BK channels modulate pre- and postsynaptic signaling at reciprocal synapses in retina

In the mammalian retina, A17 amacrine cells provide reciprocal inhibitory feedback to rod bipolar cells, thereby shaping the time course of visual signaling in vivo. Previous results indicate that A17 feedback can be triggered by Ca(2+) influx through Ca(2+) permeable AMPARs and can occur independently of voltage-gated Ca(2+) (Ca(v)) channels, whose presence and functional role in A17 dendrites have not been explored. Here, we combine electrophysiology, calcium imaging and immunohistochemistry to show that L-type Ca(v) channels in rat A17 amacrine cells are located at the sites of reciprocal synaptic feedback, but their contribution to GABA release is diminished by large-conductance Ca(2+)-activated potassium (BK) channels, which suppress postsynaptic depolarization in A17s and limit Ca(v) channel activation. We also show that BK channels, by limiting GABA release from A17s, regulate the flow of excitatory synaptic transmission through the rod pathway.