Changes in endocochlear potential during anoxia after intense noise exposure

1990 ◽  
Vol 44 (2-3) ◽  
pp. 143-149 ◽  
Author(s):  
Jian Wang ◽  
Wei-jia Dong ◽  
Ji-sheng Chen
Neuroscience ◽  
2019 ◽  
Vol 399 ◽  
pp. 184-198 ◽  
Author(s):  
S. Manohar ◽  
P.V. Ramchander ◽  
R. Salvi ◽  
G.M. Seigel

1983 ◽  
Vol 92 (6) ◽  
pp. 623-628 ◽  
Author(s):  
Joseph Sataloff ◽  
Robert T. Sataloff ◽  
Raymond A. Yerg ◽  
Hyman Menduke ◽  
Robert P. Gore

Most studies of the effects of noise upon hearing have dealt with continuous noise exposure. Previous reports on intermittent exposure to noise concluded that it causes less damage to hearing than does continuous exposure to noise of the same intensity. In this investigation, 12,000 workers were screened to find 295 subjects who met the strict criteria of the study. Most of the subjects were exposed to jackhammer noise at peak levels of 118 dBA. Intermittent exposure to intense noise results in very severe loss in high frequencies but relatively little or no hearing loss in the lower frequencies even after many years of exposure. This differs substantially from the effects of continuous exposure to noise of the same intensity. It remains to be determined whether this pattern of hearing results from intermittent exposure to all sorts of noise or only from the kinds of sources investigated in this study.


2012 ◽  
Vol 108 (4) ◽  
pp. 976-988 ◽  
Author(s):  
N. F. Manzoor ◽  
F. G. Licari ◽  
M. Klapchar ◽  
R. L. Elkin ◽  
Y. Gao ◽  
...  

Intense noise exposure causes hyperactivity to develop in the mammalian dorsal cochlear nucleus (DCN) and inferior colliculus (IC). It has not yet been established whether the IC hyperactivity is driven by hyperactivity from extrinsic sources that include the DCN or instead is maintained independently of this input. We have investigated the extent to which IC hyperactivity is dependent on input from the contralateral DCN by comparing recordings of spontaneous activity in the IC of noise-exposed and control hamsters before and after ablation of the contralateral DCN. One group of animals was binaurally exposed to intense sound (10 kHz, 115 dB SPL, 4 h), whereas the control group was not. Both groups were studied electrophysiologically 2–3 wk later by first mapping spontaneous activity along the tonotopic axis of the IC to confirm induction of hyperactivity. Spontaneous activity was then recorded at a hyperactive IC locus over two 30-min periods, one with DCNs intact and the other after ablation of the contralateral DCN. In a subset of animals, activity was again mapped along the tonotopic axis after the time course of the activity was recorded before and after DCN ablation. Following recordings, the brains were fixed, and histological evaluations were performed to assess the extent of DCN ablation. Ablation of the DCN resulted in major reductions of IC hyperactivity. Levels of postablation activity in exposed animals were similar to the levels of activity in the IC of control animals, indicating an almost complete loss of hyperactivity in exposed animals. The results suggest that hyperactivity in the IC is dependent on support from extrinsic sources that include and may even begin with the DCN. This finding does not rule out longer term compensatory or homeostatic adjustments that might restore hyperactivity in the IC over time.


1999 ◽  
Vol 20 (1) ◽  
pp. 21-32 ◽  
Author(s):  
Kenneth J. Gerhardt ◽  
Linda L. Pierson ◽  
Xinyan Huang ◽  
Robert M. Abrams ◽  
Kyle E. Rarey

Author(s):  
Courtney E Stewart ◽  
David Scott Bauer ◽  
Richard A Altschuler ◽  
William Michael King

Exposure to 120 decibel sound pressure level (dB SPL) band-limited noise results in delayed onset latency and reduced vestibular short-latency evoked potential (VsEP) responses. These changes are still present four weeks after noise overstimulation. Noise induced hearing loss (NIHL) has been shown to vary in extent and duration based on noise intensity. This study investigated whether noise-induced peripheral vestibular hypofunction (NPVH) would also decrease in extent and/or duration with less intense noise exposure. In the present study, rats were exposed to a less intense noise (110dB SPL), but for the same duration (6 hours) and frequency range (500-4000 Hz) as used in previous studies. The VsEP was assessed 1, 3, 7, 14, 21, and 28 days after noise exposure. In contrast to 120 dB SPL noise exposure, the 110 dB SPL noise exposures produced smaller deficits in VsEP responses that fully recovered in 62% of animals (13/21) within one week. These findings suggest that NPVH, a loss or attenuation of VsEP responses with a requirement for elevated stimulus intensity to elicit measurable responses, is similar to NIHL, i.e., lower sound levels produce a smaller or transient deficit. These results show it will be important to determine the extent and duration of vestibular hypofunction for different noise exposure conditions and their impact on balance.


2017 ◽  
Vol 22 (4-5) ◽  
pp. 303-310 ◽  
Author(s):  
Hao Xiong ◽  
Yongkang Ou ◽  
Yaodong Xu ◽  
Qiuhong Huang ◽  
Jiaqi Pang ◽  
...  

The sirtuin SIRT1 is a highly conserved nicotinamide adenine dinucleotide (NAD)-dependent protein deacetylase known to have protective effects against a wide range of neurological disorders. In the present study, we discovered that C57BL/6 mice fed a long-term diet supplemented with high-dose resveratrol exhibited increased cochlear SIRT1 activity and presented a better recovery of hearing and less loss of hair cells after intense noise exposure compared with those fed a standard chew. Moreover, resveratrol attenuated cochlear SIRT1 decrease and reduced oxidative stress in the cochlea after noise exposure. These results suggest a considerable therapeutic potential of resveratrol for the treatment of noise-induced hearing loss.


Sign in / Sign up

Export Citation Format

Share Document