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

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Abstract
The authors combine electrophysiology, calcium imaging and immunohistochemistry to show that L-type Cav channels in rat A17 amacrine cells are well placed to mediate reciprocal inhibitory feedback to rod bipolar cells. However, they find that the contribution of these channels to GABA release is diminished by large-conductance Ca2+-activated potassium (BK) channels, which suppress postsynaptic depolarization in A17s and limit Cav channel activation. 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 have indicated that A17 feedback can be triggered by Ca2+ influx through Ca2+-permeable AMPA receptors and can occur independently of voltage-gated Ca2+ (Cav) channels, whose presence and functional role in A17 dendrites have not yet been explored. We combined electrophysiology, calcium imaging and immunohistochemistry and found that L-type Cav channels in rat A17 amacrine cells were located at the sites of reciprocal synaptic feedback and that their contribution to GABA release was diminished by large-conductance Ca2+-activated potassium (BK) channels, which suppress postsynaptic depolarization in A17s and limit Cav channel activation. We also found that BK channels, by limiting GABA release from A17s, regulate the flow of excitatory synaptic transmission through the rod pathway.

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