It is difficult not to get excited about potassium channels, but that is exactly why they are there: – dominating the resting membrane potential, adjusting membrane time-constants, action potential thresholds, firing rates and of course, action potential repolarization and AHP generation. The number and diversity of their genes and spliced variants is exceeded only by the breadth and subtlety of their actions. And therein lies the physiological problem; most potassium channels have now been cloned and the recombinant channels characterised, but correlating the properties of these expressed channels with their native counterparts is complicated by heterogeneous subunit composition and ambiguous pharmacology. We have been studying neuronal excitability and synaptic transmission in the brainstem auditory pathway, focussing on the calyx of Held synapse onto the medial nucleus of the trapezoid body (MNTB). This glutamatergic synapse is a highly secure synapse, with over 2000 release sites generating EPSCs of up to 20 nA, giving a high safety factor for postsynaptic action potential generation in the MNTB neurone, even at frequencies in excess of 200 Hz. If it were not for the exquisite tuning of the postsynaptic excitability by a range of potassium channels, the information contained in such a large synaptic input would be lost. Combined application of voltage-clamp, specific pharmacological antagonists and immunohistochemistry, have shown that Kv3 and Kv1 channels are located in specific neuronal compartments and have distinct functions. The high-voltage activated Kv3 channels enhance repolarization and minimise action potential duration, while the low-voltage activated Kv1 channels suppress excitability at voltages around threshold (Brew & Forsythe, 1995; Dodson et al. 2002). Both channel types are present in the presynaptic calyx and have analogous functions (Dodson et al. 2003). There is also support for activity-dependent regulation of Kv3 and Kv1 conductances (Song et al. 2005; Barnes-Davies et al. 2004). In the presence of Kv1 and Kv3 antagonists (100 nM dendrotoxin-I and 3mM tetraethylammonium, respectively) half of the total outward current remains unblocked. Toxins and antagonists are available for most potassium channel subtypes, so we have taken a pharmacological, molecular and biophysical approach to characterise these other endogenous K+ currents. RT-PCR demonstrates that TASK, TWIK and TREK channels are expressed in the MNTB. Whole-cell patch recordings demonstrate that multiple twin-pore potassium channels (K2p, KCNK) dominate the resting membrane potential in the auditory brainstem and cortex. In addition, these channels make a major contribution to membrane conductance across the physiological range. I will briefly describe the basic physiology of the auditory brainstem, review the potassium channel families known to regulate excitability in this region, and present our recent evidence for the role of the twin-pore channels in regulating membrane conductance at rest and on depolarisation.