NMDA-receptor dependent, TTX-resistant membrane potential oscillations are considered to be important for the operation of the lamprey locomotor network.They involve a cyclic influx of calcium, leading to an activation of KCa-channels, which in turn contributes to the termination of the depolarized plateau and membrane repolarization.Objective To gain more specific information on the nature of calcium influx during NMDA-mediated membrane potential oscillations.Methods we have investigated the calcium dynamics in different regions of lamprey spinal neurons, using confocal calcium imaging in combination with intracellular recordings of membrane potential.Results Calcium fluctuations were observed in both the soma-proximal dendrite regions and in distal dendrites of the cell, timed to the membrane potential oscillations.The calcium level increased sharply at the onset of membrane depolarization, to reach its maximum by the end of the depolarized plateau.Calcium fluctuations were more prominent in distal dendrites than in proximal dendrites and the soma.The timing of the calcium peak could differ between different distal dendrites, but timing could also be synchronous, even between distant dendrites as revealed by high-speed line scanning.The L-type calcium channel blocker Nimodipine increased the duration of the plateau phase of the membrane potential oscillations in the majority of cells tested, while in the remaining cells oscillations ceased at a hyperpolarized level.The agonist BayK 8644 instead decreased the plateau phase duration in the majority of cells tested.Depending on dendritic location of the calcium measurement, Nimodipine either increased or decreased the amplitude of calcium fluctuations, even along restricted portions of the same distal dendrite, suggesting a non-uniform distribution of CaV1.3 calcium channels in distal dendrites.Conclusions Our results thus indicate that CaV1.3 calcium channels are activated during NMDA-mediated membrane potential oscillations.This calcium influx activates KCa channels involved in membrane repolarization at the end of thedepolarized plateau, and it may also contribute to the initiation of depolarization following the hyperpolarized phase.The activated KCa channels may be located close to the CaV1.3 channels, perhaps in distal dendrites.