Noise-Induced Hearing Loss Enhances Ca2+-Dependent Electrical Activity in Lateral Cochlear Efferents.

Exposure to loud and/or prolonged noise damages the cochlea and triggers downstream brain changes, resulting in hearing loss and altered speech comprehension. It remains unclear however whether noise exposure also compromises the cochlear efferent system; a feedback pathway originates in the brain that fine-tunes hearing sensitivity in the cochlea. Recent evidence suggests that lateral olivocochlear (LOC) efferent system supports hearing recovery by sustaining auditory nerve activity for several weeks after acoustic trauma (Sitko et al., 2025); however, the underlying neural mechanisms have not been fully elucidated. To address this gap, we examined the long-term effects of noise-induced hearing loss (NIHL) on the spontaneous action potential (AP) firing pattern in mouse LOC neurons of either sex. Under normal conditions, these neurons display a characteristic burst firing pattern driven by Ca2+ channel-mediated membrane voltage oscillations. One week following noise exposure, hearing thresholds were significantly elevated, and the duration of AP bursts was increased, as a result of an enhanced Ca2+ current. Moreover, LOC neurons exhibit Ca2+-dependent inactivation (CDI) of Ca2+ currents-a key process that shapes the duration of voltage oscillations-whose properties were also modified following noise exposure. Interestingly, our data suggest that the interplay between Ca2+ channel activation, CDI, and outward leak currents is sufficient to sustain the oscillating behavior of LOC neurons. We propose that NIHL increases efferent activity, thereby enhancing the release of neurotransmitters and neuropeptides, which may support long-lasting restoration of sensory coding in the damaged cochlea.