scholarly journals Long-term, but not transient, threshold shifts alter the morphology and increase the excitability of cortical pyramidal neurons

2012 ◽  
Vol 108 (6) ◽  
pp. 1567-1574 ◽  
Author(s):  
Sungchil Yang ◽  
Wendy Su ◽  
Shaowen Bao

Partial hearing loss often results in enlarged representations of the remaining hearing frequency range in primary auditory cortex (AI). Recent studies have implicated certain types of synaptic plasticity in AI map reorganization in response to transient and long-term hearing loss. How changes in neuronal excitability and morphology contribute to cortical map reorganization is less clear. In the present study, we exposed adult rats to a 4-kHz tone at 123 dB, which resulted in increased thresholds over their entire hearing range. The threshold shift gradually recovered in the lower-frequency, but not the higher-frequency, range. As reported previously, two distinct zones were observed 10 days after the noise exposure, an enlarged lower-characteristic frequency (CF) zone displaying normal threshold and enhanced cortical responses and a higher-CF zone showing higher threshold and a disorganized tonotopic map. Membrane excitability of layer II/III pyramidal neurons increased only in the higher-CF, but not the lower-CF, zone. In addition, dendritic morphology and spine density of the pyramidal neurons were altered in the higher-CF zone only. These results indicate that membrane excitability and neuronal morphology are altered by long-term, but not transient, threshold shift. They also suggest that these changes may contribute to tinnitus but are unlikely to be involved in map expansion in the lower-CF zone.

Marine Drugs ◽  
2021 ◽  
Vol 19 (8) ◽  
pp. 443
Author(s):  
Hyunjun Woo ◽  
Min-Kyung Kim ◽  
Sohyeon Park ◽  
Seung-Hee Han ◽  
Hyeon-Cheol Shin ◽  
...  

One of the well-known causes of hearing loss is noise. Approximately 31.1% of Americans between the ages of 20 and 69 years (61.1 million people) have high-frequency hearing loss associated with noise exposure. In addition, recurrent noise exposure can accelerate age-related hearing loss. Phlorofucofuroeckol A (PFF-A) and dieckol, polyphenols extracted from the brown alga Ecklonia cava, are potent antioxidant agents. In this study, we investigated the effect of PFF-A and dieckol on the consequences of noise exposure in mice. In 1,1-diphenyl-2-picrylhydrazyl assay, dieckol and PFF-A both showed significant radical-scavenging activity. The mice were exposed to 115 dB SPL of noise one single time for 2 h. Auditory brainstem response(ABR) threshold shifts 4 h after 4 kHz noise exposure in mice that received dieckol were significantly lower than those in the saline with noise group. The high-PFF-A group showed a lower threshold shift at click and 16 kHz 1 day after noise exposure than the control group. The high-PFF-A group also showed higher hair cell survival than in the control at 3 days after exposure in the apical turn. These results suggest that noise-induced hair cell damage in cochlear and the ABR threshold shift can be alleviated by dieckol and PFF-A in the mouse. Derivatives of these compounds may be applied to individuals who are inevitably exposed to noise, contributing to the prevention of noise-induced hearing loss with a low probability of adverse effects.


2021 ◽  
Author(s):  
Florian Occelli ◽  
Florian Hasselmann ◽  
Jérôme Bourien ◽  
Jean-Luc Puel ◽  
Nathalie Desvignes ◽  
...  

Abstract People are increasingly exposed to environmental noise through the cumulation of occupational and recreational activities, which is considered harmless to the auditory system, if the sound intensity remains <80 dB. However, recent evidence of noise-induced peripheral synaptic damage and central reorganizations in the auditory cortex, despite normal audiometry results, has cast doubt on the innocuousness of lifetime exposure to environmental noise. We addressed this issue by exposing adult rats to realistic and nontraumatic environmental noise, within the daily permissible noise exposure limit for humans (80 dB sound pressure level, 8 h/day) for between 3 and 18 months. We found that temporary hearing loss could be detected after 6 months of daily exposure, without leading to permanent hearing loss or to missing synaptic ribbons in cochlear hair cells. The degraded temporal representation of sounds in the auditory cortex after 18 months of exposure was very different from the effects observed after only 3 months of exposure, suggesting that modifications to the neural code continue throughout a lifetime of exposure to noise.


2018 ◽  
Vol 13 (2) ◽  
Author(s):  
Sjahrul Meizar Nasri ◽  
Iting Shofwati

One of preventive action methods of hearing loss that number tend to increase is by using brick that made from Styrofoam which is expected to have the ability as a soundproof that can be used to control the noise. The aim of this research is to assess the use of sound absorption material in which utilizing Styrofoam to reduce the noise exposure. In this study, cement and find aggregate that contain the Styrofoam and sand are mixed with the composition 1:4 and 1:6 and also by adding the polystyrene waste as much as 0%, 20%, 40%, 60%, and 80%.  To determine the acoustical property of the mixture, the sound absorbing coefficient (α) was determined by using Four Microphones Impedance Tube (ISO 140-3). The results showed that the highest absorption coefficient value was at frequency 800 Hz by adding 80% Styrofoam for the composition of 1:4 at 0.4100 dB and at the frequency 800 Hz by adding 40% Styrofoam for the composition 1:6 at 0.5870 dB. Based on the results of this research, further study to potentially use Styrofoam as noise barrier is suggested.


2020 ◽  
pp. 1671-1673
Author(s):  
David Koh ◽  
Tar-Ching Aw

Noise can affect hearing in the occupational setting but can have other effects where exposures are non-occupational. For clinical purposes, noise is measured in decibels weighted according to the sensitivity of the human ear (dB(A)). Regardless of source, the effects of overexposure to noise are similar. Initially there is a temporary threshold shift, where reversibility of hearing loss is possible with removal away from further noise. Noise-induced hearing loss occurs following prolonged or intense exposure, with poor prospects for improvement of hearing. The classical audiogram for noise-induced hearing loss shows a 4 kHz dip. Non-auditory effects of prolonged noise exposure include annoyance, sleep disturbance, hypertension, and cardiovascular disease, stress, and impaired cognitive performance. Prevention of noise-induced hearing loss is by reducing exposure to noise at source minimizing exposure time, using hearing protection, and participating in surveillance.


1974 ◽  
Vol 39 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Lynne Marshall ◽  
John F. Brandt

Temporary threshold shift resulting from exposure to one and five toy cap gun pistol shots was investigated using 11 normal-hearing adult subjects and one subject with a noise-induced hearing loss. The subjects fired the cap gun at arm’s length, and absolute thresholds at 4000 Hz were obtained before and after noise exposure by a fixed-frequency Bekesy technique. After exposure to one gunshot, five subjects showed a small TTS, five demonstrated no TTS, and two (including the subject with the hearing loss) exhibited negative TTS. No TTS occurred in any of the subjects after exposure to five shots. It was postulated that the small amount of TTS was due to the unexpectedly low sound pressure level produced by the cap gun and to the contraction of the middle ear muscles in some subjects prior to firing.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Moritz Gröschel ◽  
Jana Ryll ◽  
Romy Götze ◽  
Arne Ernst ◽  
Dietmar Basta

Noise exposure leads to an immediate hearing loss and is followed by a long-lasting permanent threshold shift, accompanied by changes of cellular properties within the central auditory pathway. Electrophysiological recordings have demonstrated an upregulation of spontaneous neuronal activity. It is still discussed if the observed effects are related to changes of peripheral input or evoked within the central auditory system. The present study should describe the intrinsic temporal patterns of single-unit activity upon noise-induced hearing loss of the dorsal and ventral cochlear nucleus (DCN and VCN) and the inferior colliculus (IC) in adult mouse brain slices. Recordings showed a slight, but significant, elevation in spontaneous firing rates in DCN and VCN immediately after noise trauma, whereas no differences were found in IC. One week postexposure, neuronal responses remained unchanged compared to controls. At 14 days after noise trauma, intrinsic long-term hyperactivity in brain slices of the DCN and the IC was detected for the first time. Therefore, increase in spontaneous activity seems to develop within the period of two weeks, but not before day 7. The results give insight into the complex temporal neurophysiological alterations after noise trauma, leading to a better understanding of central mechanisms in noise-induced hearing loss.


2020 ◽  
Vol 13 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Luigi De Maria ◽  
Antonio Caputi ◽  
Rodolfo Sardone ◽  
Enza Sabrina Silvana Cannone ◽  
Francesca Mansi ◽  
...  

Background: Age-Related Hearing Loss (ARHL) is a gradual and irreversible age-dependent decline in auditory function. There is still no consensus on the long-term functional effects of noise exposure on ARHL. Objective: This study aimed to compare the prevalence of ARHL in an elderly population occupationally exposed to noise in a non-exposed population. Methods: The population was divided into two groups: a group of 482 subjects professionally exposed to noise for over 10 years and a group of 1129 non-exposed subjects. Among the exposed subjects, a subgroup of 298 who worked for over 10 years in the glassware industry was selected. All the participants underwent a thorough otorhinolaryngological examination. Results: The presence of ARHL was found in 81% of exposed subjects and in 4% of non-exposed subjects. In the sub-group of glassware workers, the prevalence was 88%. The statistical analysis showed a significant association between previous occupational exposure to noise and ARHL (OR = 1.09; 95% CI = 1.067-1.124; p = 0.0012) and between exposure to the glassware industry and ARHL (OR = 1.89; 95% CI = 1.78-1.96; p = 0.006). Conclusion: Consistent with recent studies, we found a significantly higher prevalence of ARHL among workers exposed to noise; however, further studies are needed to support these findings.


2009 ◽  
Vol 123 (10) ◽  
pp. 1090-1096 ◽  
Author(s):  
L Mei ◽  
Z-W Huang ◽  
Z-Z Tao

AbstractObjective:Hearing sensitivity usually diminishes with noise exposure. In the present study, we examined the effect of 93 dB(A) wide band noise on cochlear micromechanical sensitivity in awake guinea pigs.Methods:Animals were randomly assigned to groups receiving either single or repeated noise exposure. Distortion product otoacoustic emission amplitudes were recorded before, during and after noise exposure.Results:Ninety-three decibel(A) wide band noise reduced the distortion product otoacoustic emission amplitudes at all tested frequencies. The distortion product otoacoustic emission amplitudes for higher frequencies showed a permanent reduction, whereas those for lower frequencies showed a temporary reduction. Distortion product otoacoustic emission amplitudes for middle frequencies showed prolonged enhancement after repeated noise exposure.Conclusion:Our results suggest that (1) it is likely that there are intermediate stages between permanent threshold shift and temporary threshold shift, and (2) long-term enhancement of distortion product otoacoustic emission amplitudes may be an indication of tinnitus generation.


1978 ◽  
Vol 86 (1) ◽  
pp. ORL-125-ORL-128 ◽  
Author(s):  
Allen F. Ryan ◽  
Robert C. Bone

Chinchillas were exposed to a noise band (1,414 to 5,656 Hz, 100-dB sound pressure level [SPL] for one hour) and treated with kanamycin (150 mg/kg a day until hearing loss was noted at 6.0 kHz) either separately, simultaneously, or sequentially. Simultaneous noise and kanamycin resulted in interactive potentiation of threshold shift and cochlear pathologic condition. Kanamycin treatment two months after noise exposure produced similar potentiation. No interaction was seen when noise exposure occurred one month after kanamycin treatment.


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