Enhancement of the medial olivocochlear system prevents hidden hearing loss

GÓMEZ CASATI, ME

Simposio; Closing the Auditory (Efferent) Loop III; 2018

Laboratorio de Neurobiología de la Audición de la Facultad de Medicina de la Universidad de Chile

Cochlear synaptopathy produced by exposure to noise levels which only cause transient auditory threshold elevations is a condition that affects many people and is believed to contribute to poor speech discrimination in noisy environments. These functional deficits in hearing, without changes in sensitivity, have been called hidden hearing loss (HHL). It has been proposed that activity of the medial olivocochlear (MOC) system can ameliorate acoustic trauma effects. Here we explore the role of the MOC system in HHL by comparing the performance of two different mouse models: an α9 nicotinic receptor subunit knock-out (Chrna9 KO) which lacks cholinergic transmission between efferent neurons and hair cells, and a gain of function knock-in (Chrna9L9?T KI) carrying an α9 point mutation that leads to enhanced MOC activity. Animals were exposed to sound pressure levels that in wild-type (WT) produced transient cochlear threshold shifts and a decrease in neural response amplitudes, together with the loss of ribbon synapses, indicative of cochlear synaptopathy. Moreover, a reduction in the number of efferent contacts to OHCs was observed. In Chrna9 KO ears, noise exposure produced permanent auditory threshold elevations together with cochlear synaptopathy. In contrast, the Chrna9L9?T KI was completely resistant to the same acoustic exposure protocol. These results show a positive correlation between the degree of HHL prevention and the level of MOC activity. Notably, enhancement of the MOC feedback promoted new afferent synapse formation, suggesting that it can trigger cellular and molecular mechanisms to protect and/or repair the inner ear sensory epithelium.