Color constancy is one of the most impressive features of color vision systems. Although the phenomenon has been studied for decades, its underlying neuronal mechanism remains unresolved. Literature indicates an early, possibly retinal mechanism and a late, possibly cortical mechanism. The early mechanism seems to involve chromatic spatial integration and performs the critical calculations for color constancy. The late mechanism seems to make the color manifest. We briefly review the current evidence for each mechanism. We discuss in more detail a model for the early mechanism that is based on direct measurements of goldfish outer retinal processing and induces color constancy and color contrast. In this study we extrapolate this model to primate retina, illustrating that it is highly likely that a similar mechanism is also present in primates. The logical consequence of our experimental work in goldfish and our model is that the wiring of the cone/horizontal cell system sets the reference point for color vision (i.e., it sets the white point for that animal).

The retina can function under a variety of adaptation conditions and stimulus paradigms. To adapt to these various conditions, modifications in the phototransduction cascade and at the synaptic and network levels occur. In this paper, we focus on the properties and function of a gain control mechanism in the cone synapse. We show that horizontal cells, in addition to inhibiting cones via a "lateral inhibitory pathway," also modulate the synaptic gain of the photoreceptor via a "lateral gain control mechanism." The combination of lateral inhibition and lateral gain control generates a highly efficient transformation. Horizontal cells estimate the mean activity of cones. This mean activity is subtracted from the actual activity of the center cone and amplified by the lateral gain modulation system, ensuring that the deviation of the activity of a cone from the mean activity of the surrounding cones is transmitted to the inner retina with high fidelity.