Abstract Intracellular tetanization of premotor interneurons for withdrawal in the snail. Helix lucorum produces long-term facilitation of synaptic inputs of these neurons. Using this model of plasticity we investigated the role of calcium in postsynaptic induction of synaptic facilitation. It was shown that, from the one hand, postsynaptic injection of calcium chelator EGTA completely abolishes potentiation and, from the other hand, injection of calcium chloride into the interneuron produces facilitation-like changes in the EPSP amplitude in this neuron. Therefore, not only necessity but also sufficiency of increasing of postsynaptic calcium for induction of synaptic potentiation was demonstrated. We also showed that inhibitor of nitric oxide synthase N-omega-nitro- l-arginine prevents development of postsynaptically induced facilitation what suggests that nitric oxide may participate in investigated synaptic facilitation as a retrograde messenger. These results support the idea that both invertebrates and vertebrates have common mechanisms underlying synaptic plasticity.