Auditory deficits: From bench to bedside

GÓMEZ CASATI, ME

Congreso; Congreso anual de la Sociedad de Neurociencias; 2022

The main goal of our laboratory is to increase the knowledge on the consequences of different forms of hearing loss on the normal function of hair cells in the mammalian organ of Corti and to study the role of the medial olivocochlear system (MOC). Noise and aging are the two most common causative factors among the defined etiologies of hearing loss. The clinical significance presented by noise-induced (NIHL) and age-related hearing loss (ARHL) has driven efforts to understand the underlying molecular, physiological and biochemical mechanisms of the cochlear damage. Knowing how the physical structures are affected by noise and/or age is crucial in search for therapeutic agents that act as otoprotectants against hearing loss. In the last 5 years, my lab has been trying to understand the role of the MOC system in protecting the inner ear from damage produced by overly loud sounds and this will be the focus of my talk. We have shown an inverse correlation between the activity of the alpha9alpha10 nAChR and noise-induced cochlear synaptopathy. Moreover, we have shown that the MOC system mediates resistance to ARHL – presbycusis, and that this occurs via the alpha9alpha10 nAChR complexes on OHCs. These results suggest that potentiation of the MOC feedback can trigger cellular and molecular mechanisms to protect and/or repair the inner ear sensory epithelium. These findings are beginning to bridge the gap from bench to clinics as they provide the first proof-of-principle supporting the enhancement of the MOC system as a viable approach for prevention or treatment of NIHL and/or ARHL.