Action potentials and afterpotentials were compared in giant interneurons, sensory dorsal cells and large intraspinal axons in the lamprey spinal cord. Afterpotentials of giant interneurons and dorsal cells consisted of two hyperpolarizing phases, an early and a late one, which were separated by a delayed depolarization. The afterpotentials of axons had a single hyperpolarizing phase also followed by a delayed depolarization. Tetraethyl ammonium chloride (TEA+) eliminated the early phase of the afterhyperpolarization in giant interneurons, only partially reduced the early phase in dorsal cells and did not affect the single phase of axons. The delayed depolarization of dorsal cells was attenuated by TEA+ but in axons it was unaltered. The heavy metal ions Mn2+ and Co2+ (2 mM) eliminated the late phase in giant interneurons but did not reduce the late phase in dorsal cells. The delayed depolarization remained in both types of cell in the presence of these ions. Action potentials of giant interneurons and dorsal cells, but not those of axons, were broadened by TEA+. The TEA-prolonged action potentials were narrowed by Mn2+ applied in combination with TEA+. The afterhyperpolarizations of all 3 cells were reduced by injection of negative current and enhanced by positive current. Repetitive stimulation resulted in summation of the afterhyperpolarization in giant interneurons and dorsal cells. The results suggest that different sets of potassium channels are responsible for the afterhyperpolarizations in each type of cell. In giant interneurons fast channels which are sensitive to TEA+ may underlie the early phase and slow channels activated by calcium entry may underlie the slow phase. The early phase of dorsal cells may be caused by two types of fast channel, one similar to that in giant interneurons and another less sensitive to external TEA+. This latter type may also cause the afterhyperpolarization in axons. Although calcium channels appear to contribute to the action potentials of giant interneurons and dorsal cells, the late phase of the latter neurons does not seem to be activated by calcium entry. The delayed depolarizations of the neurons appear to be due to an inward current which is not carried by calcium.