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43
Introduction
to Vision
The Virtual Lab icons direct you to specific animations and videos designed to help you visualize what you are reading about. The number beside each icon indicates the number of the clip you can access through your CD-ROM or your student website.
VVLL
OPPOSITE PAGE This painting, Arcturus II by Victor Vasarely, consists of colored squares stacked one on top of the other. The diagonals we perceive radiating from the center of these patterns are not actually in the physical stimulus, but they are perceived because of interactions between excitation and inhibition in the visual system. Hirshhorn Museum and Sculpture Garden, Smithsonian Institution, Gift of Joseph H. Hirshhorn, 1972. Photographer, Lee Stalsworth.
Chapter Contents^ C H A P T E R^3
FOCUSING LIGHT ONTO THE RETINA
Light: The Stimulus for Vision The Eye Light Is Focused by the Eye DEMONSTRATION: Becoming Aware of What Is in Focus
TRANSFORMING LIGHT INTO ELECTRICITY The Visual Receptors and Transduction How Does Transduction Occur?
PIGMENTS AND PERCEPTION Distribution of the Rods and Cones DEMONSTRATION: Becoming Aware of the Blind Spot DEMONSTRATION: Filling in the Blind Spot Dark Adaptation of the Rods and Cones METHOD: Measuring Dark Adaptation Spectral Sensitivity of the Rods and Cones
❚ TEST YOURSELF 3.
NEURAL CONVERGENCE AND PERCEPTION Why Rods Result in Greater Sensitivity Than Cones Why We Use Our Cones to See Details DEMONSTRATION: Foveal Versus Peripheral Acuity
LATERAL INHIBITION AND PERCEPTION What the Horseshoe Crab Teaches Us About Inhibition Lateral Inhibition and Lightness Perception DEMONSTRATION: Creating Mach Bands in Shadows DEMONSTRATION: Simultaneous Contrast A Display That Can’t Be Explained by Lateral Inhibition
SOMETHING TO CONSIDER: PERCEPTION IS INDIRECT
❚ TEST YOURSELF 3.
Think About It If You Want to Know More Key Terms Media Resources VL VIRTUAL LAB
44 CHAPTER 3 Introduction to Vision
Some Questions We Will Consider:
❚ How do chemicals in the eye called visual pigments affect our perception? (p. 47)
❚ How does the way neurons are “wired up” affect our perception? (p. 58)
❚ What do we mean when we say that perception is indirect? (p. 68)
N
ow that we know something about the psychophysi- cal approach to perception (Chapter 1) and basic physiological principles (Chapter 2), we are ready to apply these approaches to the study of perception. In this chap- ter we describe what happens at the very beginning of the visual system, beginning when light enters the eye, and in Chapter 4 we will consider processes that occur in VL 1 the visual areas of the brain.
Focusing Light Onto
the Retina
Vision begins when visible light is reflected from objects into the eye.
Light: The Stimulus for Vision
Vision is based on visible light, which is a band of energy within the electromagnetic spectrum. The electromag- netic spectrum is a continuum of electromagnetic energy that is produced by electric charges and is radiated as waves (Figure 3.1). The energy in this spectrum can be described by its wavelength—the distance between the peaks of the elec- tromagnetic waves. The wavelengths in the electromagnetic spectrum range from extremely short–wavelength gamma rays (wavelength about 10^12 meters, or one ten-billionth
of a meter) to long-wavelength radio waves (wavelength about 10^4 meters, or 10,000 meters). Visible light, the energy within the electromagnetic spectrum that humans can perceive, has wavelengths rang- ing from about 400 to 700 nanometers (nm), where 1 nano- meter 10 ^9 meters. For humans and some other animals, the wavelength of visible light is associated with the differ- ent colors of the spectrum. Although we will usually specify light in terms of its wavelength, light can also be described as consisting of small packets of energy called photons , with one photon being the smallest possible packet of light energy.
The Eye The eye is where vision begins. Light reflected from objects in the environment enters the eye through the pupil and is focused by the cornea and lens to form sharp images of the objects on the retina, which contains the receptors for vision (Figure 3.2a). VL^2 There are two kinds of visual receptors, rods and cones, which contain light-sensitive chemicals called visual pigments that react to light and trigger electrical signals. These signals flow through the network of neurons that make up the retina (Figure 3.2b). The signals then emerge from the back of the eye in the optic nerve, which conducts signals toward the brain. The cornea and lens at the front of the eye and the receptors and neurons in the retina lining the back of the eye shape what we see by creating the transforma- tions that occur at the beginning of the perceptual process.
Light Is Focused by the Eye Once light is reflected from an object into the eye, it needs to be focused onto the retina. The cornea, the transparent covering of the front of the eye, accounts for about 80 per- cent of the eye’s focusing power, but like the lenses in eye- glasses, it is fi xed in place, so can’t adjust its focus. The lens, which supplies the remaining 20 percent of the eye’s focus-
500 600
Gamma rays
Visible light
Infrared
X-rays
Ultra- violet rays
Infrared rays Radar^ FM^ TV^ AM^
AC circuits
Ultraviolet
Wavelength (nm)
10 –3^10 –1^10 1 103 105 10 7 10 9 10 11 10 13
400 700
Figure 3.1 ❚ The electromagnetic spectrum, showing the wide range of energy in the environment and the small range within this spectrum, called visible light, that we can see. The wavelength is in nanometers (nm), where 1 nm 10 ^9 meters.
46 CHAPTER 3 Introduction to Vision
appears double. When the pencil is about 12 inches away, focus on the pencil point. You now see the point sharply, but the faraway object you were focusing on before has become blurred. Now, bring the pencil even closer until you can’t see the point sharply no matter how hard you try. Notice the strain in your eyes as you try unsuccessfully to bring the point into focus. ❚
When you changed focus during this demonstration, you were changing your accommodation. Accommodation enables you to bring both near and far objects into focus, although objects at different distances are not in focus at the same time. But accommodation has its limits. When the pencil was too close, you couldn’t see it clearly, even though you were straining to accommodate. The distance at which your lens can no longer adjust to bring close objects into fo- cus is called the near point. The distance of the near point increases as a person gets older, a condition called presbyopia (for “old eye”). The near point for most 20-year-olds is at about 10 cm, but it increases to 14 cm by age 30, 22 cm at 40, and 100 cm at 60 (Figure 3.4). This loss of ability to accommodate occurs be- cause the lens hardens with age, and the ciliary muscles be- come weaker. These changes make it more difficult for the lens to change its shape for vision at close range. Though this gradual decrease in accommodative abil- ity poses little problem for most people before the age of 45, at around that age the ability to accommodate begins to de- crease rapidly, and the near point moves beyond a comfort- able reading distance. There are two solutions to this prob- lem. One is to hold reading material farther away. If you’ve ever seen someone holding a book or newspaper at arm’s length, the person is employing this solution. The other so- lution is to wear glasses that add to the eye’s focusing power, so it can bring light to a focus on the retina. Of course, many people who are far younger than 45 need to wear glasses to see clearly. Most of these people have myopia, or nearsightedness, an inability to see dis- tant objects clearly. The reason for this difficulty, which affects more than 70 million Americans, is illustrated in Figure 3.5a: The myopic eye brings parallel rays of light
400
70
100
60 50
Comfortable reading distance
75 50 25 10
40 30 2010
Distance of near point (cm)
Age in years
Figure 3.4 ❚ Vertical lines show how the distance of the near point (green numbers) increases with increasing age. When the near point becomes farther than a comfortable reading distance, corrective lenses (reading glasses) become necessary.
into focus at a point in front of the retina so that the image reaching the retina is blurred. This problem can be caused by either of two factors: (1) refractive myopia, in which the cornea and/or the lens bends the light too much, or (2) axial myopia, in which the eyeball is too long. Either way, images of faraway objects are not focused sharply, so objects look blurred. How can we deal with this problem? One way to create a focused image on the retina is to move the stimulus closer. This pushes the focus point farther back (see Figure 3.3b), and if we move the stimulus close enough, we can push the focus point onto the retina (Figure 3.5b). The distance at which the spot of light becomes focused on the retina is called the far point; when the spot of light is at the far point, a myope can see it clearly. Although a person with myopia can see nearby objects clearly (which is why a myopic person is called nearsighted), objects beyond the far point are still out of focus. The so- lution to this problem is well known to anyone with myo- pia: corrective eyeglasses or contact lenses. These corrective lenses bend incoming light so that it is focused as if it were at the far point, as illustrated in Figure 3.5c. Notice that the lens placed in front of the eye causes the light to enter the eye at exactly the same angle as light coming from the far point in Figure 3.5b. Although glasses or contact lenses are the major route to clear vision for people with myopia, surgical procedures in which lasers are used to change the shape of the cor- nea have been introduced that enable people to experience good vision without corrective lenses. More than 1 million Americans a year have laser-assisted in situ keratomileusis (LASIK) surgery. LASIK involves sculpting the cornea with a type of laser called an excimer laser, which does not heat tissue. A small flap, less than the thickness of a human hair, is cut into the surface of the cornea. The flap is folded out of the way, the cornea is sculpted by the laser so that it focuses light onto the retina, and the flap is then folded back into place. The result, if the procedure is successful, is good vi- sion without the need for glasses. A person with hyperopia, or farsightedness, can see distant objects clearly but has trouble seeing nearby objects.
In the hyperopic eye, the focus point for parallel rays of light is located behind the retina, usually because the eyeball is too short. By accommodating to bring the focus point back to the retina, people with hyperopia are able to see distant objects clearly. Nearby objects, however, are more difficult for a per- son with hyperopia to deal with because a great deal of ac- commodation is required to return the focus point to the retina. The constant need to accommodate when looking at nearby objects (as in reading or doing close-up work) results in eyestrain and, in older people, headaches. Headaches do not usually occur in young people because they can accom- modate easily, but older people, who have more difficulty accommodating because of presbyopia, are more likely to
experience headaches and may therefore require a corrective lens that brings the focus point forward onto the retina. Focusing the image clearly onto the retina is the initial step in the process of vision. But it is important to real- ize that although a sharp image on the retina is essential for clear vision, we do not see the image on the retina. Vi- sion occurs not in the retina, but in the brain, and before the brain can create vision, the light on the retina must be transformed into electricity.
Transforming Light
Into Electricity
The transformation of light into electricity is the process of transduction we introduced in Chapter 1 (p. 7).
The Visual Receptors and Transduction Transduction is carried out by receptors , neurons specialized for receiving environmental energy and transforming this energy into electricity (see page 7). The receptors for vision are the rods and the cones. As we will see shortly, the rods and cones have different properties that affect our perception. However, they both function similarly during transduction, so to describe transduction we will focus on the rod recep- tor shown in Figure 3.6. The key part of the rod for transduction is the outer segment, because it is here that the light acts to create electricity. Rod outer segments contain stacks of discs (Figure 3.6a). Each disc contains thousands of visual pig- ment molecules, one of which is highlighted in Figure 3.6b. Zooming in on an individual molecule, we can see that the molecule is a long strand of protein called opsin, which loops back and forth across the disc membrane seven times (Figure 3.6c). Our main concern is one particular place where a molecule called retinal is attached. Each visual pig- ment molecule contains only one of these tiny retinal mol- ecules. The retinal is crucial for transduction, because it is the part of the visual pigment that is sensitive to light. Transduction is triggered when the light-sensitive reti- nal absorbs one photon of light. (Remember that a photon is the smallest possible packet of light energy.) Figure 3.7 shows what happens. Before light is absorbed, the retinal is next to the opsin (Figure 3.7a). (Only a small part of the opsin, where the retinal is attached, is shown here). When a photon of light hits the retinal, it changes shape, so it is sticking out from the opsin. This change in shape is called isomerization, and it is this step that triggers the transformation of the light en- tering the eye into electricity in the receptors.
How Does Transduction Occur? Saying that isomerization of the visual pigment results in transduction is just the first step in explaining how light is
(a) Focus in front of retina
(b) Far point
(c) Corrective lens
A)
A)
Figure 3.5 ❚ Focusing of light by the myopic (nearsighted) eye. (a) Parallel rays from a distant spot of light are brought to a focus in front of the retina, so distant objects appear blurred. (b) As the spot of light is moved closer to the eye, the focus point is pushed back until, at the far point, the rays are focused on the retina, and vision becomes clear. (c) A corrective lens, which bends light so that it enters the eye at the same angle as light coming from the far point, brings light to a focus on the retina. Angle A is the same in (b) and (c).
Transforming Light Into Electricity 47
Pirenne, 1942) was able to draw conclusions about the phys- iology of transduction by determining a person’s ability to see dim flashes of light.
Hecht’s Psychophysical Experiment The starting point for Hecht’s experiment was his knowledge that transduction is triggered by the isomerization of visual pigment molecules and that it takes just one photon of light to isomerize a visual pigment molecule. With these facts in hand, Hecht did a psychophysical experiment that enabled him to determine how many visual pigment molecules need to be isomerized for a person to see. He accomplished this by using the method of constant stimuli (see page 14) to de- termine a person’s absolute threshold for seeing a brief flash of light. What was special about this experiment is that Hecht used a precisely calibrated light source, so he could determine the threshold in terms of the number of photons needed to see. Hecht found that a person could detect a flash of light that contained 100 photons. To determine how many visual pigment molecules were isomerized by this flash, he con- sidered what happened to those 100 photons before they reached the visual pigment. The first thing that happens is that about half the photons bounce off the cornea or are absorbed by the lens and by the vitreous humor, a jellylike substance that fi lls the inside of the eye (Figure 3.9). Thus, only 50 of the original 100 photons actually reach the ret- ina at the back of the eye. But of these 50, only about 7 are absorbed by the light-sensitive retinal part of the visual pig- ment. The rest hit the larger opsin (which is not sensitive to light) or may slip between the visual receptors. This means that a person sees a flash of light when only 7 visual pig- ment molecules are isomerized (also see Sackett, 1972, who obtained a similar result). But Hecht wasn’t satisfied just to show that a person sees a light when 7 visual pigment molecules are activated.
He also wanted to determine how many visual pigment mol- ecules must be isomerized to activate a single rod receptor. We can understand how he determined this by looking at Figure 3.10, which shows that the light flash Hecht’s observ- ers saw covered about 500 receptors. Because Hecht had de- termined that the observers saw the light when only 7 visual pigment molecules were isomerized, the figure shows the 7 photons that cause this isomerization approaching the 500 receptors. With this picture of 7 photons approaching 500 recep- tors in mind, Hecht asked the following question: What is the likelihood that any two of these photons would enter the same receptor? The answer to this question is “very small.” It
Transforming Light Into Electricity 49
Experience and action
Physiological processes Stimuli
PP
PH
PH
Hecht’s experiment— psychophysical
Hecht’s conclusions— physiological
Figure 3.8 ❚ The three main components of the perceptual process (see Figures 1.1 and 1.10). Hecht was able to draw physiological (PH) conclusions based on the measurement of a psychophysical (PP) relationship.
100 photons to eye
Vitreous humor
50 photons reach retina 7 photons absorbed by visual pigment
50 photons reflected or absorbed by eye structures
Figure 3.9 ❚ The observer in Hecht et al.’s (1942) experiment could see a spot of light containing 100 photons. Of these, 50 photons reached the retina, and 7 photons were absorbed by visual pigment molecules.
500 receptors
7 photons that will each isomerize a single visual pigment molecule
Light flash
Figure 3.10 ❚ How Hecht reasoned about what happened at threshold, when observers were able to see a flash of light when 7 photons were absorbed by visual pigment molecules. The 7 photons that were absorbed are shown poised above 500 rod receptors. Hecht reasoned that because there were only 7 photons but 500 receptors, it is likely that each photon entered a separate receptor. Thus, only one visual pigment molecule was isomerized per rod. Because the observer perceived the light, each of 7 rods must have been activated.
50 CHAPTER 3 Introduction to Vision
is therefore unlikely that 2 of the 7 visual pigment molecules that each absorbed a photon Hecht’s experiment would be in the same receptor. Hecht concluded that only 1 visual pig- ment molecule per receptor was isomerized when his observ- er’s reported seeing the light; therefore, a rod receptor can be activated by the isomerization of only 1 visual pigment mol- ecule. Hecht’s conclusions can be summarized as follows:
- A person can see a light if 7 rod receptors are activated simultaneously.
- A rod receptor can be activated by the isomerization of just 1 visual pigment molecule. The beauty of Hecht’s experiment is that he used the psychophysical approach, measuring relationship PP in Figure 3.8, to draw conclusions about the physiological operation of the visual system. You will see, as you read this book, that this technique of discovering physiological mechanisms from psychophysical results has been used to study the physiological mechanisms responsible for percep- tions ranging from color and motion in vision to the pitch of sounds for hearing to the ability to perceive textures with the sense of touch.
The Physiology of Transduction Hecht’s dem- onstration that it takes only one photon to activate a rod receptor posed a challenge for physiological researchers, because they needed to explain how isomerization of just one of the millions of visual pigment molecules in a rod can activate the receptor. Hecht carried out his experiment in the 1940s when physiological and chemical tools were not
available to solve this problem, so it wasn’t until 30 years later that researchers in physiology and chemistry labora- tories were able to discover the mechanism that explained Hecht’s result. Physiological and chemical research determined that isomerization of a single visual pigment molecule triggers thousands of chemical reactions, which in turn trigger thousands more (Figure 3.11). A biological chemical that in small amounts facilitates chemical reactions in this way is called an enzyme ; therefore, the sequence of reactions trig- gered by the activated visual pigment molecule is called the enzyme cascade. Just as lighting one match to a fuse can trigger a fireworks display consisting of thousands of points of light, isomerizing one visual pigment molecule can cause a chemical effect that is large enough to activate the entire rod receptor. For more specific details as to how this is ac- complished, see “If You Want to Know More #3” at the end of this chapter.
Pigments and Perception
Vision can occur only if the rod and cone visual pigments transform the light entering the eye into electricity. We will now see, however, that these pigments not only determine whether or not we see, but also shape specific aspects of our perceptions. We will show how the properties of visual pigments help determine how sensitive we are to light, by comparing perception determined by the rod receptors to perception determined by the cone receptors. To accom- plish this, we need to consider how the rods and cones are distributed in the retina.
Distribution of the Rods and Cones From the cross section of the retina in Figure 3.2b you can see that the rods and cones are interspersed in the retina. In the part of the retina shown in this picture, there are more rods than cones. The ratio of rods and cones depends, however, on location in the retina. Figure 3.12, which shows how the rods and cones are distributed in the retina, indicates that
- There is one small area, the fovea, that contains only cones. When we look directly at an object, its image falls on the fovea.
- The peripheral retina, which includes all of the retina outside of the fovea, contains both rods and cones. It is important to note that although the fovea is the place where there are only cones, there are many cones in the peripheral retina. The fovea is so small (about the size of this “o”) that it contains only about 1 per- cent, or 50,000, of the 6 million cones in the retina (Tyler, 1997a, 1997b).
- There are many more rods than cones in the periph- eral retina because most of the retina’s receptors are located there and because there are about 120 million rods and 6 million cones.
Visual pigment molecule
The enzyme cascade
Figure 3.11 ❚ This sequence symbolizes the enzyme cascade that occurs when a single visual pigment molecule is activated by absorption of a quantum of light. In the actual sequence of events, each visual pigment molecule activates hundreds more molecules, which, in turn, each activate about a thousand more molecules. Thus, isomerization of one visual pigment molecule activates about a million other molecules.
52 CHAPTER 3 Introduction to Vision
D E M O N S T R AT I O N
Becoming Aware of the Blind Spot
Place the book on your desk. Close your right eye, and posi- tion yourself above the book so that the cross in Figure 3.15 is aligned with your left eye. Be sure the page is flat and, while looking at the cross, slowly move closer. As you move closer, be sure not to move your eye from the cross, but at the same time keep noticing the circle off to the side. At some point, around 3 to 9 inches from the book, the circle should disap- pear. When this happens the image of the circle is falling on your blind spot. ❚
Figure 3.15 ❚
Why aren’t we usually aware of the blind spot? One rea- son is that the blind spot is located off to the side of our visual field, where objects are not in sharp focus. Because of this and because we don’t know exactly where to look for it (as opposed to the demonstration, in which we are focusing our attention on the circle), the blind spot is hard to detect. But the most important reason that we don’t see the blind spot is that some mechanism in the brain “fills in” the place where the image disappears (Churchland & Ramachandran, 1996). The next demonstration illustrates an important property of this filling-in process.
D E M O N S T R AT I O N
Filling in the Blind Spot Close your right eye and, with the cross in Figure 3.16 lined up with your left eye, move the “wheel” toward you. When the center of the wheel falls on your blind spot, notice how the spokes of the wheel fill in the hole (Ramachandran, 1992). ❚ VL^3
Optic nerve
Blind spot
Ganglion cell fibers
Receptors
Figure 3.14 ❚ There are no receptors at the place where the optic nerve leaves the eye. This enables the receptor’s ganglion cell fibers to flow into the optic nerve. The absence of receptors in this area creates the blind spot.
These demonstrations show that the brain does not fi ll in the area served by the blind spot with “nothing”; rather, it creates a perception that matches the surrounding pat- tern—the white page in the first demonstration, and the spokes of the wheel in the second one.
Dark Adaptation of the Rods and Cones A recent episode of the Mythbusters program on the Dis- covery Channel (2007) was devoted to investigating myths about pirates (Figure 3.17). One of the myths explored was that pirates wore eye patches to preserve night vision in one eye, so when they went from the bright light outside to the darkness belowdecks they could see with their previously patched eye. To determine whether this works, the myth- busters carried out some tasks in a dark room just after both of their eyes had been in the light and did some differ- ent tasks with an eye that had just previously been covered with a patch for 30 minutes. It isn’t surprising that they completed the tasks much more rapidly when using the eye that had been patched. Anyone who has taken sensation and perception could have told the mythbusters that the eye patch would work because keeping an eye in the dark trig-
Figure 3.16 ❚ View the pattern as described in the text, and observe what happens when the center of the wheel falls on your blind spot. (From Ramachandran, 1992.)
gers a process called dark adaptation, which causes the eye to increase its sensitivity in the dark. (Whether pirates actu- ally used patches to dark adapt their eyes to help them see when going belowdecks remains a plausible, but unproven, hypothesis.) We are going to describe dark adaptation and show how it can be used to illustrate a difference between the rods and cones. You may have noticed that when the lights are turned off it is difficult to see at first, but that eventually you begin seeing things that were previously not visible. However, as you experience your eye’s increasing sensitivity in the dark, it is probably not obvious that your eyes increase their sensi- tivity in two distinct stages: an initial rapid stage and a later, slower stage. These two stages are revealed by measurement of the dark adaptation curve—a plot of how visual sensitiv- ity changes in the dark, beginning with when the lights are extinguished. We will now describe three ways of measuring the dark adaptation curve, to show that the initial rapid stage is due to adaptation of the cone receptors and the second, slower stage is due to adaptation of the rod receptors. We will first describe how to measure a two-stage dark adaptation curve that is caused by both the rods and the cones. We will then measure the dark adaptation of the cones alone and of the rods alone and show how the different adaptation rates of the rods and the cones can be explained by differences in their visual pigments. In all of our dark adaptation experiments, we ask our observer to adjust the intensity of a small, flashing test light so that he or she can just barely see it. This is similar to the psychophysical method of adjustment that we described in Chapter 1 (see page 14). In the first experiment, our observer looks at a small fi xation point while paying attention to a flashing test light that is off to the side (Figure 3.18). Be- cause the observer is looking directly at the fi xation point, its image falls on the fovea, and the image of the test light falls in the periphery. Thus, the test light stimulates both rods and cones. The dark adaptation curve is measured as follows.
The dark adaptation curve shows that as dark adapta- tion proceeds, the observer becomes more sensitive to the light. Note that higher sensitivity is at the bottom of this graph, so as the dark adaptation curve moves downward, the observer’s sensitivity is increasing. The dark adaptation curve indicates that the observ- er’s sensitivity increases in two phases. It increases rapidly for the first 3 to 4 minutes after the light is extinguished and then levels off; it begins increasing again at about 7 to 10 minutes and continues to do so until about 20 or 30 minutes after the light was extinguished (red curve in Figure 3.19). The sensitivity at the end of dark adaptation, labeled dark-adapted sensitivity, is about 100,000 times greater than the light-adapted sensitivity measured before dark adaptation began. Measuring Cone Adaptation To measure dark adaptation of the cones alone, we have to ensure that the image of the test light stimulates only cones. We achieve this by having the observer look directly at the test light so its image will fall on the all-cone fovea, and by making the test light small enough so that its entire image falls within the fovea. The dark adaptation curve determined by this procedure is indicated by the green line in Figure 3.19. This
Pigments and Perception 53
Figure 3.17 ❚ Why did pirates wear eye patches? Did they all have exactly the same eye injury? Were they trying to look scary? Or were they dark adapting the patched eye?
Peripheral retina Fixation point
Test light
Fovea
Figure 3.18 ❚ Viewing conditions for a dark adaptation experiment. The image of the fixation point falls on the fovea, and the image of the test light falls in the peripheral retina.
METHOD ❚ Measuring Dark Adaptation
The first step in measuring dark adaptation is to light adapt the observer by exposure to light. While the adapt- ing light is on, the observer indicates his or her sensitiv- ity by adjusting the intensity of a test light so it can just barely be seen. This is called the light-adapted sensitivity, because it is measured while the eyes are adapted to the light. Once the light-adapted sensitivity is determined, the adapting light is extinguished, so the observer is in the dark. The course of dark adaptation is usually mea- sured by having the observer turn a knob to adjust the intensity of the test light so it can just barely be seen. Because the observer is becoming more sensitive to the light, he or she must continually decrease the light’s in- tensity to keep it just barely visible. The result, shown as the red curve in Figure 3.19, is a dark adaptation curve.
Why do the rods take about 20 to 30 minutes to reach their maximum sensitivity (point R on the curve), compared to only 3 to 4 minutes for the cones (point C)? The answer to this question involves a process called visual pigment regeneration, which occurs more rapidly in the cones than in the rods.
Visual Pigment Regeneration When light hits the light-sensitive retinal part of the visual pigment mol- ecule, it is isomerized and triggers the transduction pro- cess (Figure 3.7). It then separates from the opsin part of the molecule. This separation causes the retina to become lighter in color, a process called visual pigment bleaching. This bleaching is shown in Figure 3.20, which shows a pic- ture of a frog retina that was taken moments after it was il- luminated with light (Figure 3.20a). The red color is the vi- sual pigment. As the light remains on, more and more of the pigment’s retinal is isomerized and breaks away from the opsin, so the retina’s color changes (Figures 3.20b and c). Does this mean that all of our pigment eventually be- comes bleached if we stay in the light? This would be a bad situation because we need intact visual pigment molecules to see. Luckily, even in the light, as some molecules are ab- sorbing light, isomerizing, and splitting apart, molecules that have been split apart are undergoing a process called visual pigment regeneration in which the retinal and opsin become rejoined. As you look at the page of this book, some of your visual pigment molecules are isomerizing and bleaching, as shown in Figure 3.20, and others are regenerating. This means that under most normal light levels your eye always contains some bleached visual pigment and some intact visual pig- ment. If you were to turn out the lights, then bleached vi- sual pigment would continue to regenerate, but there would
be no more isomerization, so eventually your retina would contain only intact (unbleached) visual pigment molecules. As retinal combines with opsin in the dark, the pigment regains its darker red color. William Rushton (1961) devised a procedure to measure the regeneration of visual pigment in humans by measuring this darkening of the visual pig- ment that occurs during dark adaptation. Rushton’s mea- surements showed that cone pigment takes 6 minutes to regenerate completely, whereas rod pigment takes more than 30 minutes. When he compared the course of pigment regeneration to the rate of psychophysical dark adaptation, he found that the rate of cone dark adaptation matched the rate of cone pigment regeneration and the rate of rod dark adaptation matched the rate of rod pigment regeneration. Rushton’s result demonstrated two important connec- tions between perception and physiology:
1. Our sensitivity to light depends on the concentration of a chemical—the visual pigment. 2. The speed at which our sensitivity is adjusted in the dark depends on a chemical reaction—the regenera- tion of the visual pigment.
We can appreciate the fact that the increase in sensitiv- ity we experience during dark adaptation is caused by visual pigment regeneration by considering what happens when the visual pigment can’t regenerate because of a condition called detached retina. A major cause of detached retinas is traumatic injuries of the eye or head, as when a base- ball player is hit in the eye by a line drive. When part of the retina becomes detached, it has become separated from a layer that it rests on, called the pigment epithelium, which contains enzymes that are necessary for pigment regenera- tion (see Figure 3.2b). The result is that once visual pigments
(a) (b) (c)
Retinal
Opsin Opsin Opsin
Figure 3.20 ❚ A frog retina was dissected from the eye in the dark and then exposed to light. (a) This picture was taken just after the light was turned on. The dark red color is caused by the high concentration of visual pigment in the receptors that are still in the unbleached state, as indicated by the closeness of the retinal and opsin in the diagram above the retina. Only a small part of the opsin molecule is shown. (b, c) As the pigment isomerizes, the retinal and opsin break apart, and the retina becomes bleached, as indicated by the lighter color.
Bruce Goldstein
Pigments and Perception 55
56 CHAPTER 3 Introduction to Vision
are bleached, so the retinal and opsin are separated, they can no longer be recombined in the detached part of the ret- ina, and the person becomes blind in the area of the visual field served by this area of the retina.
Spectral Sensitivity of
the Rods and Cones
Another way to show that perception is determined by the properties of the visual pigments is to compare rod and cone spectral sensitivity—an observer’s sensitivity to light at each wavelength across the visible spectrum.
Measuring Spectral Sensitivity In our dark adaptation experiments, we used a white test light, which contains all wavelengths in the visible spectrum. To deter- mine spectral sensitivity, we use flashes of monochromatic light, light that contain only a single wavelength. We deter- mine the threshold for seeing these monochromatic lights for wavelengths across the visible spectrum (see Figure 3.1). For example, we might first determine the threshold for see- ing a 420-nm (nanometer) light, then a 440-nm light, and so on, using one of the psychophysical methods for measur- ing threshold described in Chapter 1. The result is the curve in Figure 3.21a, which shows that the threshold for seeing light is lowest in the middle of the spectrum; that is, less light is needed to see wavelengths in the middle of the spec- trum than to see wavelengths at either the short- or long- wavelength ends of the spectrum. The ability to see wavelengths across the spectrum is often plotted not in terms of threshold versus wavelength as in Figure 3.21a, but in terms of sensitivity versus wave- length. We can convert threshold to sensitivity with the fol- lowing equation: sensitivity 1/threshold. When we do this for the curve in Figure 3.21a, we obtain the curve in Figure 3.21b, which is called the spectral sensitivity curve. We measure the cone spectral sensitivity curve by hav- ing people look directly at the test light, so that it stimu- lates only the cones in the fovea, and presenting test flashes of wavelengths across the spectrum. We measure the rod spectral sensitivity curve by measuring sensitivity after the eye is dark adapted (so the rods control vision because they are the most sensitive receptors) and presenting test flashes off to the side of the fi xation point. The cone and rod spectral sensitivity curves, shown in Figure 3.22, show that the rods are more sensitive to short- wavelength light than are the cones, with the rods being most sensitive to light of 500 nm and the cones being most sensitive to light of 560 nm. This difference in the sensitiv- ity of the cones and the rods to different wavelengths means that as vision shifts from the cones to the rods during dark adaptation, we become relatively more sensitive to short- wavelength light—that is, light nearer the blue and green end of the spectrum. You may have noticed an effect of this shift to short- wavelength sensitivity if you have observed how green foli- age seems to stand out more near dusk. The shift from cone
Figure 3.21 ❚ (a) The threshold for seeing a light versus wavelength. (b) Relative sensitivity versus wavelength—the spectral sensitivity curve. (Adapted from Wald, 1964.)
Relative sensitivity
High
Low 400 500 600 700
Relative threshold
High
Low 400 500 600 700 (a) Wavelength (nm)
(b) Wavelength (nm)
Threshold curve
Spectral sensitivity curve
Relative sensitivity
Wavelength (nm)
0
Rod vision Cone visionCone vision
400 500 600 700
Figure 3.22 ❚ Spectral sensitivity curves for rod vision (left) and cone vision (right). The maximum sensitivities of these two curves have been set equal to 1.0. However, the relative sensitivities of the rods and the cones depend on the conditions of adaptation: The cones are more sensitive in the light, and the rods are more sensitive in the dark. The circles plotted on top of the rod curve are the absorption spectrum of the rod visual pigment. (From Wald, 1964; Wald & Brown, 1958.)
58 CHAPTER 3 Introduction to Vision
- Where on the retina does a researcher need to pres- ent a stimulus to test dark adaptation of the cones? How can adaptation of the rods be measured without any interference from the cones?
- Describe how rod and cone sensitivity changes starting when the lights are turned off and how this change in sensitivity continues for 20–30 minutes in the dark.
- What happens to visual pigment molecules when they (a) absorb light and (b) regenerate? What is the connection between visual pigment regeneration and dark adaptation?
- What is spectral sensitivity? How is a cone spectral sensitivity curve determined? A rod spectral sensi- tivity curve?
- What is an absorption spectrum? How do rod and cone pigment absorption spectra compare, and what is their relationship to rod and cone spectral sensitivity?
Neural Convergence
and Perception
We’ve seen how perception can be shaped by properties of the visual pigments in the receptors. We now move past the receptors to show how perception is also shaped by neural circuits in the retina. Figure 3.25a is a cross section of the retina that has been stained to reveal the retina’s layered structure. Figure 3.25b shows the five types of neurons that make up these layers. Signals generated in the receptors (R) travel to the bipolar cells (B) and then to the ganglion cells (G). The receptors and bipolar cells do not have long axons, but the ganglion cells have axons like the neurons in Figure 2.4. These axons transmit signals out of the retina in the optic VL 5, 6 nerve (see Figure 3.14). In addition to the receptors, bipolars, and ganglion cells, there are two other types of neurons, the horizontal cells and amacrine cells, which connect neurons across the retina. Signals can travel between receptors through the horizontal cells and between bipolar cells and between ganglion cells through the amacrine cells. We will return to the horizontal and amacrine cells later in the chapter. For now we will focus on the direct pathway from the receptors to the ganglion cells. We focus specifically on the property of neural convergence (or just convergence for short) that occurs when one neuron receives signals from many other neurons. We introduced convergence in Chapter 2 (page 33). Now let’s see how it applies to the neurons in the retina. In Figure 3.25b the ganglion cell on the right receives sig- nals from three receptors (indicated by light color). A great deal of convergence occurs in the retina because there are 126 million receptors, but only 1 million ganglion cells. Thus, on the average, each ganglion cell receives signals from 126 re- ceptors. We can show how convergence can affect perception
by continuing our comparison of the rods and cones. An im- portant difference between rods and cones is that the signals from the rods converge more than do the signals from the cones. We can appreciate this difference by noting that there are 120 million rods in the retina, but only 6 million cones. On the average, about 120 rods pool their signals to one ganglion cell, but only about 6 cones send signals to a single ganglion cell. This difference between rod and cone convergence be- comes even greater when we consider the foveal cones. (Re- member that the fovea is the small area that contains only cones.) Many of the foveal cones have “private lines” to gan- glion cells, so that each ganglion cell receives signals from only one cone, with no convergence. The greater conver- gence of the rods compared to the cones translates into two differences in perception: (1) the rods result in better sensi- tivity than the cones, and (2) the cones result in better detail vision than the rods.
Why Rods Result in Greater Sensitivity Than Cones One reason rod vision is more sensitive than cone vision is that it takes less light to generate a response from an indi- vidual rod receptor than from an individual cone receptor (Barlow & Mollon, 1982; Baylor, 1992). But there is another reason as well: The rods have greater convergence than the cones. We can understand why the amount of convergence is important for determining sensitivity by expanding our dis- cussion of neurotransmitters from Chapter 2 (see page 31). We saw that the release of excitatory transmitter at the syn- apse increases the chances that the receiving neuron will fire. This means that if a neuron receives excitatory transmitter from a number of neurons it will be more likely to fire. Keeping this basic principle in mind, we can see how the difference in rod and cone convergence translates into dif- ferences in the maximum sensitivities of the cones and the rods. In the two circuits in Figure 3.26, five rod receptors converge onto one ganglion cell and five cone receptors each send signals onto their own ganglion cells. We have left out the bipolar, horizontal, and amacrine cells in these circuits for simplicity, but our conclusions will not be affected by these omissions. For the purposes of our discussion, we will assume that we can present small spots of light to individual rods and cones. We will also make the following additional assumptions:
1. One unit of light intensity causes the release of one unit of excitatory transmitter, which causes one unit of excitation in the ganglion cell. 2. The threshold for ganglion cell fi ring is 10 units of excitation. That is, the ganglion cell must receive 10 units of excitation to fi re. 3. The ganglion cell must fi re before perception of the light can occur.
When we present spots of light with an intensity of 1 to each receptor, the rod ganglion cell receives 5 units of excitation, 1 from each of the 5 rod receptors. Each of the cone ganglion cells receives 1 unit of excitation, 1 from each cone receptor. Thus, when intensity 1, neither the rod nor the cone ganglion cells fire. If, however, we increase the intensity to 2, as shown in the figure, the rod ganglion cell receives 2 units of excitation from each of its 5 receptors, for a total of 10 units of excitation. This total reaches the threshold for the rods’ ganglion cell, it fires, and we see the
light. Meanwhile, at the same intensity, the cones’ ganglion cells are still below threshold, each receiving only 2 units of excitation. For the cones’ ganglion cells to fire, we must increase the intensity to 10. VL^7 The operation of these circuits demonstrates that one reason for the rods’ high sensitivity compared to the cones’ is the rods’ greater convergence. Many rods summate their responses by feeding into the same ganglion cell, but only one or a few cones send their responses to a single ganglion cell. The fact that rod and cone sensitivity is determined
Neural Convergence and Perception 59
Image not available due to copyright restrictions
The books on the top shelf represent the details we see when viewing the books in the light, when our cones are control- ling vision. The books on the middle shelf represent how we might perceive the details midway through the process of dark adaptation, when the rods are beginning to determine our vision, and the books on the bottom shelf represent the poor detail vision of the rods. (Also note that color has dis- appeared. We will describe why this occurs in Chapter 9.) The poor detail vision of the rods is why it is difficult to read in dim illumination. We can understand how differences in rod and cone wir- ing explain the cones’ greater acuity by returning to our rod and cone neural circuits. As we stimulate the receptors in the circuits in Figure 3.28 with two spots of light, each with
an intensity of 10, we will ask the following question: Under what conditions can we tell, by monitoring the output of the ganglion cells, that there are two separate spots of light? We begin by presenting the two spots next to each other, as in Figure 3.28a. When we do this, the rod ganglion cell fires, and the two adjacent cone ganglion cells fire. The firing of the single rod ganglion cell provides no hint that two sepa- rate spots were presented, and the firing of the two adjacent cone ganglion cells could have been caused by a single large spot. However, when we spread the two spots apart, as in Figure 3.28b, the output of the cones signals two separate spots, because there is a silent ganglion cell between the two that are firing, but the output of the rods’ single ganglion cell still provides no information that would enable us to say that there are two spots. Thus, the rods’ convergence VL 8 decreases their ability to resolve details (Teller, 1990). We have seen that the large amount of convergence that occurs in the rods results in high sensitivity, and the low amount of convergence of the cones results in high acu- ity. This is an example of how what we see depends both on what’s out there in the environment and on the physiologi- cal workings of our visual system. When we are looking di- rectly at something under high illumination, cone vision, aided by low neural convergence, enables us to see details, as in the top shelf of the bookcase in Figure 3.27. When we are looking at something under low illumination, rod vision, aided by high neural convergence, enables us to make out things that are dimly illuminated, but we see few details, as in the bottom shelf of the bookcase. In the next section we will consider how another physiological mechanism—the decrease in the rate of nerve firing caused by inhibition—can also influence what we perceive.
Lateral Inhibition
and Perception
The neural circuit in Figure 3.29 may look familiar because it is the circuit from Chapter 2 that introduced the idea that neural processing is achieved by convergence and inhibition. We saw that the convergence and inhibition in this circuit caused neuron B to respond best to stimulation by a small
(a)
(b)
Figure 3.28 ❚ Neural circuits for the rods (left) and the cones (right). The receptors are being stimulated by two spots of light.
7 6 5 4 3 2 1
Lateral^4 inhibition
3–5 2–6 1–
7 6 5 4 3 2 1
Receptors stimulated
Firing rate of “B”
1 2 3 4
B
A C
5 6 7
Figure 3.29 ❚ Circuit with convergence and inhibition from Figure 2.16. Lateral inhibition arrives at neuron B from A and from C.
Lateral Inhibition and Perception 61
62 CHAPTER 3 Introduction to Vision
spot of light on receptors 3, 4, and 5. We are now going to look at some perceptual effects of inhibition by focusing on lateral inhibition—inhibition that is transmitted across the retina. An example of lateral inhibition is the connec- tions between neurons A and B and C and B in Figure 3.29. Notice that activation of neurons A or C results in the re- lease of inhibitory transmitter onto neuron B. To understand how lateral inhibition can cause percep- tual effects, we will look at an experiment using a primitive animal called the Limulus, more familiarly known as the horseshoe crab (Figure 3.30).
What the Horseshoe Crab Teaches Us About Inhibition In an experiment that is now considered a classic, Keffer Hartline, Henry Wagner, and Floyd Ratliff (1956) used the Limulus to demonstrate how lateral inhibition can affect the response of neurons in a circuit. They chose the Limulus be- cause the structure of its eye makes it possible to stimulate individual receptors. The Limulus eye is made up of hun- dreds of tiny structures called ommatidia, and each omma- tidium has a small lens on the eye’s surface that is located directly over a single receptor. Each lens and receptor is roughly the diameter of a pencil point (very large compared to human receptors), so it is possible to illuminate and re- cord from a single receptor without illuminating its neigh- boring receptors. When Hartline and coworkers recorded from the nerve fiber of receptor A, as shown in Figure 3.31a, they found that illumination of that receptor caused a large response. But when they added illumination to the three nearby receptors at B, the response of receptor A decreased (Figure 3.31b). They also found that increasing the illumination of B de- creased A’s response even more (Figure 3.31c). Thus, illu- mination of the neighboring receptors inhibited the firing of receptor A. This decrease in the firing of receptor A is
caused by lateral inhibition that is transmitted across the Limulus ’s eye by the fibers of the lateral plexus, shown in Figure 3.31. VL^9 Just as the lateral plexus transmits signals laterally in the Limulus, the horizontal and amacrine cells (see Figure 3.25) transmit signals across the human retina. We will now see how lateral inhibition may influence how humans perceive light and dark.
Lateral Inhibition and Lightness Perception We will now describe three perceptual phenomena that have been explained by lateral inhibition. Each of these phenom- ena involves the perception of lightness—the perception of shades ranging from white to gray to black. The Hermann Grid: Seeing Spots at Inter- sections Notice the ghostlike gray images at the inter- sections of the white “corridors” in the display in Figure 3.32,
Figure 3.30 ❚ A Limulus, or horseshoe crab. Its large eyes are made up of hundreds of ommatidia, each containing a single receptor.
Lateral eye
Bruce Goldstein
(a)
A only
(b)
A + B
(c)
A + B (increased intensity at B)
Electrode recording from A
Lateral plexus
B A
Light (^) Light
Figure 3.31 ❚ A demonstration of lateral inhibition in the Limulus. The records show the response recorded by the electrode in the nerve fiber of receptor A: (a) when only receptor A is stimulated; (b) when receptor A and the receptors at B are stimulated together; (c) when A and B are stimulated, with B at an increased intensity. (Adapted from Ratliff, 1965.)
