Rita Yammine
Research Mentor: Gabriel Corfas
Mentor Department: Kesge Hearing Research Institute, Medicine
Author(s): Rita Yammine, Luis Cassinotti, Deepika Tripu, Beatriz Borges, Colin Greineder, Peter Tessier, Gabriel Corfas
Session: Session 7 (4:00 PM – 4:50 PM)
Presentation Type: Poster 5
Abstract
Hearing loss is prevalent among military personnel due to frequent exposure to high levels of noise during training and operational activities. This noise-induced hearing loss (NIHL) results from disruptions in the structure and function of the organ of Corti, the part of the inner ear responsible for transducing sounds into neuronal signals. Depending on their level, duration, and recurrence, noise exposures cause varying degrees of organ of Corti injury, with milder exposures leading to the loss of synapses between spiral ganglion neurons (SGNs) and inner hair cells (IHCs), whereas greater exposures destroy hair cells. Unfortunately, either the loss of IHC synapses or of IHCs eventually leads to SGN loss, resulting in permanent hearing loss that cannot be treated even with cochlear implants. Thus, treatments that induce IHC synapse protection or regeneration and/or promote SGN survival after noise exposure could help millions of active military and veterans preserve their hearing. The tyrosine kinase receptors TrkB and TrkC and their ligands, the neurotrophins BDNF and Ntf3, are essential for the development and survival of vestibular and cochlear sensory neurons during embryogenesis. Our lab has also demonstrated that Neurotrophin/Trk signaling regulates hair cell ribbon-synapse formation in the neonatal cochlea and vestibular epithelia. Furthermore, studies in rodent models suggest that neurotrophins could serve as treatments for NIHL, slow age-related hearing loss. In this work, we test the hypothesis that induction of TrkB signaling in the inner ear after military-relevant noise exposures via IV administration of TrkB agonist antibodies protects against NIHL and the loss of IHC synapses.
