Evoked transmitter release is abnormal at the larval neuromuscular junctions of two Drosophila mutants. Following a single nerve impulse, the increased calcium conductance at the nerve terminal, which lasts for 1 ms in normal larvae, lasts for at least 60 ms in one mutant and several seconds in the other. Both mutations appear to affect the same gene on the X-chromosome. Normal larvae treated with 4-aminopyridine, a potassium channel blocking agent, mimic the abnormal synaptic transmission of one mutant. Normal larvae treated with tetraethylammonium, another potassium channel blocking agent, mimic the abnormal synaptic transmission of the other mutant. From these and other experiments, we suggest that the abnormal neuromuscular transmission in these mutants may be caused by defective potassium channels in the nerve terminal membrane.