Optics of Vision
OPTICS OF THE EYE: The Eye act as camera.
The lens system of the eye is composed of four refractive interfaces: (1) the interface between air and the anterior surface of the cornea, (2) the interface between the posterior surface of the cornea and
the aqueous humor, (3) the interface between the aqueous humor and the anterior surface of the lens of the eye, and
(4) the interface between the posterior surface of the lens and the vitreous humor. The internal index of air is 1; the
cornea, 1.38; the aqueous humor, 1.33; the crystalline lens
(on average), 1.40; and the vitreous humor, 1.34.
Consideration of All Refractive Surfaces of the Eye
as a Single Lens—The “Reduced” Eye. If all the refractive surfaces of the eye are algebraically added together and then considered to be one single lens, the optics of the normal eye may be simplified and represented schematically as a “reduced eye. In the reduced eye, a single refractive surface is considered to exist, with its central point 17 millimeters in front of the retina and total refractive power of 59 diopters when the lens is accommodated for distant vision.
About two-thirds of the 59 diopters of refractive power of the eye is provided by the anterior surface of the cornea
(not by the eye lens).
The principal reason for this phenomenon is that the refractive index of the cornea is markedly different from that of air, whereas the refractive index of the eye lens is not greatly different from the indices of the aqueous humor and vitreous humor.
The total refractive power of the internal lens of the eye is only 20 diopters
Formation of an Image on the Retina:
The lens system of the eye can focus an image on the retina. The image is inverted and reversed with
respect to the object. However, the mind perceives objects in the upright position despite the upside-down orientation on the retina because the brain is trained to consider an inverted image as normal.
MECHANISM OF “ACCOMMODATION”
In children, the refractive power of the lens of the eye can be increased voluntarily from 20 diopters to about
34 diopters, which is an “accommodation” of 14 diopters. To make this accommodation, the shape of the lens is
changed from that of a moderately convex lens to that of a very convex lens.
In a young person, the lens is composed of a strong elastic capsule filled with viscous, proteinaceous, but
transparent fluid. When the lens is in a relaxed state with no tension on its capsule, it assumes an almost spherical
shape, owing mainly to the elastic retraction of the lens capsule.
About 70 suspensory ligaments attach radially around the lens, pulling the lens edges toward the outer circle of the
eyeball. These ligaments are constantly tensed by their attachments at the anterior border of the choroid and
retina. The tension on the ligaments causes the lens to remain relatively flat under normal conditions of the eye
Also located at the lateral attachments of the lens ligaments to the eyeball is the ciliary muscle, which itself has
two separate sets of smooth muscle fibers meridional fibers and circular fibers.
The meridional fibers extend from the peripheral ends of the suspensory ligaments to the corneoscleral junction. When these muscle fibers contract, the peripheral insertions of the lens ligaments are pulled medially toward the edges of the cornea, thereby releasing the ligaments’ tension on the lens.
The circular fibers are arranged circularly all the way around the ligament attachments so that when they contract, a
sphincter-like action occurs, decreasing the diameter of the circle of ligament attachments; this action also allows
the ligaments to pull less on the lens capsule.
Accommodation Is Controlled by Parasympathetic
The ciliary muscle is controlled almost entirely by parasympathetic nerve signals transmitted to the eye
through the third cranial nerve from the third nerve nucleus in the brain stem.
Presbyopia—Loss of Accommodation by the Lens.
The ability of the lens to change shape decreases with age. The power of accommodation decreases from about 14 diopters in a child to less than 2 diopters by the time a person reaches 45 to 50 years and to essentially 0 diopters at age 70 years. Thereafter, the lens remains almost totally non accommodating, a condition known as presbyopia.
To see clearly both in the distance and nearby, an older person must wear bifocal glasses, with the upper segment focused for far-seeing and the lower segment focused for near-seeing.
Iris controls the amount of light that enters the eye. The amount of light that enters the eye through
the pupil is proportional to the area of the pupil or to the square of the diameter of the pupil. The pupil of the
human eye can become as small as about 1.5 millimeters and as large as 8 millimeters in diameter. The quantity of
light entering the eye can change about 30-fold as a result of changes in pupillary aperture.
“Depth of Focus” of the Lens System Increases with
Decreasing Pupillary Diameter:
When a lens system has a great depth of focus, the retina can be displaced considerably from the focal plane of the lens strength can change considerably from normal and the image will still remain nearly in sharp focus, whereas when a lens system has a “shallow” depth of focus, moving the retina only slightly away from the focal plane causes extreme
The greatest possible depth of focus occurs when the pupil is extremely small. The reason for this is that, with
a very small aperture, almost all the rays pass through the center of the lens and the central-most rays are always in
focus, as explained earlier.
Errors of Refraction:
Emmetropia (Normal Vision). The eye is considered to be normal, or “emmetropic,” if parallel light rays from distant objects are in sharp focus on the retina when the ciliary muscle is completely relaxed. This means that the emmetropic eye can see all distant objects clearly with its ciliary muscle relaxed. However, to focus objects at close range, the eye must contract its ciliary muscle and thereby provide appropriate degrees of accommodation.
Hyperopia (Farsightedness). Hyperopia, which is also known as “farsightedness,” is usually due to either an eyeball
that is too short or, occasionally, a lens system that is too weak. In this condition, parallel light rays are not bent sufficiently by the relaxed lens system to come to focus by the time they reach the retina. To overcome this abnormality, the ciliary muscle must contract to increase the strength of the lens. By using the mechanism of accommodation, a farsighted person is capable of focusing distant objects on the retina. If the person has used only a small amount of strength in the ciliary muscle to accommodate for the distant objects, he or she still has much accommodative power left, and objects closer and closer to the eye can also be focused
sharply until the ciliary muscle has contracted to its limit. In old age, when the lens becomes “presbyopic,” a farsighted person is often unable to accommodate the lens sufficiently to focus even distant objects, much less near objects.
Myopia (Nearsightedness). In myopia, or “ “nearsightedness,” when the ciliary muscle is completely relaxed, the light rays coming from distant objects are focused in front of the retina. This condition is usually due to too long an eyeball, but it also can result from too much refractive power in the lens system of the eye. No mechanism exists by which the eye can decrease the strength of its lens to less than that which exists when the ciliary muscle is completely relaxed. A myopic person has no mechanism by which to focus distant objects sharply on the retina. However, as an object moves nearer to the person’s eye, it finally gets close enough that its image can be focused. Then, when the object comes still closer to the eye, the person can use the mechanism of accommodation to keep the image focused clearly. A myopic person has a definite limiting “far point” for clear vision.
Receptor and Neural Function of the Retina
ANATOMY AND FUNCTION OF THE STRUCTURAL ELEMENTS OF THE RETINA
Layers of the Retina:
(1) pigmented layer, (2) layer of rods and cones projecting to the pigment, (3) the outer nuclear layer containing the cell bodies of the rods and cones, (4) outer plexiform layer, (5) inner nuclear layer, (6) inner plexiform layer, (7) ganglionic layer, (8) layer of optic nerve fibers, and (9) inner limiting membrane.
Light enters the lens, it passes first through the ganglion cells and then through the plexiform and nuclear layers before it finally reaches the layer of rods and cones. This distance is a thickness of several hundred micrometers; visual acuity (sharpness of vision) is decreased by this passage through such nonhomogeneous tissue. However, in the central foveal region of the retina, as discussed subsequently, the inside layers are pulled aside to decrease this loss of acuity.
Foveal Region of the Retina and Its Importance in Acute Vision.
The fovea is a minute area in the center of the retina, occupying 1 square millimeter; it is especially
capable of acute and detailed vision. The central fovea, is 0.3 millimeter in diameter, is composed almost
entirely of cones. These cones have a special structure that aids their detection of detail in the visual image
Rods and Cones: In the peripheral portions of the retina, the rods are 2 to 5 micrometers in diameter,
whereas the cones are 5 to 8 micrometers in diameter; in the central part of the retina, in the fovea, there are no
rods and the cones are slender and have a diameter of only 1.5 micrometers
The major functional segments of either a rod or cone are (1) the outer segment, (2) the inner segment, (3) the nucleus, and (4) the synaptic body.
The light-sensitive photochemical is found in the outer segment. In the case of the rods, this photochemical is
rhodopsin; in the cone phytochemicals, usually called simply color pigments, that function almost exactly the same as rhodopsin except for differences in spectral sensitivity. In the outer segments of the rods and cones, large numbers of discs are found. Each disc is actually an infolded shelf of the cell membrane. There are as many as 1000 discs in each rod or cone. Both rhodopsin and the color pigments are conjugated proteins. They are incorporated into the membranes of the discs in the form of transmembrane proteins. The concentrations of these photosensitive pigments in the discs are so great that the pigments themselves constitute about 40 percent of the entire mass of the outer segment.
The inner segment of the rod or cone contains the usual cytoplasm with cytoplasmic organelles. Especially important are the mitochondria, which, as explained later, play the important role of providing energy for function of the
The synaptic body is the portion of the rod or cone that connects with subsequent neuronal cells, the horizontal
and bipolar cells, which represent the next stages in the vision chain.
Pigment Layer of the Retina. The black pigment melanin in the pigment layer prevents light reflection
throughout the globe of the eyeball, which is extremely important for clear vision Without it, light rays would be
reflected in all directions within the eyeball and would cause diffuse lighting of the retina rather than the normal
the contrast between dark and light spots required for the formation of precise images.
Melanin in the pigment layer is absent in albinos. When an albino enters a bright room, the light that impinges on the retina is reflected in all directions inside the eyeball by the unpigmented surfaces of the retina and by the underlying sclera, so a single discrete spot of light that would normally excite only a few rods or cones is reflected everywhere and excites many receptors. Therefore, the visual acuity of albinos, even with the best optical correction, is seldom better than 20/100 to 20/200 rather than the normal 20/20 values. The pigment layer also stores large quantities of
vitamin A. This vitamin A is exchanged back and forth through the cell membranes of the outer segments of the rods and cones, which themselves are embedded in the pigment.
PHOTOCHEMISTRY OF VISION:
RHODOPSIN-RETINAL VISUAL CYCLE AND EXCITATION OF THE RODS
Rhodopsin and Its Decomposition by Light Energy.
The outer segment of the rod that projects into the pigment layer of the retina has a concentration of about
40 percent of the light-sensitive pigment called rhodopsin, or visual purple. This substance is a combination of the
protein scotopsin and the carotenoid pigment retinal (also called “retinene”). Furthermore, the retinal is a particular
type called the 11-cis retinal. This cis form of retinal is important because only this form can bind with scotopsin to
When light energy is absorbed by rhodopsin, the rhodopsin begins to decompose within a very small fraction
of a second, The cause of this rapid decomposition is photoactivation of electrons in the retinal portion of the rhodopsin, which leads to an instantaneous change of the cis form of retinal into the all-trans form that has the same chemical structure as the cis form but a different physical structure. it is a straight molecule rather than an angulated molecule. Because the three-dimensional orientation of the reactive sites of the all-trans-retinal no longer fits with the orientation of the reactive sites on the protein scotopsin, the all-trans-retinal begins to pull away from the scotopsin. The immediate product is bathorhodopsin, which is a partially split combination of the all-trans-retinal and scotopsin.
Bathorhodopsin is extremely unstable and decays in nanoseconds to lumirhodopsin. This product then decays
in microseconds to metarhodopsin I, then in about a millisecond to metarhodopsin II, and finally, much more
slowly (in seconds), into the completely split products scotopsin and all-trans-retinal. It is the metarhodopsin II, also called activated rhodopsin, that excites electrical changes in the rods, and the rods then transmit the visual image into the central nervous system in the form of the optic nerve action potential.
Re-Formation of Rhodopsin. The first stage in the re-formation of rhodopsin is to reconvert the all-trans-retinal into 11-cis retinal. This process requires metabolic energy and is catalyzed by the enzyme retinal isomerase. Once the 11-cis retinal is formed, it automatically recombines with the scotopsin to re-form rhodopsin, which then remains stable until
its decomposition is again triggered by the absorption of light energy.
Role of Vitamin A for Formation of Rhodopsin:
In the second route the all-trans retinal first converted into all-trans retinol, which is one form of
vitamin A. Then the all-trans retinol is converted into 11-cis retinol under the influence of the enzyme isomerase. Finally, the 11-cis retinol is converted into 11-cis retinal, which combines with scotopsin to form new
rhodopsin. Vitamin A is present both in the cytoplasm of the rods and in the pigment layer of the retina. Therefore,
vitamin A is normally always available to form new retinal when needed. Conversely, when there is excess retinal in the retina, it is converted back into vitamin A, thus reducing the amount of light-sensitive pigment in
Night Blindness. Night blindness occurs in persons with severe vitamin A deficiency because without vitamin
A, the amounts of retinal and rhodopsin that can be formed are severely depressed. This condition is called night blindness because the amount of light available at night is
too little to permit adequate vision in vitamin A–deficient
For night blindness to occur, a person usually must remain on a vitamin A-deficient diet for months because
large quantities of vitamin A are normally stored in the liver and can be made available to the eyes. Once night blindness develops, it can sometimes be reversed in less than 1 hour by intravenous injection of vitamin A.
Excitation of the Rod When Rhodopsin Is Activated by Light
The Rod Receptor Potential is Hyperpolarizing, Not
When the rod is exposed to light, the resulting receptor potential is different from the receptor
potentials in almost all other sensory receptors because excitation of the rod causes increased negativity of the
intrarod membrane potential, which is a state of hyperpolarization. This is exactly opposite to the decreased negativity (the process of “depolarization”) that occurs in almost all other sensory receptors.
How does activation of rhodopsin cause hyperpolarization? The answer is that when rhodopsin decomposes, it decreases the rod membrane conductance for sodium ions in the outer segment of the rod. This causes
hyperpolarization of the entire rod membrane in the following way. The inner segment continually pumps sodium from inside the rod to the outside, and potassium ions are pumped to the inside of the cell. Potassium ions leak out of the cell through nongated potassium channels that are confined to the inner segment of the rod. As in other cells, this sodium-potassium pump creates a negative potential on the inside of the entire cell. However, the outer segment
of the rod, where the photoreceptor discs are located, is entirely different; here, the rod membrane, in the dark
state, is leaky to sodium ions that flow through cyclic guanosine monophosphate (cGMP)-gated channels. In
the dark state, cGMP levels are high, permitting positively charged sodium ions to continually leak back to the inside
1onditions, when the rod is not excited, there is reduced electronegativity inside the membrane of the rod, measuring about −40 millivolts rather than the usual −70 to −80
millivolts found in most sensory receptors.
When the rhodopsin in the outer segment of the rod is exposed to light, it is activated and begins to
decompose. The cGMP-gated sodium channels are then closed, and the outer segment membrane conductance of sodium to the interior of the rod is reduced by a three-step process (Figure 51-7): (1) light is absorbed
by the rhodopsin, causing photoactivation of the electrons in the retinal portion, as previously described;
(2) the activated rhodopsin stimulates a G protein called transducin, which then activates cGMP phosphodiesterase, an enzyme that catalyzes the breakdown of cGMP to 5′-cGMP; and (3) the reduction in cGMP closes the
cGMP-gated sodium channels and reduces the inward sodium current. Sodium ions continue to be pumped
outward through the membrane of the inner segment. Thus, more sodium ions now leave the rod than leak
back in. Because they are positive ions, their loss from inside the rod creates increased negativity inside the
membrane, and the greater the amount of light energy striking the rod, the greater the electronegativity
becomes that is, the greater is the degree of hyperpolarization. At maximum light intensity, the membrane
potential approaches −70 to −80 millivolts, which is near the equilibrium potential for potassium ions across the
Duration of the Receptor Potential, and Logarithmic Relation of the Receptor Potential to Light Intensity.
When a sudden pulse of light strikes the retina, the transient hyperpolarization (receptor potential) that
occurs in the rods reaches a peak of about 0.3 seconds and lasts for more than a second. In cones, the change occurs
four times as fast as in the rods. A visual image impinged on the rods of the retina for only one-millionth of a second
can sometimes cause the sensation of seeing the image for longer than a second.
The mechanism by Which Rhodopsin Decomposition Decreases Membrane Sodium Conductance—The
” Under optimal conditions, a
single photon of light, the smallest possible quantal unit
of light energy, can cause a receptor potential of about 1
millivolt in a rod. Only 30 photons of light will cause half
saturation of the rod. How can such a small amount of
light cause such great excitation? The answer is that the
photoreceptors have an extremely sensitive chemical
cascade that amplifies the stimulatory effects about a millionfold, as follows:
- The photon activates an electron in the 11-cis retinal
a portion of the rhodopsin; this activation leads to the
formation of metarhodopsin II, which is the active
form of rhodopsin, as already discussed and shown
in Figure 51-5.
- The activated rhodopsin functions as an enzyme to
activate many molecules of transducin, a protein
present in an inactive form in the membranes of the
discs and cell membrane of the rod.
- The activated transducin activates many more molecules of phosphodiesterase.
- Activated phosphodiesterase is another enzyme; it
immediately hydrolyzes many molecules of cGMP,
thus destroying it. Before being destroyed, the
cGMP had been bound with the sodium channel
protein of the rod’s outer membrane in a way that
“splints” it in the open state. However, in light,
hydrolyzation of the cGMP by phosphodiesterase
removes the splinting and allows the sodium channels to close. Several hundred channels close for
each originally activated molecule of rhodopsin.
Because the sodium flux through each of these
channels have been extremely rapid, the flow of more
then a million sodium ions is blocked by the channel
closure before the channel opens again. This diminution of sodium ion flow is what excites the rod,
as already discussed.
- Within about a second, another enzyme, rhodopsin
kinase, which is always present in the rod, inactivates the activated rhodopsin (the metarhodopsin
II), and the entire cascade reverses back to the
normal state with open sodium channels.
Thus, the rods have developed an important chemical cascade that amplifies the effect of a single photon of
light to cause the movement of millions of sodium ions. This mechanism explains the extreme sensitivity of the rods
under dark conditions. The cones are about 30 to 300 times less sensitive than
the rods, but even this degree of sensitivity allows color vision at any intensity of light greater than extremely dim
Photochemistry of cones
Only one of three types of color pigments is present in each of the different cones, thus making the cones selectively sensitive to different colors: blue, green, or red. These color pigments are called, respectively, blue-sensitive pigment, green-sensitive pigment, and red-sensitive pigment. The absorption characteristics of the pigments in the three types of cones show peak absorbencies at light wavelengths of 445, 535, and 570 nanometers, respectively. These wavelengths are also the wavelengths for peak light sensitivity for each type of cone, which begins to explain how the retina differentiates the colors. The approximate absorption curves for these three pigments are shown in Figure. Also
shown is the absorption curve for the rhodopsin of the rods, with a peak at 505 nanometers.
AUTOMATIC REGULATION OF
RETINAL SENSITIVITY—LIGHT AND
If a person has been in bright light for hours, large portions of the phytochemicals 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 process is called light
Conversely, if a person remains in darkness for a
long time, the retinal and opsins in the rods and cones
are converted back into light-sensitive pigments.
Furthermore, vitamin A is converted back into the retinal to
increase light-sensitive pigments, the final limit being
determined by the number of opsins in the rods and cones
to combine with the retinal. This process is called dark
From the preceding sections, we learned that different cones are sensitive to different colors of light. This section
is a discussion of the mechanisms by which the retina detects the different gradations of color in the visual
OF COLOR DETECTION
All theories of color vision are based on the well-known
the observation that the human eye can detect almost all
gradations of colors when only red, green, and blue
monochromatic lights are appropriately mixed in different combinations.
Spectral Sensitivities of the Three Types of Cones. On
the basis of color vision tests, the spectral sensitivities of
the three types of cones in humans have proved to be
essentially the same as the light absorption curves for the
three types of pigment found in the cones. an orange monochromatic light with a wavelength of 580 nanometers
stimulates the red cones to a value of about 99 (99 percent of the peak stimulation at optimum wavelength); it
stimulates the green cones to a value of about 42, but the blue cones are not stimulated at all. Thus, the ratios
of stimulation of the three types of cones in this instance are 99 : 42 : 0. The nervous system interprets this set of
ratios as the sensation of orange. Conversely, a monochromatic blue light with a wavelength of 450 nanometers
stimulates the red cones to a stimulus value of 0, the green cones to a value of 0, and the blue cones to a value of 97. This set of ratios—0 : 0 : 97—is interpreted by the nervous system as blue. Likewise, ratios of 83: 83 : 0 are
interpreted as yellow, and ratios of 31 : 67 : 36 are interpreted as green.
Perception of White Light. About equal stimulation of
all the red, green, and blue cones give one the sensation
of seeing white. Yet, there is no single wavelength of light
corresponding to white; instead, white is a combination
of all the wavelengths of the spectrum. Furthermore, the
perception of white can be achieved by stimulating the
a retina with a proper combination of only three chosen
colors that stimulate the respective types of cones about
Red-Green Color Blindness. When a single group of colorreceptive cones is missing from the eye, the person is
unable to distinguish some colors from others. For instance,
one can see in Figure 51-10 that green, yellow, orange,
and red colors, which are the colors between the wavelengths of 525 and 675 nanometers, are normally distinguished from one another by the red and green cones.
If either of these two cones is missing, the person
cannot use this mechanism for distinguishing these four
colors; the person is especially unable to distinguish red
from green and is therefore said to have red-green color
A person with loss of red cones is called a protanope;
the overall visual spectrum is noticeably shortened at the
long wavelength end because of a lack of the red cones. A
color-blind person who lacks green cones is called a deuteranope; this person has a perfectly normal visual spectral
width because red cones are available to detect the long
wavelength red color.
Red-green color blindness is a genetic disorder that
occurs almost exclusively in males. That is, genes in the
female X chromosome code for the respective cones. Yet
color blindness almost never occurs in females because at
least one of the two X chromosomes almost always has a
normal gene for each type of cone. Because the male has
only one X chromosome, a missing gene can lead to color
Because the X chromosome in the male is always inherited from the mother, never from the father, color blindness
is passed from mother to son, and the mother is said to be
a color blindness carrier; about 8 percent of all women are
color blindness carriers.
Blue Weakness. Only rarely are blue cones missing,
although sometimes they are underrepresented, which is a
genetically inherited condition giving rise to the phenomenon called blue weakness