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Basic Mechanisms Underlying Noise-Induced Hearing Loss

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Free Radicals in ENT Pathology

Abstract

The basic concept of noise-induced hearing loss (NIHL) is relatively simple: the development of a hearing dysfunction following exposure to a loud sound. However, there are many complexities in the types of hearing dysfunctions that can follow noise and the mechanisms underlying these changes. There have been several classical ways of differentiating types of NIHL. One such division is based on changes in the thresholds for detection of a sound, a reflexive behavioral response to a sound, an auditory brain stem response (ABR) evoked by sound, or some other sound-evoked physiological response in the central auditory pathways. If the amount of signal needed to generate detection or response becomes greater following a noise, this is considered a threshold shift. The threshold shift following noise can be temporary (a temporary threshold shift or TTS) or permanent (a permanent threshold shift or PTS). A PTS generally involves loss of sensory cells and can be further divided into cell death following apoptosis versus cell death by necrosis. TTS and the two types of PTS are all considered to have different causes and underlying mechanisms.

Another canonical way of classifying NIHL is by the causes, which can be strictly mechanical, a consequence of metabolic/intracellular influences, initiation of cell death pathways, or some combination thereof. Finally, one can divide the NIHL effects into those from predominantly peripheral consequences, from central auditory changes, or from both. This chapter will first focus on the peripheral events occurring in the cochlea. It will consider TTS and how our understanding of TTS has changed based on recent studies showing “permanent” auditory neuropathy occurring along with traditional “temporary” components of TTS (J Neurosci 26(7):2115–2123, 2006; J Neurosci 29(45):14077–14085, 2009). It will then consider the different types of PTS. For both types of threshold shifts, this chapter will consider the structural, cellular, and intracellular elements involved, the mechanical and metabolic/intracellular pathway influences, and how our understanding has progressed. Because the role of oxidative stress and free radicals in these mechanisms is the subject of many other chapters in this volume (Chaps. 2, 10, 13, and 19), specific pathways for formation of free radicals and their influence on cell function and cell death will not be detailed in this chapter. The chapter will assume their significant role in NIHL and consider strategies for protection and treatment given this role. The chapter will conclude with consideration of central auditory effects.

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Acknowledgments

We would like to thank the editors, specifically Josef Miller and Colleen LePrell for their contributions to this chapter. This work is supported by NIH grants R01 DC011294 and P30 DC005188 and DOD grant Army W81XWH-11-1-0414.

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Authors and Affiliations

  1. Department of Otolaryngology—Head & Neck Surgery, Kresge Hearing Research Institute, 5443 Medical Science Building 1, Ann Arbor, MI, 48109, USA

    Richard A. Altschuler Ph.D.

  2. Department of Cell & Developmental Biology, University of Michigan, Ann Arbor, MI, 48109, USA

    Richard A. Altschuler Ph.D. & David Dolan

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  1. Richard A. Altschuler Ph.D.
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Correspondence to Richard A. Altschuler Ph.D. .

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Editors and Affiliations

  1. Cochlear Signaling & Tissue Engin., University of Michigan Kresge Hearing Research Institute, Ann Arbor, Michigan, USA

    Josef Miller

  2. Dept of Speech , Lang & Hearing Sci, Univ of Florida Health Sciences Center, Gainesville, Florida, USA

    Colleen G. Le Prell

  3. Div . of Otolaryngology Head & Neck Surgery, SIU School of Medicine, Springfield, Illinois, USA

    Leonard Rybak

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Altschuler, R.A., Dolan, D. (2015). Basic Mechanisms Underlying Noise-Induced Hearing Loss. In: Miller, J., Le Prell, C., Rybak, L. (eds) Free Radicals in ENT Pathology. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Cham. https://doi.org/10.1007/978-3-319-13473-4_7

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