Résumé
Background: Speech intelligibility in quiet is critically dependent on the temporal envelope of a sound signal. An abnormal coding of this temporal cue (due to infectious, immune, genetic, tumoral or environmental of origin) implies a decrease of speech recognition scores. The current proxy to probe deafness in clinical framework (Compound Action Potential of the auditory nerve, auditory brainstem responses) uses simplistic stimuli (clicks, tone bursts) to detect a such abnormal coding of the temporal cues. The aim of this study was to develop a new electrophysiology method in murins able to measure the auditory nerve responses to amplitude-modulation stimuli.Material and methods: The electrophysiology response of the auditory nerve was recorded using an electrode implanted onto the round window niche on normal-hearing gerbil cochlea and aging rat cochlea. The acoustical stimuli consisted of 20 seconds sinusoidally amplitude-modulated noise-band centered on 4, 8 and 16 kHz. We have studied varying sound level, the modulation depth, the modulation frequency and the carrier frequency.Results: Our study on the selective fiber loss ouabain model show the mass potentials recorded at the round window enable the detection of low spontaneous rate fibers in gerbil auditory nerve. This result is important because the current clinical used tests aren’t enough sensitive to detect a such coding impairment (CAP, ABR) (Batrel, Huet, Hasselmann et al., 2017). Then we combined the stimulus of this previous study with a sinusoidal function to develop a new method to assess the envelope coding by the auditory nerve. We validated this new method. Last, we used our method on an aging model (Sprague-Dawley rat). Our results suggest aging leads to a phenotype change of auditory nerve fibers without associated fiber loss (article Occelli, Hasselmann et al, submitted to eNeuro).Conclusion: Our study shows it’s indispensable to expand the number of tools to probe the cochlea because the current clinical used tests aren’t enough sensitive to detect subtle deficits of encoding in the auditory nerve. The recording of the fiber sustained activity enable to detect the selective loss of low-spontaneous rate neurons. A such loss is undetectable with classical clinical tools. The phenotype change of fibers we observed in aging Sprague-Dawley rats is detectable with our method whereas it’s not using the compound action potential of the auditory nerve.