Abstract
While exposure to high levels of noise damages the sensory hair cells of the organ of Corti and causes permanent hearing loss; exposure to moderate levels of noise leads to temporary hearing loss. However, although temporary, this deafness can be accompanied by a synaptic disconnection between the sensory hair cells and the auditory nerve fibers. Once disconnected from the sensory cells, the auditory fibers can no longer communicate acoustic information to the central nervous system and ultimately degenerate. Surprisingly, the proportion of disconnected auditory fibers can reach more than 50% without affecting hearing thresholds, but speech understanding in a noisy background is compromised. As these damage to the auditory nerve does not cause an increase in hearing thresholds, it cannot be detected by a standard audiometric testing, so this condition has been termed a "hidden" hearing loss.Most of the studies conducted on hidden hearing loss have used noise exposure paradigms that are very different from the exposure conditions that patients face in their daily life. Exposure to non-fluctuating, stable frequency, narrowband noise for several hours is rare in personal and professional settings. The transient impulse noise encountered during certain professional and leisure activities (explosions, firearms, industrial or construction machines and tools...) are particularly dangerous for hearing.The objective of my thesis was to determine whether an impulse noise mimicking the detonation of a gunshot could cause a temporary threshold shift associated with hidden hearing loss. To do so, we developed an impulse noise exposure paradigm to induce a temporary threshold shift in mice. We were able to demonstrate that exposure to impulse noise (145 dB SPL peak, 700 impulses, 1 impulse/second) caused an acute mean increase in auditory thresholds of 30 dB shortly after exposure. After 2 weeks, the hearing thresholds returned to their initial levels except for the most apical cochlear regions where a slight threshold shift persisted.Despite the recovery of auditory thresholds, ABR wave I amplitudes were permanently reduced, indicating a loss of synapses between the inner hair cells and the auditory nerve fibers. We also observed damages to the stereocilia of the outer hair cells, mainly in the apical region of the cochlea, which could explain the permanent increase in low-frequency hearing thresholds. Quantification of auditory synapses revealed moderate but reversible synaptic loss in the basal part of the cochlea. The evolution of the ribbon’s spatial organization as well as their ultrastructures disturbed by impulse noise exposure revealed a partial and incomplete repair of these structures 2 weeks after exposure. We observed an increase in oxidative stress in the cochlea following impulse noise exposure. Finally, an increase in the acoustic startle response was also observed in some noise-exposed animals suggesting the occurrence of hyperacusis.Altogether, these results demonstrate that impulse noise, like continuous noise, can cause a "hidden" hearing loss in the basal part of the cochlea and that exposure to impulse noise at moderate levels could have long-term consequences on auditory perception and speech intelligibility in noise.