Abstract
Noise-exposure at levels low enough to avoid a permanent threshold shift has been found to cause a massive, delayed degeneration of spiral ganglion neurons (SGNs) in mouse cochleae. Damage to the afferent innervation was initiated by a loss of synaptic ribbons, which is largely irreversible in mice. A similar delayed loss of SGNs has been found in guinea pig cochleae, but at a reduced level, suggesting a cross-species difference in SGN sensitivity to noise. Ribbon synapse damage occurs “silently” in that it does not affect hearing thresholds as conventionally measured, and the functional consequence of this damage is not clear. In the present study, we further explored the effect of noise on cochlear afferent innervation in guinea pigs by focusing on the dynamic changes in ribbon counts over time, and resultant changes in temporal processing. It was found that (1) contrary to reports in mice, the initial loss of ribbons largely recovered within a month after the noise exposure, although a significant amount of residual damage existed; (2) while the response threshold fully recovered in a month, the temporal processing continued to be deteriorated during this period.
Highlights
Noise exposure is the most common cause of sensorineural hearing loss (SNHL), which is one of the most common neurological disorders [1] in modern society
The effect of noise exposure on afferent innervation to the cochlea of guinea pigs was explored at two noise levels, and 105 dB SPL was found to be the maximal noise level that did not cause permanent threshold shift (PTS) for a brief exposure of 2 h
Corresponding to the compound action potential (CAP) recovery after 105 dB noise exposure, the noise induced damage on ribbon synapses appears to be largely reversible in guinea pigs, unlike in the cochleae of mice [2]
Summary
Noise exposure is the most common cause of sensorineural hearing loss (SNHL), which is one of the most common neurological disorders [1] in modern society. Similar noise exposure in guinea pigs was found to cause a similar delayed SGN death process, but on a much smaller scale [3] This SGN damage is ‘‘silent’’ in that it will not be detected by standard tests of auditory threshold. These reports suggest that ‘‘silent’’ SGN death is likely a common phenomenon in mammalian ears, but that quantitatively large cross-species differences may exist. This cross-species variation must be studied before extrapolation to humans is possible
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