Light evokes Ca2+ spikes in the axon terminal of a retinal bipolar cell

Bipolar cells in the vertebrate retina have been characterized as nonspikin g interneurons. Using patch-clamp recordings from goldfish retinal slices, we find, however, that the morphologically well-defined Mb1 bipolar cell is capable of generating spikes. Surprisingly, in dark-adapted retina, spikes were reliably evoked by light flashes and had a long (1-2 s) refractory pe riod. In light-adapted retina, most Mb1 cells did not spike. However, an L- type Ca2+ channel agonist could induce periodic spiking in these cells. Spi kes were determined to be Ca2+ action potentials triggered at the axon term inal and were abolished by 2-amino-4-phosphonobutyric acid (APB), an agonis t that mimics glutamate. Signaling via spikes in a specific class of bipola r cells may serve to accelerate and amplify small photoreceptor signals, th ereby securing the synaptic transmission of dim and rapidly changing visual input.