Effects of loud noise on the efferent system of the inner ear

BOERO L; GOUTMAN J; ELGOYHEN AB; GOMEZ CASATI ME

Congreso; XXIX Congreso Anual de la Sociedad Argentina de Investigación en Neurociencia; 2014

Noise induced hearing loss (NIHL) is a major hazard in society that leads to considerable communication problems for affected individuals. Despite several identified details about its etiology, the underlying mechanisms that induce NIHL have been only partially identified. Here, we intend to address the issue of NIHL and the role of the efferent olivocochlear system in this process. We made use of a murine model of enhanced noise protection, the Chrna9L9?T knock-in (KI), a mouse in which the α9 nicotinic receptor subunit bears a mutation and leads to enhanced medial efferent activity and a mouse model lacking the 9 subunit of the nicotinic receptor (Chrna9 knockout (KO)). We exposed WT, Chrna9L9?T KI and α9 KO mice to loud sounds (1-16 kHz, 100 dB SPL, 1hr) and measured auditory brainstem responses (ABR), which reflect synchronized discharges from neurons along the auditory pathway. We also tested outer hair cell function by recording the distortion product otoacoustic emissions (DPOAEs). Acoustic trauma produced large auditory threshold shifts in WT and Chrna9 KO mice the next day of exposure. However, one week after, thresholds returned to normal in WT whereas in the Chrna9 KO they did not recovered. In contrast, Chrna9L9?T KI mice were resistant to the same noise exposure. Suprathreshold ABR amplitudes were reduced in both WT and Chrna9 KO mice. Notably, they did not recover 1 week after exposure, suggesting an irreversible loss of cochlear nerve synapses. In contrast, Chrna9L9?T KI mice showed no changes following noise trauma. Finally, we used immunohistochemistry to visualize efferent neurons and found disorganized terminals after trauma. These findings will contribute to the understanding of how normal hair cell function is affected by loud noise and the role of the efferent system.