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Age-related hearing loss (ARHL) is largely attributed to structural changes and functional declines in the peripheral auditory system, which include synaptopathy at the inner hair cell/spiral ganglion cell (SGC) connection and the loss of SGCs. However, functional changes at the central terminals of SGCs, namely the auditory nerve synapses in the cochlear nucleus, are not yet fully understood during ARHL. With the use of young (1–3 mo) and old (25–30 mo) CBA/CaJ mice, this study evaluated the intrinsic properties of the bushy neurons postsynaptic to the endbulb of Held synapses, and the firing properties of these neurons to direct current injections as well as to synaptic inputs from the auditory nerve. Results showed that bushy neurons in old mice are more excitable and are able to fire spikes at similar rate and timing to direct current injections as those in young mice. In response to synaptic inputs, however, bushy neurons from old mice fired spikes with significantly decreased rate and reduced temporal precision to stimulus trains at 100 and 400 Hz, with the drop in firing probability more profound at 400 Hz. It suggests that transmission of auditory information at the endbulb is declined in both rate and timing during aging, which signifies the loss of sensory inputs to the central auditory system under ARHL. The study proposes that, in addition to damages at the peripheral terminals of SGCs as well as the loss of SGCs, functional decline at the central terminals of surviving SGCs is also an essential component of ARHL.

Transmission of auditory sensory information decreases in rate and temporal precision at the endbulb of Held synapse during age-related hearing loss