Auditory efferent feedback system deficits precede age‐related hearing loss: Contralateral suppression of otoacoustic emissions in mice

Abstract

The C57BL/6J mouse has been a useful model of presbycusis, as it displays an accelerated age-related peripheral hearing loss. The medial olivocochlear efferent feedback (MOC) system plays a role in suppressing cochlear outer hair cell (OHC) responses, particularly for background noise. Neurons of the MOC system are located in the superior olivary complex, particularly in the dorsomedial periolivary nucleus (DMPO) and in the ventral nucleus of the trapezoid body (VNTB). We previously discovered that the function of the MOC system declines with age prior to OHC degeneration, as measured by contralateral suppression (CS) of distortion product otoacoustic emissions (DPOAEs) in humans and CBA mice. The present study aimed to determine the time course of age changes in MOC function in C57s. DPOAE amplitudes and CS of DPOAEs were collected for C57s from 6 to 40 weeks of age. MOC responses were observed at 6 weeks but were gone at middle (15-30 kHz) and high (30-45 kHz) frequencies by 8 weeks. Quantitative stereological analyses of Nissl sections revealed smaller neurons in the DMPO and VNTB of young adult C57s compared with CBAs. These findings suggest that reduced neuron size may underlie part of the noteworthy rapid decline of the C57 efferent system. In conclusion, the C57 mouse has MOC function at 6 weeks, but it declines quickly, preceding the progression of peripheral age-related sensitivity deficits and hearing loss in this mouse strain.

Effects of age and background noise on processing a mistuned harmonic in an otherwise periodic complex sound

“…Animal studies have shown that aging impairs inhibitory processes in the dorsal cochlear nucleus (Caspary et al, 2005). In humans, distortion product otoacoustic emissions are reduced when white noise is presented to the contralateral ear (Berlin et al, 1993;Chery-Croze et al, 1993;Moulin et al, 1992;Williams et al, 1994), and this contralateral suppression has been found to weaken with increasing age (Keppler et al, 2010;Kim et al, 2002;Yilmaz et al, 2007;Zhu et al, 2007). This lack of suppression is consistent with reduced inhibitory control from the medial olivocochlear system on the outer hair cells which could also influence the amplitude and latency of cortical evoked responses.…”

Tinnitus with a Normal Audiogram: Physiological Evidence for Hidden Hearing Loss and Computational Model

“…This suggests that deafferentation following noise damage predominantly affects high-threshold AN fibers, while sufficient numbers of low-threshold AN fibers remain responsive to sound. Normal hearing thresholds can also be accompanied by impaired function of efferent fibers that project from the brainstem to the cochlea (Kim et al, 2002;Jacobson et al, 2003;Zettel et al, 2007;Zhu et al, 2007).…”

Sound-Evoked Olivocochlear Activation in Unanesthetized Mice

“…The functional status of MOC efferents has been noninvasively assayed in many other mammals through measurement of the MOC reflexes in which the amplitude of otoacoustic emissions are modulated upon sound presentation to the contralateral or ipsilateral ear (Boyev et al 2002;Harrison et al 2008;Henin et al 2011;Moulin et al 1993). However, reduced otoacoustic emission amplitudes following contralateral acoustic stimulation (CAS) in mice have only been reported by one group Zhu et al 2007), and the role of the MOC system rather than other feedback systems such as the middle ear muscle reflex has not been directly demonstrated. In addition, olivocochlear reflex strength in mice has only been studied under anesthesia, a condition likely to reduce the excitability of MOC neurons, thereby interfering with the MOC-mediated inhibition of OHCs (Avan et al 1996;Boyev et al 2002;Guitton et al 2004;Kujawa and Liberman 2001;Liberman and Brown 1986).…”