hearing loss in the quiet environment-reared cats ranged from 6 to 32 kHz with the largest loss (on average, 40 dB) ranging from 24 to 32 kHz. In contrast, the hearing loss in the enriched-environment cats was restricted to 6 -8 kHz at a level of, on average, 35 dB and with 16 -32 kHz having normal thresholds. Despite the remaining hearing loss for the enriched-environment cats in the 6 -8 kHz range, plastic tonotopic map changes in primary auditory cortex could no longer be demonstrated, suggesting that the enriched acoustic environment prevents this reorganization. This finding has implications for the treatment of hearing disorders, such as tinnitus, that have been linked to cortical tonotopic map reorganization.

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“…11 and 12 indicates that while ATS across all tested frequencies was similar, there was a large difference in OHC loss between the G and the two nonG groups [i.e., between the b(t) exposed in the industrial noise environment the above result emphasizes the often-observed lack of correlation between various measures of threshold having a recoverable component (i.e., compound threshold shifts) and permanent threshold shifts. Interrupting a noise exposure for a significant period of time over the course of a chronic exposure should lead to a reduced traumatic effect either as a consequence of the partial or complete recovery of thresholds during the silent periods, or as a result of the toughening effect (Miller et al, 1963;Clark et al, 1987;and others), or under some conditions of exposure, the conditioning effect (Canlon et al, 1988). The above statement can be tested by comparing the results of the 5 day continuous exposures and the 19 day interrupted exposures, i.e., a comparison between pairs of G and nonG groups shown in Figs.…”

Section: Fig 7 Group Mean (A) Permanent Threshold Shift (Pts) (B) mentioning

confidence: 99%

“…The experiments described below were designed to test this hypothesis. However, the experimental design also allowed for (a) a replication or reinforcement of earlier results that showed increased trauma produced by nonG exposures relative to equivalent energy G exposures (Hamernik et al, 2003b;Hamernik and Qiu, 2001;Lei et al, 1994); (b) an evaluation of the equal energy principle as it applies to interrupted/intermittent noise exposures Hamernik et al, 2007); and (c) the effect of toughening/conditioning (Miller et al, 1963;Clark et al, 1987;Canlon et al, 1988;Hamernik et al, 2003aHamernik et al, , 1994Hamernik and Ahroon, 1999) on the resultant hearing and sensory cell loss.…”

Section: Introductionmentioning

confidence: 99%

The value of a kurtosis metric in estimating the hazard to hearing of complex industrial noise exposures

Qiu

Hamernik

Davis

2013

The Journal of the Acoustical Society of America

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A series of Gaussian and non-Gaussian equal energy noise exposures were designed with the objective of establishing the extent to which the kurtosis statistic could be used to grade the severity of noise trauma produced by the exposures. Here, 225 chinchillas distributed in 29 groups, with 6 to 8 animals per group, were exposed at 97 dB SPL. The equal energy exposures were presented either continuously for 5 d or on an interrupted schedule for 19 d. The non-Gaussian noises all differed in the level of the kurtosis statistic or in the temporal structure of the noise, where the latter was defined by different peak, interval, and duration histograms of the impact noise transients embedded in the noise signal. Noise-induced trauma was estimated from auditory evoked potential hearing thresholds and surface preparation histology that quantified sensory cell loss. Results indicated that the equal energy hypothesis is a valid unifying principle for estimating the consequences of an exposure if and only if the equivalent energy exposures had the same kurtosis. Furthermore, for the same level of kurtosis the detailed temporal structure of an exposure does not have a strong effect on trauma.

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Protection against noise trauma by pre-exposure to a low level acoustic stimulus

Cited by 181 publications

References 18 publications

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Changes in Guinea Pig Cochlear Hair Cells after Sound Conditioning and Noise Exposure

Enriched Acoustic Environment after Noise Trauma Reduces Hearing Loss and Prevents Cortical Map Reorganization

The value of a kurtosis metric in estimating the hazard to hearing of complex industrial noise exposures

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