In neurons of the suprachiasmatic nucleus, spike frequency adaptation and membrane afterhyperpolarization occur during a train of action potentials. Extracellular Ca 2+ may regulate neuronal excitability by several mechanisms, including activation of small conductance and large conductance Ca 2+-activated K + channels. The overall goal of this study was to examine the role of Ca 2+-activated K + currents in individual suprachiasmatic nucleus neurons. To this end, we used the nystatin-perforated patch technique to record currents from suprachiasmatic nucleus neurons. Iberiotoxin and tetraethylammonium, antagonists of large conductance Ca 2+-activated K + channels, had no effect on the membrane afterhyperpolarization. However, antagonists of small conductance Ca 2+-activated K + channels, apamin and d-tubocurarine, reduced the amplitude of the membrane afterhyperpolarization and inhibited the spike frequency adaptation that occurred during a train of action potentials. Although there was no significant difference in membrane AHP between different portions of the circadian day, apamin and d-tubocurarine increased the spontaneous firing frequency of suprachiasmatic nucleus neurons during the daytime. In voltage-clamp mode, membrane depolarization-activated currents were followed by an outward tail current reversing near the K + equilibrium potential. The tail current decayed with a time constant of 220 ms at +20 mV and 149 ms at −40 mV. Apamin irreversibly and d-tubocurarine reversibly inhibited the tail current. The tail current amplitude was also reduced by the GABA A receptor antagonist, bicuculline methiodide, while picrotoxin (another GABA A receptor antagonist) was without effect. Removal of extracellular Ca 2+ or the addition of Cd 2+ reversibly inhibited the tail current. These results indicate that apamin- and d-tubocurarine-sensitive small conductance Ca 2+-activated K + channels have a modulatory function on the action potential firing frequency as well as the membrane afterhyperpolarization that follows a train of action potentials in suprachiasmatic nucleus neurons. Importantly, our data also indicate that a portion of the effects of bicuculline methiodide on suprachiasmatic nucleus neurons may be mediated by inhibition of small conductance Ca 2+-activated K + channels.