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Key points Kv4 channels generate A‐type current known to regulate neuronal excitability. Its role in processing timing information is understudied, especially in the auditory system where temporal information is crucial for hearing. In the cochlear nucleus, principal bushy neurons are specialized for temporal processing with distinct biophysical properties owing to their expression of various voltage‐gated ion channels. Previous studies reported conflicting information regarding the expression and potential role of Kv4 channels in these neurons. We explored these questions using electrophysiology in CBA/CaJ mice of either sex. A‐type current was isolated from 88% of bushy neurons using Kv4 channel‐selective blocker Jingzhaotoxin‐X (JZ‐X), which increased the intrinsic excitability of bushy neurons without altering their synaptic input. During high‐rate activity, JZ‐X treatment significantly increased the spike jitter and reduced the firing threshold of bushy neurons. In old mice, A‐type current in bushy neurons reduced in magnitude but maintained current density, accompanied by decreased membrane surface area. In contrast, TEA‐sensitive Kv3 current reduced in both magnitude and current density, indicative of a greater contribution to the altered biophysical properties of bushy neurons during ageing. Our findings suggest that Kv4 channels play significant roles in regulating neuronal excitability and improving the temporal processing of bushy neurons. Such function is likely retained with age and is not the primary mechanism driving compromised temporal processing under age‐related hearing loss. Most bushy neurons of the cochlear nucleus exhibit Kv4‐mediated A‐type current. A‐type current regulates neuronal excitability of bushy neurons without contributing to the synaptic transmission at the endbulb of Held. A‐type current increases the firing threshold and improves the temporal precision of spikes in bushy neurons during high‐rate activity. A‐type current reduces peak amplitude in bushy neurons during ageing but maintains current density. Decreased Kv3 current, rather than Kv4 current, likely play more significant roles in altering the biophysical properties of bushy neurons during ageing, contributing to compromised temporal processing during age‐related hearing loss. [ABSTRACT FROM AUTHOR]

• Different subtypes of AN synapses converge onto individual CN neurons. • Non-type Ia synapses preferentially degenerate during aging. • Bushy neurons also differentially degenerate during ARHL with compromised output. • Reduced input to d -stellate neurons contributes to weakened inhibition in the CN. Sound information is transduced from mechanical vibration to electrical signals in the cochlea, conveyed to and further processed in the brain to form auditory perception. During the process, spiral ganglion neurons (SGNs) are the key cells that connect the peripheral and central auditory systems by receiving information from hair cells in the cochlea and transmitting it to neurons of the cochlear nucleus (CN). Decades of research in the cochlea greatly improved our understanding of SGN function under normal and pathological conditions, especially about the roles of different subtypes of SGNs and their peripheral synapses. However, it remains less clear how SGN central terminals or auditory nerve (AN) synapses connect to CN neurons, and ultimately how peripheral pathology links to structural alterations and functional deficits in the central auditory nervous system. This review discusses recent progress about the morphological and physiological properties of different subtypes of AN synapses and associated postsynaptic CN neurons, their changes during aging, and the potential mechanisms underlying age-related hearing loss. [ABSTRACT FROM AUTHOR]