V-107
Sensory and Motor Systems
Role of the Medial Olivocochlear System in Sound Hypersensitivity
Joaquín Gigena2,4, Amanda Lauer3, Ana Belén Elgoyhen1, María Eugenia Gómez-Casati2, Jimena Ballestero2
1. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Dr. Héctor N. Torres, Consejo Nacional de Investigaciones Científicas y Técnicas, CABA, Argentina.
2. Instituto de Farmacología, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina y Consejo Nacional de Investigaciones Científicas y Técnicas, Argentina.
3. Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine; Baltimore, Maryland, United States.
4. Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, CABA, Argentina.
Presenting Author:
joacogghh@gmail.com
Noise-induced auditory disorders represent a significant global health concern, with hyperacusis—an intolerance to everyday sound levels—constituting a particularly challenging condition. Hyperacusis is thought to result from maladaptive plasticity within the central auditory system, whereby a compensatory increase in neural gain exaggerates sound-evoked responses, often following peripheral auditory damage. The mammalian auditory system possesses an endogenous protective mechanism known as the medial olivocochlear (MOC) reflex. In the organ of Corti, the neurosensory epithelium of the auditory system, inner hair cells (IHCs) transduce auditory signals, whereas outer hair cells (OHCs) mechanically amplify sound-induced vibrations. The MOC efferent system projects directly to OHCs and, when activated by sound, inhibits their amplifying activity. This reflex is considered an important mechanism for protecting the cochlea from acoustic trauma. The aim of this project was to investigate the role of the MOC system in hyperacusis. Using the auditory startle response as a behavioral assay, we evaluated sound sensitivity in wild-type mice and in genetically modified mouse lines that either lack MOC efferent activity (α9 KO) or exhibit enhanced MOC efferent activity (α9 KI).
