Abstract
Recent studies demonstrated that reversible continuous noise exposure may induce a temporary threshold shift (TTS) with a permanent degeneration of auditory nerve fibers, although hair cells remain intact. To probe the impact of TTS-inducing impulse noise exposure on hearing, CBA/J Mice were exposed to noise impulses with peak pressures of 145 dB SPL. We found that 30 min after exposure, the noise caused a mean elevation of ABR thresholds of ~30 dB and a reduction in DPOAE amplitude. Four weeks later, ABR thresholds and DPOAE amplitude were back to normal in the higher frequency region (8–32 kHz). At lower frequencies, a small degree of PTS remained. Morphological evaluations revealed a disturbance of the stereociliary bundle of outer hair cells, mainly located in the apical regions. On the other hand, the reduced suprathreshold ABR amplitudes remained until 4 weeks later. A loss of synapse numbers was observed 24 h after exposure, with full recovery two weeks later. Transmission electron microscopy revealed morphological changes at the ribbon synapses by two weeks post exposure. In addition, increased levels of oxidative stress were observed immediately after exposure, and maintained for a further 2 weeks. These results clarify the pathology underlying impulse noise-induced sensory dysfunction, and suggest possible links between impulse-noise injury, cochlear cell morphology, metabolic changes, and hidden hearing loss.
Highlights
Noise-induced hearing loss (NIHL) acquired in leisure or occupational settings is a common cause of hearing impairment in industrialized countries, with a prevalence second only to age-related hearing loss (ARHL) [1,2]
Our results showed that 30 min after exposure, mice displayed an elevation of Auditory Brainstem Response (ABRs) thresholds of ≥30 dB for all frequencies (Figure 2A)
Synapses ning To electron microscopy (SEM), which allows the visualization surface of the organ determine the contribution of the loss of ribbon synapses of in the impulse noise-induced of Twenty-four hours after exposure, disturbance of stereocilial morphology reduction of ABR wave-I amplitudes at suprathreshold levels, we examined IHCswas by observed mainlypresynaptic in outer hairand cells located in the regions coding frequencies from 4 to double-labeling postsynaptic structures and 3Dthe confocal imaging analy16 [40]
Summary
Noise-induced hearing loss (NIHL) acquired in leisure or occupational settings is a common cause of hearing impairment in industrialized countries, with a prevalence second only to age-related hearing loss (ARHL) [1,2]. This temporary loss is known as a temporary threshold shift (TTS), and is probably due to reversible damage to the stereocilia of hair cells [5] and/or swelling, followed by recovery, of cochlear nerve terminals [6,7]. Some recent studies demonstrated that TTS exposure may cause the loss of more than 50% of the synapses that lie between the cochlear nerve fibers and inner hair cells (IHCs), without hair-cell damage and without alteration in hearing thresholds [8,9]. This selective synaptopathy occurring after noise exposure was named “hidden hearing
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