Abstract
Hidden hearing refers to the functional deficits in hearing without deterioration in hearing sensitivity. This concept is proposed based upon recent finding of massive noise-induced damage on ribbon synapse between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in the cochlea without significant permanent threshold shifts (PTS). Presumably, such damage may cause coding deficits in auditory nerve fibers (ANFs). However, such deficits had not been detailed except that a selective loss of ANFs with low spontaneous rate (SR) was reported. In the present study, we investigated the dynamic changes of ribbon synapses and the coding function of ANF single units in one month after a brief noise exposure that caused a massive damage of ribbon synapses but no PTS. The synapse count and functional response measures indicates a large portion of the disrupted synapses were re-connected. This is consistent with the fact that the change of SR distribution due to the initial loss of low SR units is recovered quickly. However, ANF coding deficits were developed later with the re-establishment of the synapses. The deficits were found in both intensity and temporal processing, revealing the nature of synaptopathy in hidden hearing loss.
Highlights
Time points after such a no-permanent threshold shift (PTS) noise exposure in guinea pigs
Similar to our previous reports[3,4], a brief exposure to a broadband noise at 105 dB SPL produced a significant temporal threshold shift (TTS) of moderate degree as tested in the audiogram of auditory brainstem responses (ABR) at 1 day post noise (1DPN); no significant difference in ABR thresholds was seen between the control and those tested at 1 week and 1 month post noise (1WPN and 1MPN, Supplementary Fig. 1), suggesting that the noise exposure did not cause a PTS
In addition to the total recovery of ABR threshold, there was a total recovery in distortion product of otoacoustic emission (DPOAE, sFig. 2), suggesting a virtually total recovery of outer hair cell (OHC) function
Summary
Time points after such a no-PTS noise exposure in guinea pigs. We found that the number of synapses (verified in immunohistology staining against presynaptic ribbons and postsynaptic terminals) are largely recovered following a massive initial reduction[3,4]. Functional deterioration in signal processing, especially the temporal processing ability appeared at later phase (towards one month after the noise) when the ribbon synapse numbers were largely recovered. This result suggested that the repaired synapses are functionally abnormal. We investigated the dynamic changes of coding activities of single ANF units after a no-PTS noise exposure that was similar to what was utilized in in our previous studies[3,4]. The repaired synapses are functionally abnormal in both intensity and temporal coding
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