Patch-clamp and calcium-indicator measurements were used to examine the electrical excitability of large-terminal bipolar neurons from goldfish retina. Large, transient increases in intracellular calcium occurred spontaneously in the synaptic terminal but not in the soma of bipolar neurons. Calcium transients were blocked by hyperpolarization, by external application of calcium-channel blockers, and by the neurotransmitters GABA and glutamate. These observations suggest that calcium action potentials are responsible for the spontaneous increases in intraterminal calcium, which was directly confirmed by electrical recordings of calcium-dependent action potentials in both whole-cell and perforated-patch recordings. We suggest that regenerative depolarization produced by the opening of calcium channels in the synaptic terminal of on-type bipolar neurons represents an amplification mechanism in the high-sensitivity ON pathway in the dark-adapted fish retina.