Abstract
Noise exposure at low levels or low doses can damage hair cell afferent ribbon synapses without causing permanent threshold shifts. In contrast to reports in the mouse cochleae, initial damage to ribbon synapses in the cochleae of guinea pigs is largely repairable. In the present study, we further investigated the repair process in ribbon synapses in guinea pigs after similar noise exposure. In the control samples, a small portion of afferent synapses lacked synaptic ribbons, suggesting the co-existence of conventional no-ribbon and ribbon synapses. The loss and recovery of hair cell ribbons and post-synaptic densities (PSDs) occurred in parallel, but the recovery was not complete, resulting in a permanent loss of less than 10% synapses. During the repair process, ribbons were temporally separated from the PSDs. A plastic interaction between ribbons and postsynaptic terminals may be involved in the reestablishment of synaptic contact between ribbons and PSDs, as shown by location changes in both structures. Synapse repair was associated with a breakdown in temporal processing, as reflected by poorer responses in the compound action potential (CAP) of auditory nerves to time-stress signals. Thus, deterioration in temporal processing originated from the cochlea. This deterioration developed with the recovery in hearing threshold and ribbon synapse counts, suggesting that the repaired synapses had deficits in temporal processing.
Highlights
Noise exposure at relatively low levels or doses has been found to cause ‘‘silent’’ damage to the afferent cochlear innervation [1,2,3]
Instead of observing the auditory brainstem responses (ABRs), we focused on cochlear responses by measuring the compound action potential (CAP) to time-stress signals
Damage to and repair of afferent innervation to inner hair cells (IHC) Frequency-specific ABRs showed a clear threshold elevation across the whole frequency range tested at 1 DPN and a total recovery at 1 WPN, as reported previously [2]
Summary
Noise exposure at relatively low levels or doses has been found to cause ‘‘silent’’ damage to the afferent cochlear innervation [1,2,3]. It has been called ‘‘silent’’ damage because the noise exposure does not cause a permanent threshold shift in hearing, which is currently the major criterion for noise-induced hearing loss and noise safety standards In both mice and guinea pigs, noise exposure can cause massive damage in the ribbon synapses between inner hair cells (IHC) and type I spiral ganglion neurons (SGN) [1,2,3]. The temporal processing resolution of the auditory system, as tested with paired click-evoked auditory brainstem responses (ABRs), deteriorated in guinea pigs within a month after noise exposure, while the hearing threshold recovered fully during this period [2] These results suggest a clear cross-species difference in the repair process around the ribbon synapses, and that the repaired synapses are not fully functionally intact. We observed the damage and the repair of ribbon synapses at both pre- and post-synaptic sites in an attempt to provide insight into the plastic changes to the ribbon synapses during the repair process
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