Many auditory neurons fire action potentials at high rates with high temporal precision. These include neurons of the medial nucleus of the trapezoid body (MNTB) and anterior ventral cochlear nucleus (AVCN), which participate in circuits that detect the locations of sounds in space. The expression of several different potassium channel subunits in these cells permits accurate phase-locking of their action potentials to different stimulus frequencies. Our laboratory has focused on the role of the voltage-dependent potassium channel subunit Kv3.1b, and on Slick and Slack, two potassium channel subunits that are present at high levels in these neurons and that are activated by increases in intracellular sodium ions. The ability of MNTB and AVCN neurons to fire at high frequencies can be attributed to the presence of high levels of the Kv3.1b potassium channel, which allows neurons to follow synaptic stimuli at high frequencies. In rats or mice, inhibition of Kv3.1 channels or knockout of the Kv3.1 gene prevents MNTB neurons from following high frequency stimulation (>200 Hz). Nevertheless, high levels of Kv3.1b current degrade the accuracy of action potential timing at lower frequencies of firing. The amplitude of Kv3.1b currents can be regulated by protein kinase C (PKC), which suppresses current by direct phosphorylation of serine 503 at the C-terminus of the protein. Using a phospho-specific antibody to serine 503 of Kv3.1b we find that, in a quiet auditory environment, Kv3.1b is basally phosphorylated by this enzyme, providing maximal timing accuracy at low firing frequencies. In vivo acoustic stimulation of animals, or high frequency stimulation of the afferent input of MNTB neurons in brainstem slices, results in a rapid and reversible decrease in the level of phosphorylation. This dephosphorylation permits neurons to fire at higher rates, albeit with lower temporal accuracy. Phosphorylation of Kv3.1b therefore appears to be a mechanism that rapidly adjusts the intrinsic electrical properties of neurons to the pattern of incoming auditory stimuli. MNTB and AVCN neurons also express the Slack and Slick genes, which encode large conductance sodium-activated potassium channels (KNa channels). Both whole-cell and single channel recordings have demonstrated that channels gated by intracellular sodium are present at the somata of MNTB neurons, and that their biophysical and pharmacological properties match those of Slick and or Slack/Slick channels. Manipulations of the level of KNa current in MNTB neurons, either by increasing levels of internal sodium or by exposure to a pharmacological activator of Slack channels, increases the accuracy of timing of action potentials at high frequencies of stimulation. These findings suggest that KNa channels, like Kv3.1b, influence the fidelity of information transfer through the MNTB and that modulation of these potassium channels constitutes a mechanism that allows neurons to adjust to different frequencies of stimulation.