Dopamine's effect on calcium influx into the bursting neuron, R15, of Aplysia californica was tested by tail current measurements and by measurement of absorbance of intracellular Arsenazo III, a calcium-sensitive indicator. Slow outward tail currents were elicited by subthreshold depolarization in voltage clamp and were demonstrated to be dependent upon transient increases in intracellular calcium activity, (Ca)i), using calcium-free seawater, calcium blockers (Mn2+ and La3+), and intracellular injection of EGTA. Dopamine reduces these tail currents as it reduces the slow inward current. Next, the transient elevations of (Ca)i accompanying subthreshold depolarization were measured directly in Arsenazo III-loaded neurons. Dopamine did not reduce the rise in (Ca)i measured in the soma during depolarization. However, when absorbance of the axodendritic region was monitored, dopamine did reduce calcium influx. Voltage monitoring in the axon indicated that the reduced calcium influx could not simply be ascribed to altered space clamp. In keeping with the apparent axodendritic location of dopamine action, isolation of the soma by ligation of the axon markedly reduced the dopamine response. Dopamine seems to reduce calcium influx into R15, but this effect is topographically limited to nonsomatic membrane, an area of the neuron not usually monitored in optical studies of (Ca)i.