In ocular physiology, adaptation is the ability of the eye to adjust to various levels of darkness and light.
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The human eye can function from very dark to very bright levels of light; its sensing capabilities reach across nine orders of magnitude. This means that the brightest and the darkest light signal that the eye can sense are a factor of roughly 1,000,000,000 apart. However, in any given moment of time, the eye can only sense a contrast ratio of one thousand. What enables the wider reach is that the eye adapts its definition of what is black. The light level that is interpreted as "black" can be shifted across six orders of magnitude—a factor of one million.
The eye takes approximately 20–30 minutes to fully adapt from bright sunlight to complete darkness and become ten thousand to one million times more sensitive than at full daylight. In this process, the eye's perception of color changes as well. However, it takes approximately five minutes for the eye to adapt to bright sunlight from darkness. This is due to cones obtaining more sensitivity when first entering the dark for the first five minutes but the rods take over after five or more minutes.[1]
A minor mechanism of adaptation is the pupillary light reflex, adjusting the amount of light that reaches the retina. A dilation of the pupil from 2mm to 10mm only increases the area of light entering the eye by a factor of 25.
Changes in the sensitivity of rods and cones in the eye are the major contributors to dark adaptation. Rods are more sensitive to light and so take longer to fully adapt to the change in light. Rods, whose photopigments regenerate more slowly, do not reach their maximum sensitivity for about half an hour.[1][2] Cones take approximately 9–10 minutes to adapt to the dark.[1] Sensitivity to light is modulated by changes in intracellular calcium ions and cyclic guanosine monophosphate.[3] Inhibition by one neuron on another is just as important as activation in synapses. Together with the bleaching of a rod or cone pigment, merging of signals on ganglion cells are inhibited, reducing convergence. Alpha adaptation, i.e. rapid sensitivity fluctuations, is powered by nerve control.
The merging of signals by virtue of the diffuse ganglion cells, as well as horizontal and amacrine cells, allow a cumulative effect. This means that area of stimulation varies inversely with the intensity, a strong stimulus over 100 rods or less is equivalent to one that is weak and over 1,000 rods. In sufficiently bright light, convergence is low, but during dark adaptation, convergence of rod signals boost. This is not due to structural changes, but by a possible shutdown of inhibition that stops convergence of messages in bright light. If only one eye is open, the closed eye must adapt separately upon reopening to match the already adapted eye.[1]
The fovea is blind to dim light (due to its cone-only array) and the rods are more sensitive, so a dim star on a moonless night must be viewed from the side, so it stimulates the rods. This is not due to pupil width since an artificial fixed-width pupil gives the same results.[1]
Insufficiency of adaptation most commonly presents as insufficient adaptation to dark environment, called night blindness or nyctalopia. The opposite problem, known as hemeralopia, that is, inability to see clearly in bright light, is much rarer.