Research PaperTime course of organ of Corti degeneration after noise exposure
Introduction
Excessive exposure to noise is a common phenomenon for members of the military (e.g., Humes et al., 2005), workers in industries such as mining and manufacturing (e.g., McBride, 2004) as well as people engaged in typical activities of everyday life (e.g., Flamme et al., 2012, Le Prell et al., 2012). Excessive exposure to noise results in the degeneration of cells in the inner ear and may lead to the development of a permanent hearing loss (PTS). Noise effects on hearing and the inner ear have been studied in depth since World War II in humans (e.g., Ward and Glorig, 1961, Taylor et al., 1965, Bredberg, 1968, Mills et al., 1970, Melnick, 1976, Humes et al., 2005) and in experimental animals (e.g., Hawkins et al., 1943; Davis and Associates, 1953, Bohne, 1976a, Bohne, 1976b, Bohne, 1976c, Liberman and Kiang, 1978, Wang et al., 2002, Chen and Fechter, 2003).
From such studies, important information has been obtained including species differences and how the pattern and magnitude of damage change as a function of frequency, intensity and duration of the noise exposure. However, despite the extensive history of noise research, certain fundamental questions remain such as 'when is degeneration of hair cells (HCs) and supporting cells (SCs) completed after a damaging noise exposure?' For compensatory and therapeutic purposes, it is important to determine when hearing loss has stabilized and when cells in the organ of Corti (OC) have stopped degenerating as a result of the exposure. The present study was conducted to address this latter question.
Section snippets
Data set
From our permanent collection of plastic-embedded flat preparations of the chinchilla's cochlea, 22 controls and 199 ears exposed to an octave band of noise (OBN) with a center frequency of 0.5 or 4 kHz met our requirements for determining when OC degeneration and re-epithelization of the basilar membrane (BM) were completed. The main requirement for the exposed ears was that they have a wide range of postexposure survivals before fixation so that the time(s) for stabilization of HC and SC
Controls
This group had 22 ears from 20 animals. The apex-to-base median loss of OHCs and IHCs was 0.9% and 0.35% and the median loss plus one quartile was 1.3% and 0.7%, respectively. Five ears had 1–3 focal IHC lesions in the apical or basal half of the OC, ranging in length from 0.03 to 0.11 mm. MNF degeneration was noted medial to the 0.11-mm lesion (10% loss, dieback - code 1). Median OP and IP losses plus one quartile were 3 and 2, respectively. There were no OC WOs or regions of stria-vascularis
Noise-induced degeneration of HCs
All degeneration from a particular noise exposure is not completed in ears having short postexposure survivals (e.g., Bohne, 1971, Fredelius, 1988). Our data showed that a variable number of OHCs die by one h postexposure (see Fig. 11), with many OHCs in the maximally stimulated area dying nearly simultaneously. In contrast, IHCs die in much smaller #s initially. The death of IHCs was spread out over days to months postexposure (e.g., compare cytocochleograms in Fig. 11, Fig. 12, Fig. 13,
Conclusions
All OC degeneration from a particular noise is not completed in ears with short postexposure survivals. Analysis of our data showed that a # of HCs and SCs died days to months postexposure. To our knowledge, this is the first study to demonstrate quantitatively the delayed and continuing cell and nerve fiber degeneration which occurs after termination of a damaging noise exposure.
OHCs were the first cells to degenerate from noise. Generally, this degeneration began during the exposure and
Recommendations
- 1.
Researchers who study death pathways in noise-damaged ears have used short postexposure survivals (e.g., Hu et al., 2000, Hu et al., 2006, Bohne et al., 2007). Short postexposure times are suitable for studying death pathways in OHCs only. To study death pathways in IHCs, OPs, IPs and DCs, longer postexposure survival times must be employed.
- 2.
Because much noise-induced loss of IHCs, OPs and IPs occurs gradually over weeks to months postexposure, researchers should test pharmacological agents at
Acknowledgments
Exposure of the chinchillas to noise, and fixation, embedment, dissection and analysis of their cochleae for HC loss was supported from 1970 to 2013 by the Department of Otolaryngology, Washington University School of Medicine, and by grants from the NIH, NIOSH, and NOHR. The current study is based on an analysis of cell losses and an assessment of SC pathology in some of the previously fixed and dissected ears.
Sincere thanks to Mr. Valentin Militchin for writing and trouble-shooting the CYTOS
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