INCREASED EXPRESSION OF KV3.1B CHANNEL IS NOT RESPONSIBLE FOR THE DEVELOPMENTALREFINEMENT OF ACTION POTENTIALS IN FUSIFORM NEURONS FROM THE DORSAL COCHLEAR NUCLEUS OF MICE.

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 the onset of hearing at postnatal day 14 along with the refinement of the action potential waveform, which becomes faster and shorter. We then tested whether Kv3.1 channels influence the developmental maturation of action potentials in DCN fusiform neurons. For this, we used Swiss mice from post-natal day 8 to 25 and divided them into pre-hearing (<p14) and post-hearing (>14). We measured Kv currents and action potentials using whole-cell patch-clamp recordings. Tetraethylammonium (TEA) was applied at a concentration of 1-5 mM to block Kv3 channels, and we detected Kv3.1b subunit expression by immunocytochemistry. 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 TEA broadens action potential waveforms similarly in neurons from both groups while maintaining the developmental differences between groups. On the other hand, TEA affected the ability of post-hearing fusiform neurons to fire at high frequencies. 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 influenced their ability to fire at high frequencies.