The active and passive electrical properties of the after‐hyperpolarizing (AH) cell of the guinea‐pig myenteric plexus were analysed using a single‐electrode voltage or current clamp. Action potentials were compared under normal conditions, in the presence of tetrodotoxin (TTX) and in the presence of both TTX and tetraethylammonium chloride (TEA). Calcium action potentials were studied by examining their calcium dependence, the actions of manganese and the effect of substituting barium for calcium. The maximum rate of rise of the action potential did not increase in calcium concentrations above 10 mM. The half‐saturation concentration was 2 mM‐calcium. AH cells exhibited five predominant currents consisting of an inward sodium current, an inward calcium current and three outward currents. There was a transient outward current which was inactivated at holding potentials more positive than ‐65 mV and was suppressed by 4‐aminopyridine and barium but not by external TEA. A second outward current observed in the presence of 10 mM‐external TEA had properties consistent with that of the delayed rectifier (Hodgkin & Huxley, 1952). A third outward current was the calcium‐dependent slow after‐hyperpolarizing current (Hirst, Johnson & van Helden, 1985). The voltage dependence, the action of calcium antagonists, the effect of barium substitution and the temporal characteristics of calcium currents were studied. The peak calcium current density was in excess of 100 microA/cm2 in 2.5 mM‐calcium solution at 35 degrees C for depolarizations to ‐10 mV. Calcium currents showed at least two phases of inactivation. Both calcium and barium currents showed early inactivation with decay occurring over the first 10‐40 ms. The calcium‐activated current precluded direct measurement of slow inactivation of the calcium current. Barium currents studied over the first 100‐150 ms had a very slow inactivating component.