Impacts of Kv3.1 Channels on Action Potentials in Fusiform Neurons From the Dorsal Cochlear Nucleus of Mice Before and After Hearing Onset

Abstract Purpose Kv3.1 channels are high-voltage-activated potassium channels that facilitate high-frequency firing in auditory brainstem neurons. Fusiform neurons in the dorsal cochlear nucleus (DCN) can fire rapid trains of action potentials and express Kv3.1 channels. Their ability to fire high-frequency action potential trains increases after hearing onset at postnatal day 14. Simultaneously, the action potentials become shorter and faster. We tested whether Kv3.1 channels drive the developmental maturation of action potentials in DCN fusiform neurons. Methods We used Swiss female mice from postnatal day 8 to 25 and divided them into pre-hearing (< P14) and post-hearing (> P14). We measured Kv currents and action potentials in whole-cell patch-clamp. Tetraethylammonium (TEA) was applied at a concentration of 1–5 mM to block Kv3 channels, and we detected the expression of Kv3.1b channel subunits by immunocytochemistry. Results We found increased Kv3.1b subunit expression in the DCN after hearing onset, suggesting that this subunit could be responsible for the electrophysiological changes in post-hearing fusiform neurons. TEA-sensitive high-threshold currents were a significant component of voltage-dependent potassium currents in both pre- and post-hearing fusiform neurons, with similar magnitudes in both groups. However, blocking Kv3 currents with 1–5 mM TEA broadens action potential waveforms in neurons from both groups while maintaining the developmental differences between groups. On the other hand, TEA was more effective at reducing the firing of post-hearing neurons. Conclusions We conclude that the rise in Kv3.1b channel expression in DCN fusiform neurons after hearing does not account for the shorter, faster action potentials observed at that time, but could contribute to their ability to fire action potentials at high frequencies.