Remodeling of Cochlear Efferent Innervation Following Noise Exposure

Noise-induced hearing loss is one of the leading causes of sensory disability worldwide. Exposure to intense sounds damages cochlear sensory hair cells and their synaptic contacts with the auditory nerve. The activity of these cells is modulated by the olivocochlear efferent system, which originates in the brainstem. Numerous studies suggest that this system contributes to protecting the cochlea from acoustic trauma. The efferent system has been shown to undergo alterations in animal models of hearing loss caused by aging or genetic mutations that impair mechanotransduction. These alterations include changes in synaptic targets and ion channel expression, suggesting a reversion to an early developmental state. Whether these changes are a consequence of cochlear damage or represent a protective response remains an open question. Here, we investigated whether noise exposure similarly induces efferent plasticity in C57BL/6J mice, a strain highly susceptible to noise-induced damage. Mice were exposed to intense noise, and auditory brainstem responses were recorded one day before, one day after, and one week after acoustic trauma to monitor auditory function. One week after acoustic trauma, cochlear tissue was collected and processed for immunohistochemistry. Efferent innervation and ion channel expression were examined to characterize noise-induced changes in the olivocochlear system.