Muscle fibers in the swim appendages of the mollusk Aplysia brasiliana are innervated by cholinergic motoneurons. Serotonin (5-HT) causes an increase in amplitude of junctional potentials and muscle contractions at this neuromuscular synapse. We studied motoneurons with intracellular current-clamp recording and single-electrode voltage-clamp analysis to determine the effects of 5-HT on somatic currents in these presynaptic neurons. Serotonin was found to have no effect on action potential duration in motoneurons bathed in normal seawater, and no effect of 5-HT could be detected on K currents, indicating that 5-HT does not indirectly enhance calcium currents by prolonging the action potential. Calcium currents were isolated by replacing extracellular sodium with TEA and adding tetrodotoxin and other K -channel blockers. Under these conditions motoneuron action potentials were greatly prolonged and could be blocked with Co² or Cd² . Addition of 5-HT increased the duration of these Ca² spikes by about 35%. In motoneurons studied with voltage clamp, the amine produced a 58% increase in total inward calcium current. Use of the calcium channel blockers nifedipine, nimodipine, ω-conotoxin GVIA, and ω-agatoxin TK revealed that motoneurons express varying amounts of L-, N- and P-like calcium channels, but only an agatoxin-sensitive, P-type channel is sensitive to 5-HT. It is concluded that 5-HT acts directly to increase a P-type Ca² current during a normal spike. The resulting increase in intracellular calcium could contribute to an increase in transmitter release and account for the increase in junctional potentials in swim muscles.