The photosensitive element is rhodopsin, which is composed of opsin (a protein) belonging to the superfamily of G-protein-coupled receptors and retinal (an aldehyde of vitamin A).
Under optimal conditions, a single photon of light, the smallest possible quantal unit of light energy, can cause a measurable receptor potential in a rod of about 1mV. Only 30 photons of light will cause half saturation of the rod. The small amount of light can cause such a great excitation because the photoreceptors are extremely sensitive chemical cascade that amplifies the stimulatory effects about a millafold!
1. photon activates an electron in 11-cis retinal portion of rhodopsin, this leads to the formation of metarhodopsin 2, which is the active form of rhodopsin.
2. The activated rhodopsin functions as an enzyme to activate many molecules of transducin
3. Activated transducin activates many more molecules of phosphodiesterase.
4. Activated phosphodiesterase immediately hydrolyzes many molecules of cGMP thus destroying it. cGMP is bound to a sodium channel in such away that splits it open allowing sodium into the cell and depolarizing it before it is destroyed, after being destroyed the sodium channel closes and therefore the cell hyperpolarizes. Several hundred channels close for each originally activated molecule of rhodopsin.
5. Within about a second, another enzyme, rhodopsin kinase, which is always present within the rod, inactivates activated rhodopsin (metarhodopsin 2) and the entire cascade reverses back to the normal state with open sodium channels.
If a person has been in bright light for hours, large portions of the photochemicals in both the rods and the cones will have been reduced to retinal and opsins. Furthermore, much of the retinal of both the rods and the cones will have been converted into vitamin A. Because of these two effects, the concentrations of the photosensitive chemicals remaining in the rods and cones are considerably reduced, and the sensitivity of the eye to light is correspondingly reduced. This is called light adaptation.
Conversely, if a person remains in darkness for a long time, the retinal and opsins in the rods and cones are converted back into the light-sensitive pigments. Furthermore, vitamin A is converted back into retinal to increase light-sensitive pigments, the final limit being determined by the amount of opsins in the rods and cones to combine with the retinal. This is called dark adaptation.
Figure 50-9 Dark adaptation, demonstrating the relation of cone adaptation to rod adaptation.
Figure 50-9 shows the course of dark adaptation when a person is exposed to total darkness after having been exposed to bright light for several hours. Note that the sensitivity of the retina is very low on first entering the darkness, but within 1 minute, the sensitivity has already increased 10-fold—that is, the retina can respond to light of one tenth the previously required intensity. At the end of 20 minutes, the sensitivity has increased about 6000-fold, and at the end of 40 minutes, about 25,000-fold.
The resulting curve of Figure 50-9 is called the dark adaptation curve. Note, however, the inflection in the curve. The early portion of the curve is caused by adaptation of the cones because all the chemical events of vision, including adaptation, occur about four times as rapidly in cones as in rods. However, the cones do not achieve anywhere near the same degree of sensitivity change in darkness as the rods do. Therefore, despite rapid adaptation, the cones cease adapting after only a few minutes, while the slowly adapting rods continue to adapt for many minutes and even hours, their sensitivity increasing tremendously.