Changes of Hair Cell Stereocilia and Threshold Shift after Acoustic Trauma in Guinea Pigs: Comparison between Inner and Outer Hair Cells

Abstract

The vulnerability of inner hair cells (IHCs) and outer hair cells (OHCs) to acoustic overstimulation is still controversially discussed. The present study was undertaken to investigate the vulnerability of IHCs and OHCs and the relation between chronological changes of auditory threshold shifts and stereocilia damages on IHCs and OHCs in guinea pigs after moderate acoustic trauma, caused by a single continuous exposure to pink noise (20 Hz to 20 kHz) of around 106 ± 2 dB SPL for 44 h. Stereocilia changes and threshold shifts of auditory brainstem responses (ABR) were assessed at regular intervals after noise exposure for 9 weeks. Scanning electron microscopy demonstrated the morphological changes of steriocilia as early as 1 day after noise exposure. The morphological changes included fused, bent, collapsed, and even missing stereocilia. These damages were more prominent on IHCs than on OHCs. The shift of ABR threshold was not parallel to the chronological change of the stereocilia on IHCs as well as OHCs. The elevation of the ABR threshold (40–60 dB SPL) was greatest on the 1st day after noise exposure, whereas the stereocilia showed the most damage 7 days after noise exposure. Combined with the results from previous studies, we conclude that moderate-level (around 105–110 dB) noise tends to induce more damage to the stereocilia of IHCs than of OHCs. Other damage (e.g., metabolic disturbance) than morphological damage of hair cell stereocilia may contribute partially to the hearing threshold shift induced by moderate acoustic overstimulation.

A behavioral measure of the cochlear changes underlying temporary threshold shifts

“…This may indicate temporary morphological changes to IHCs, such as tip link and MET ion channel dysfunction, causing a reduction in IHC transduction and a concurrent loss of sensitivity. This is consistent with morphological studies (Chen et al, 2003). However, as testing for the present study occurred at least 15 min post-exposure, this mechanism is probably not the cause of the TTS observed in the present study.…”

Hair cell counts in a rat model of sound damage: Effects of tissue preparation & identification of regions of hair cell loss

“…The dendritic terminals that make contact with IHC have been shown to swell in regions with CFs greater than or equal to the frequency of the damaging stimulus[2, 23]. Stereocilia can also be immediately damaged in specific frequency regions, although studies on this topic are in conflict showing exclusively IHC[24], exclusively OHC[25], or a mixture of IHCs and OHCs[6] being damaged in the area of maximal basilar membrane displacement. Lateral wall pathology has also been observed in discrete regions as a result of acoustic trauma[15].…”

“…Damage to the sensory hair cells in the auditory periphery manifests functionally as noise-induced hearing loss (NIHL) [4, 5]. Hyperacusis and tinnitus can also occur as the result of peripheral or central damage and remodeling [6, 7]. The relationship between hair cell (HC) damage and subsequent manifestations of auditory pathology is complex[8], and HC lesions alone do not always provide a sufficient explanation for any resulting functional pathology post sound-exposure.…”

The possible impact of noise-induced Ca 2+ -dependent activity in the central auditory pathway: A manganese-enhanced MRI study

“…Furthermore, partly irreversible peripheral effects after moderate noise exposure have been reported at the level of inner and outer hair cells in different species (Bohne et al, 2007;Chen et al, 2003;Clark and Pickles, 1996;Nordmann et al, 2000;Vazquez et al, 2001). A dramatic loss of synaptic connections at the ribbon synapses between IHCs and the spiral ganglion neurons without changes in auditory threshold was found after an acute 100 dB-exposure in mice.…”