Glycinergic feedback enhances synaptic gain in the distal retina

Abstract

Glycine input originates with interplexiform cells, a group of neurons situated within the inner retina that transmit signals centrifugally to the distal retina. The effect on visual function of this novel mechanism is largely unknown. Using gramicidin-perforated patch whole-cell recordings, intracellular recordings, and specific antibody labeling techniques, we examined the effects of the synaptic connections between glycinergic interplexiform cells, photoreceptors, and bipolar cells. To confirm that interplexiform cells make centrifugal feedback on bipolar cell dendrites, we recorded the post-synaptic glycine currents from axon-detached bipolar cells while stimulating pre-synaptic interplexiform cells. The results show that glycinergic interplexiform cells activate bipolar cell dendrites that express the α3 subunit of the glycine receptor, as well as a subclass of unidentified receptors on photoreceptors. By virtue of their synaptic contacts, glycine centrifugal feedback increases glutamate release from photoreceptors, and suppresses the uptake of glutamate by the EAAT2 transporter on photoreceptors. The net effect is a significant increase in the synaptic gain between photoreceptors and their second-order neurons.