To survive in the wild small rodents evolved specialized retinas. To escape predators, looming shadows need to be detected with speed and precision. To evade starvation, small seeds, grass, nuts and insects need to also be detected quickly. Some of these succulent seeds and insects may be camouflaged offering only low contrast targets.Moreover, these challenging tasks need to be accomplished continuously at dusk, night, dawn and daytime. Crossover inhibition is thought to be involved in enhancing contrast detectionin the microcircuits of the inner plexiform layer of the mammalian retina. The AII amacrine cells are narrow field cells that play a key role in crossover inhibition. Our lab studies the synaptic physiology that regulates glycine release from AII amacrine cellsin mouse retina. These interneurons receive excitation from rod and conebipolar cells and transmit excitation to ON-type bipolar cell terminals via gap junctions. They also transmit inhibition via multiple glycinergic synapses onto OFF bipolar cell terminals.AII amacrine cells are thus a central hub of synaptic information processing that cross links the ON and the OFF pathways. What are the functions of crossover inhibition? How does it enhance contrast detection at different ambient light levels? How is the dynamicrange, frequency response and synaptic gain of glycine release modulated by luminance levels and circadian rhythms? How is synaptic gain changed by different extracellular neuromodulators, like dopamine, and by intracellular messengers like cAMP, phosphateand Ca2+ ions from Ca2+ channels and Ca2+ stores? My talk will try to answer some of these questions and will pose additional ones. It will end with further hypothesis and speculations on the multiple roles of crossover inhibition.