![]() Hair cell damage can be visible within minutes after overexposure, and hair cell death can continue for days ( Wang et al., 2002). Hair cells normally transduce sound-evoked mechanical motion into receptor potentials, which lead to transmitter release at their glutamatergic synapses with cochlear afferent fibers (see Fig. Permanent NIHL is due to destruction of cochlear hair cells or damage to their mechano-sensory hair bundles ( Liberman and Dodds, 1984). Thresholds may fully recover (“temporary” threshold shift) or stabilize at an elevated value (“permanent” threshold shift). After overexposure, NIHL recovers with an exponential time course ( Miller et al., 1963) for 2–3 weeks, depending on initial severity. Noise-induced hearing loss (NIHL) is a major health problem ( DHHS, 2009), because opportunities for overexposure abound, and exposures that damage hearing are not necessarily painful or even annoying. This primary neurodegeneration should add to difficulties hearing in noisy environments, and could contribute to tinnitus, hyperacusis, and other perceptual anomalies commonly associated with inner ear damage. Results suggest that noise-induced damage to the ear has progressive consequences that are considerably more widespread than are revealed by conventional threshold testing. Here, we show, using cochlear functional assays and confocal imaging of the inner ear in mouse, that acoustic overexposures causing moderate, but completely reversible, threshold elevation leave cochlear sensory cells intact, but cause acute loss of afferent nerve terminals and delayed degeneration of the cochlear nerve. ![]() Postexposure recovery of threshold sensitivity has been assumed to indicate reversal of damage to delicate mechano-sensory and neural structures of the inner ear and no persistent or delayed consequences for auditory function. Overexposure to intense sound can cause temporary or permanent hearing loss.
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