Why does it take so long for our vision to adjust to a darkened theater after we come in from bright sunlight?

Rafael Caruso, an investigator in the National Eye Institute's Ophthalmic Genetics & Visual Function Branch in Bethesda, Md., guides us to an answer.

If we go from the outdoors on a bright sunny day into a very dimly lit room, we are hardly able to see our surroundings at first. As time goes by, however, we gradually become able to detect the room's contents. This phenomenon is known as "dark adaptation," and it typically takes between 20 and 30 minutes to reach its maximum, depending on the intensity of light exposure in the previous surroundings.

The human retina can perform its light-detection function in an astounding range of light intensities, from bright sunlight to dim starlight, by relying on two types of light-sensitive cells, or photoreceptors. The first, the cones, evolved for day vision and can respond to changes in brightness even in extremely high levels of illumination. (Cones are unable to respond to light reliably in dim illumination, however.)

Photoreceptors for night vision are called rods. Rods can act as light detectors even in extremely low levels of illumination but are ineffective—they are known to "saturate"—in bright light. Remarkably, rods can respond reliably to a single visible light photon, so they operate at the physical limit of light detection.

Both cones and rods participate in dark adaptation, slowly increasing their sensitivity to light in a dim environment. Cones adapt faster, so the first few minutes of adaptation reflect cone-mediated vision. Rods work slower, but since they can perform at much lower levels of illumination, they take over after the initial cone-mediated adaptation period. This is actually a general feature of many sensory systems: if a sensation relies on stimulation of more than one type of receptor cell, the most sensitive receptor type at any given time is the one that mediates sensation.

So, what happens in the cones and rods during dark adaptation? To attempt to answer this question we need to first consider the mechanism underlying cone and rod function. The only light-mediated event in vision is the interaction of visible light photons with protein molecules in the photoreceptors known as cone or rod opsins, which are also known as "visual pigments." Human cones have one of three types of opsin, each with a slightly different sensitivity to the spectrum of light, which is relevant for color vision. Rods, on the other hand, have a single form of opsin called rhodopsin. In vertebrates, all photoreceptor opsins contain a molecule called retinal, or retinaldehyde. (The ultimate source of retinal is dietary vitamin A; this is the reason why an early sign of vitamin A deficiency is night blindness.)

The absorption of a photon by a molecule of retinal induces a change in the molecular configuration of its hydrocarbon chain—a process known as photoisomerization. After photoisomerization, opsin becomes chemically active and is able to initiate a series of biochemical events in the cones and rods that ultimately lead to a change in the number of glutamate molecules released by the photoreceptor. Glutamate, an amino acid and neurotransmitter, acts as a messenger that conveys to other retinal cells information about light stimulation of photoreceptors. Following its activation by light, an opsin molecule releases its transformed retinal molecule. Free opsin—an opsin that has released its retinal molecule—is likely to be the molecule responsible for the retina's reduced sensitivity to light.

Dark adaptation is required for the recovery of this sensitivity. It is accomplished through a restoration of the original biochemical configuration of visual pigments. This involves a recombination of free opsin with an untransformed retinal—which results in a regeneration of cone opsins and rhodopsin. The rate of delivery of retinal to the photoreceptors is the probable reason for the relatively slow rate of dark adaptation. Since this process evolved to adapt to the slow changes in illumination that occur during the transition from day to night, the rate of change in sensitivity is quite adequate to compensate for changes in natural lighting.

Many diseases that interfere with the complex molecular mechanism underlying dark adaptation lead to night blindness. In addition to vitamin A deficiency, which is the most common cause of night blindness in the nonindustrialized world, inherited eye diseases can cause this condition. Many of these diseases, such as retinitis pigmentosa, are caused by mutations in the genes that code for the many proteins that drive the elegant molecular machinery involved in light detection.

For further reading:

Phototransduction, Dark Adaptation, and Rhodopsin Regeneration. T. D. Lamb and E. N. Pugh, Jr., in Investigative Ophthalmology & Visual Science, Vol. 47, pages 5138–5152; 2006.

The First Steps in Seeing. Chapters 4, 6, 7 and 8. R. W. Rodieck. Sinauer Associates, 1998.

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