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

BOERO, L; GOUTMAN, JD; ELGOYHEN, AB; GÓMEZ CASATI, ME

Huerta Grande, Cordoba

Congreso; Reunión Anual de la Sociedad Argentina de Neurociencia; 2014

Sociedad Argentina de Neurociencias

Noise induced hearing loss (NIHL) is a major hazard in society. Despite several identified details about its etiology, the underlying mechanisms that induce NIHL have been only partially identified. Here, we intend to address the role of the efferent olivocochlear system in NIHL. We made use of a murine model of enhanced noise protection, the Chrna9L9'T knock-in (KI), a mouse in which the alpha9 nicotinic receptor subunit bears a mutation and leads to enhanced medial efferent activity and a mouse model lacking the alpha9 subunit of the nicotinic receptor (Chrna9 knockout (KO)). We exposed mice to noise 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. Acoustic trauma produced large auditory threshold shifts in WT and Chrna9 KO mice one day after exposure. However, one week later, thresholds returned to normal in WT, whereas in the Chrna9 KO they did not recover. 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. We used immunohistochemistry to visualize efferent neurons and found disorganized terminals after trauma.