Noise exposure triggers changes in synptic function in mammalian hair cells

GÓMEZ-CASATI, MARÍA EUGENIA; RUTHERFORD, MARK A.; BOERO, LUIS EZEQUIEL; GOUTMAN, JUAN DIEGO

Villa Carlos Paz

Congreso; XXXIV Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; 2019

Sociedad Argentina de Investigación en Neurociencias

Noise-induced hearing loss has gained relevance as one of the most important sources of hearing loss. It has been shown that acoustic trauma (AT) producing only transient auditory threshold shifts also produces long-term reductions in the number of synapses between inner hair cells (IHCs) and afferent neurons. Here we intend to address if the capacity of IHCs to release neurotransmitter is altered after AT.Mice were exposed to loud sounds for 1 hour, and evaluated one day later for cochlear function. Exocytosis in IHC was tested by measuring changes in membrane capacitance (∆Cm) triggered by step depolarizations.IHCs from exposed WT mice displayed larger ∆Cm jumps compared to unexposed IHCs using short pulses at different voltages. Larger differences were found at the maximal release points in the curve. Also, exposed IHCs showed augmented ∆Cm with pulses of extended duration, longer than 100 ms. No differences in calcium entry between exposed and control cells 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 was observed in WT mice. These results suggest that AT potentiates vesicle release in IHC, possibly by accelerating vesicle recruitment, and this would be dependent upon the intense glutamate release.