Noise-induced hearing loss has gained relevance as one of the most important sources of hearing loss. Acoustic trauma (AT) can alter auditory function and reduce the number of synapses between inner hair cells (IHCs) and afferent neurons but less is known about its impact in the ability of IHCs to signal auditory information. Here we intend to address if the capacity of IHCs to release neurotransmitter is altered after AT.
Auditory function tests and confocal imaging confirmed that one day after exposure to a 120 dB noise for 1 hour, mice displayed elevated hearing thresholds and a reduction in the number of synapses per IHC. We measured changes in membrane capacitance (∆Cm) triggered by step depolarizations as a proxy of IHC exocytosis. IHCs from noise-exposed mice displayed larger ∆Cm jumps compared to unexposed IHCs. Using depolarizations of increasing duration, we found larger Cm for pulses longer than 100 ms. No differences in calcium entry were observed for any of the applied depolarizations. To determine if this potentiated release was triggered by glutamate released during AT and acting retrogradely, we made use of the vesicular transporter vGluT3 knock-out (KO) mouse. Exposed KO showed reduced ∆Cm compared to controls, in contrast to what has been observed in WT mice. These results suggest that AT enhances vesicle release in IHC, possibly by accelerating vesicle recruitment, and this would be dependent upon the intense glutamate release.