Plasticity at the neuronal level commonly involves use-dependent changes in strength of particular synaptic pathways or regulation of postsynaptic properties by modulatory transmitters. Here we analyze a novel form of short-term plasticity mediated by use-dependent facilitation of postsynaptic responsiveness. Using current- and voltage-clamp recordings, we found that all spinal ventral horn neurons able to generate plateau potentials showed depolarization-induced facilitation of the underlying inward current. Facilitation was noticeable when the neurons were depolarized to more than -50 mV at intervals <4 s. When stimulation with fast triangular voltage ramps was used, the inward current activated at a less depolarized potential during the second ramp. The inward current and facilitation was eliminated by nifedipine, a selective antagonist of L-type calcium channels. Depolarization-induced facilitation of low-voltage-activated L-type calcium channels is suggested to be the underlying mechanism. It is noted that facilitation occurs on a time scale compatible with a role in phasic motor activity.