1. Acutely isolated Xenopus spinal neurons possess a slowly activating Ca(2+)-dependent outward current which was revealed either by removal of external Ca2+ or by the addition of the Ca2+ channel blocker, 150 microM Cd2+. 2. The Ca(2+)-sensitive current was very slow to activate and had a mean time constant of activation of 437 ms at 0 mV. The current also had very long tail currents which were blocked by Cd2+. The rate of decay of the slowest component of the Ca(2+)-dependent tail currents was insensitive to membrane potential suggesting that the relaxation of the Ca(2+)-dependent current may only be weakly voltage dependent. 3. The reversal potential of the Ca(2+)-sensitive tail currents depended on the concentration of external K+ in a manner predicted by the Nernst equation. Thus the Ca(2+)-sensitive current was carried by K+. 4. The toxin apamin (10 nM to 2 microM) selectively blocked the Ca(2+)-dependent K+ current without affecting voltage-gated K+ currents. This current may be analogous to a small-conductance Ca(2+)-dependent K+ (SK) current; however, unlike some SK currents, the Ca(2+)-dependent K+ current was also sensitive to 500 microM tetraethylammonium chloride (TEA). 5. Applications of 10 nM apamin to spinalized embryos did not perturb the motor pattern for swimming. However, the cycle periods over which the locomotor rhythm generator could generate appropriate motor activity were lengthened by about 10% and the mean duration of swimming episodes was increased by approximately 40%. 6. We therefore propose that the Ca(2+)-dependent K+ current plays an important role in the self-termination of motor activity.