Abstract
Abstract: :
Purpose: ON and OFF bipolar cells drive diverse amacrine cells at the inner plexiform layer. Bipolar cells also receive feedback inhibition from amacrine cells. Could amacrine cell feedback mediate interactions between similar and different bipolar cell types? We studied these bipolar–bipolar interactions to identify specific pathways, and analyzed their role in information processing. Methods: Bipolar cells were whole–cell patch–clamped in rabbit retina slices. Excitatory and inhibitory currents and voltage responses were recorded under normal and pharmacologically–blocked conditions. Photopic light stimuli included narrow– and wide–field flashes, and sinusoidally flickering stimuli of various contrasts and temporal frequencies. Results: We found three types of interaction between excitation and inhibition: 1) Most OFF bipolar cells and about half of ON bipolar cells show opposite polarity inputs: When excitation increased, inhibition decreased, and vice–versa. These out–of–phase inputs reinforce each other, yielding a stronger voltage response than would result from either input alone. 2) In Rod bipolar cells and some ON cone bipolar cells, excitation and inhibition increased simultaneously with increased light intensity, canceling each other. 3) For a set of bipolar cells stratifying in the middle of the ON sublamina, inhibition canceled excitation, but is delayed by about 50ms, causing the cell to respond preferentially to high temporal frequencies. Light responses were elicited over a region less than 200 µm wide. Pharmacological results indicate that reinforcing inhibitory signals, likely carried between sub–laminae by vertically oriented diffuse amacrine cells, are glycinergic, while canceling inhibitory signals are not. Conclusions: We found three main forms of interaction between bipolar cells carried by amacrine feedback: Reinforcing feedback acts to maintain robust signaling in the majority of pathways; cancellation acts to suppress rod bipolars under photopic conditions; and delayed cancellation is likely the origin of transience in ON transient ganglion cells.
Keywords: bipolar cells • retinal connections, networks, circuitry • retina: proximal (bipolar, amacrine, and ganglion cells)