The retina compensates for rod death and deteriorating cones to retain high-fidelity visual signaling to the brain.

Mice can detect changes in hue independent of luminance, with differing sensitivity to hue and luminance in different parts of visual space.

Signals from primate rod photoreceptors do not exhibit the light-level-dependent routing through parallel retinal circuits observed in rodents and often invoked in interpreting psychophysical experiments.

A single class of neurons switches both its sensory detection and neurotransmission mechanisms to support transient or sustained physiological output.

Heterogeneity in perceptual sensitivity of human cone-mediated vision across wavelength originates in the cone photoreceptors, where S cones exhibit distinct functional properties in comparison to L and M cones.

Mouse retina manifests homeostatic plasticity and adapts to photoreceptor degeneration to resist visual decline.

A combination of physiological and perceptual experiments show that the responses of rod photoreceptors inhibit those of cones more than vice versa, and reveal both the site of the retinal interaction and the underlying mechanism.

Endocannabinoid activation of the CB1 receptor on retinal ganglion cells in the eye results in enhanced excitability and responsiveness to visual stimulation through a novel mechanism involving intracellular chloride regulation.

Retinal visual response properties in awake mice are similar to those under anesthesia or ex vivo, but not exactly the same, so knowledge of retinal function cannot be simply translated from ex vivo to in vivo.