Acoustic Over-Exposure Triggers Study by Pilati et al.

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Table of Contents

Introduction
Tinnitus Development
Conclusion
Reference

Introduction

In their article, Pilati et al. (2012) explore the topic of acoustic over-exposure (AOE), which represents the harmful processes occurring due to the subjection of the ears to high-decibel noise. AOE can take place because of a single and very loud noise or due to exposure to high decibels over prolonged periods of time. The authors have stated that AOE results in deafness in both humans and animals, further leading to the deterioration of auditory nerves. Some period of time (usually weeks) after being subjected to AOE, the body experiences a rise in the cells’ impulsivity or excitability within the dorsal cochlear nucleus (DCN). This is considered a possible neural correspondent to tinnitus, which is characterized by one or both ears experiencing ringing and other noises. Pilati et al. (2012) mention that the roots of tinnitus linked to DCN remain unknown; however, there is evidence that it is linked to the neurons that lie within the fusiform cell (FC) layer.

Tinnitus Development

To explore the impact of AOE, the researchers examined the changes in cells’ excitability within the fusiform cells after AOE involving the experiment with Wistar rats. The lab animals were exposed to a loud single tone of sound for four hours, with the recording of their auditory brainstem responses between three to four days after exposure. It was revealed that after acoustic over-exposure, some fusiform cells tend to illustrate a distinct bursting firing pattern, which, in turn, leads to them losing the ability to fire regularly or at high frequencies of firing. Based on the researchers’ findings, it can be suggested that the decreased balancing of HVA K+ currents in fusiform cell layers is the mechanism that contributes to the post-AOE change of activity.

Finding the difference in firing capacity in FCs is important because, at their regular patterns, they can fire trains of action potential that are reliable and precise when responding to depolarizations. Nevertheless, as a result of acoustic over-exposure, the firing patterns switched gradually for several days post-AOE intervals, which suggests that the change does not occur immediately, with over-exposure to loud sounds having a rather accumulative effect on hearing. In addition, it was revealed that, in general, tinnitus was induced after one ear’s exposure to loud sounds, which means that the application of the same sound to both ears could limit the likelihood of tinnitus onset (Pilati et al., 2012). Moreover, even though the research cited in the article found that bursts could be reported five to six days after the exposure of both ears to AOE, a relationship between the bursts of cellular excitability and the hyperactivity of the dorsal cochlear nucleus is to be found in the future.

Conclusion

Overall, there is a lack of consensus among researchers regarding the neuronal mechanisms leading to tinnitus development, which means that there is still no effective treatment that can be used. Among the common approaches to addressing tinnitus has been the local anesthetic lidocaine application; however, the effects are often short-term. Therefore, it is essential to consider treating the initial acoustic over-exposure symptoms immediately after exposure to slow tinnitus development later. The study provides a comprehensive scientific overview of the effects of acoustic over-exposure on hearing, delving deeper into the mechanisms causing tinnitus sometime after the exposure. The implications of the study are vast, mainly because the researchers have cited contradictory studies.

Reference

Pilati, N., Large, C., Forsythe, I. D., & Hamann, M. (2012). Acoustic over-exposure triggers burst firing in dorsal cochlear nucleus fusiform cells. Hearing Research, 283, 98-106.

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Acoustic Over-Exposure Triggers Study by Pilati et al.

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