Adaptation of mammalian photoreceptors to background light: putative role for direct modulation of phosphodiesterase.

All sensory receptors adapt. As the mean level of light or sound or odor is altered, the sensitivity of the receptor is adjusted to permit the cell to function over as wide a range of ambient stimulation as possible. In a rod photoreceptor, adaptation to maintained background light produces a decrease (or "sag") in the response to the prolonged illumination, as well as an acceleration in response decay time and a Weber-Fechner-like decrease in sensitivity. Earlier work on salamander indicated that adaptation is controlled by the intracellular concentration of Ca(2+). Three Ca(2+)-dependent mechanisms were subsequently identified, namely, regulation of guanylyl cyclase, modulation of activated rhodopsin lifetime, and alteration of channel opening probability, with the contribution of the cyclase thought to be the most important. Later experiments on mouse that exploit the powerful techniques of molecular genetics have shown that cyclase does indeed play a significant role in mammalian rods, but that much of adaptation remains even when regulation of cyclase and both of the other proposed pathways have been genetically deleted. The identity of the missing mechanism or mechanisms is unclear, but recent speculation has focused on direct modulation of spontaneous and light-activated phosphodiesterase.