1. Describe the characteristics of light and color, outline the anatomy of the eye and its connections with the brain, and describe the process of transduction of visual information.
2. Describe the coding of visual information by photoreceptors and ganglion cells in the retina.
3. Describe the striate cortex and discuss how its neurons respond to orientation, movement, and spatial frequency.
4. Discuss how neurons in the striate cortex respond to retinal disparity and color, and explain the modular organization of striate cortex and the phenomenon of blindsight.
5. Describe the anatomy of the visual association cortex and discuss the location and functions of the two streams of visual analysis that take place there.
6. Discuss the perception of color and the analysis of form by neurons in the ventral stream.
7. Describe the two basic forms of visual agnosia: apperceptive visual agnosia and associative visual agnosia.
8. Describe how neurons in extrastriate cortex respond to movement and location, and discuss the effects of brain damage on perception of these features.

• The brain performs two major functions: It controls the movements of the muscles. It regulates the body’s internal environment. Ways in which sensory organs detect changes in the environment and the ways in which the brain interprets neural signal from these organs.
• We receive information about the environment from sensory receptors- specialized neurons that detect a variety of physical events. Stimuli interact with the receptors and alter their membrane potentials. This process is known as sensory transduction because sensory events are transduced ("transferred") into changes in the cells’ membrane potential. These electrical changes are called receptor potentials.
• People often say that we have five senses: sight, hearing, smell, taste, and touch. Certainly, we should add the vestibular senses. As well as providing us with auditory information, the inner ear supplies information about head orientation and movement.

• The perceived color of light is determined by three dimensions: hue, saturation, and brightness. Wavelength determines the first of the three perceptual dimensions of light: hue. The visible spectrum displays the range of hues that our eyes can detect.
• Light can also vary in intensity, which corresponds to the second perceptual dimension of light: brightness. The third dimension, saturation, of one wave length, the perceived color is pure, or fully saturated. Conversely, if the radiation contains all wavelengths, it produces no sensation of hue-it appears white.

• The eyes are suspended in the orbits, bony pockets in the front of the skull. They are held in place and moved by six extraocular muscles attached to the tough, white outer coat of the eye called the sclera. These mucous membranes line the eyelid and fold back to attach to the eye.
• The outer layer of most of the eyes, the sclera, is opaque and does not permit entry of light. The cornea, the outer layer at the front of the eye, is transparent and admits light. The amount of light that enters is regulated by the size of the pupil, which is an opening I the iris, the pigmented ring of muscles situated behind the cornea. The lens, situated immediately behind the iris, consists of a series of transparent, onionlike layers. Its shape can be altered by contraction of the ciliary muscles. These changes in shape permit the eye to focus images of near or distant objects on the retina- a process called accommodation.
• After passing through the lens, light passes through the main part of the eye, which contains the vitreous humor ("glassy liquid"). After passing through the vitreous humor, light falls on the retina, the interior lining of the back of the eye. In the retina are located the receptor cells, the rods and cones (named for their shapes),collectively known as photoreceptors. The human retina contains approximately 120 million rods and 6 million cones. Although they are greatly outnumbered by rods, cones provide us with most of the information about our environment. In particular, they are responsible for our daytime vision. They provide us with information about small features in the environment and thus are the source of vision of the highest sharpness, or acuity (from acus, "needle"). The fovea, or central region of the retina, which mediates our most acute vision, contains only cones. Cones are also responsible for color vision- our ability to discriminate light of different wavelengths. Although rods do not detect different colors and provide vision of poor acuity, they are more sensitive to light.
• Another feature of the retina is the optic disk, where axons conveying visual information gather together and leave the eye through the optic nerve. The optic disk produces a blind spot because no receptors are located there.
• Close examination of the retina shows that it consists of several layers of neuron cell bodies, their axons and dendrites, and the photoreceptors.
• The photoreceptors form synapses with bipolar cells, neurons whose two arms connect the shallowest and deepest layers of the retina. In turn, these neurons form synapses with the ganglion cells, neurons whose axons travel through the optic nerves ( the second cranial nerves) and carry visual information into the brain. In addition, the retina contains horizontal cells and amacrine cells, both of which transmit information in a direction parallel to the surface of the retina and thus combine messages from adjacent photoreceptors.

• Let’s consider the nature of transduction of visual information. The first step in the chain of events that leads to visual perception involves a special chemical called a photopigment. Photopigments are special molecules embedded in the membrane of the lamellae; a single human rod contains approximately 10 million of them. The molecules consist of two parts: an opsin (a protein) and rhodpsin consists of rod opsin plus retinal. (Rhod- refers to the Greek rhodon, "rose," not to rod. Before it is bleached by the action of light, rhodspin has a pinkish hue.) Retinal is synthesized from vitamin A, which explains why carrots, rich in this vitamin, are said to be good for your eyesight.
• When a molecule of rhodspin is exposed to light, it breaks into its two constituents, rod opsin and retinal. When that happens, the rod opsin changes from its rosy color to a pale yellow; hence, we say that the light bleaches the photopigment. The splitting of the photopigment causes a change in the membrane potential of the photoreceptor (the receptor potential), which changes the rate ate which the photoreceptor releases its neurotransmitter, glutamate.
• The first two types of cells in the circuit-photreceptors and bipolar cells-do not produce action potentials. Instead, their release of neurotransmitter is regulated by the value of their membrane potential; depolarizations increase the release, and hyperpolarizations decrease it.
• The hyperpolarization reduces the release of neurotramsitter by the photoreceptor. Because the neurotransmitter normally hyperpolarizes the dendrites of the bipolar cell, a reduction in its release causes the membrane of the bipolar cell to depolarize. Thus, light hyperpolarizes the photoreceptor and depolarizes the bipolar cell. The depolarization causes the bipolar cell to release more neurotransmitter, which depolarizes the membrane of the ganglion cell, causing it to increase its rate of firing. Thus, light shining on the photoreceptor causes excitation of the ganglion cell.

• The axons of the retinal ganglion cell bring information to the rest of the rbain. They ascend through the optic nerves and reaches the dorsal lateral geniculate nucleus of the thalamus. This nucleus receives its name from its resemblence to a bent knee. It contains six layers of neurons, each of which receives input from only one eye. The neurons in the two inner layers contain cell bodies that are larger than those in the outer four layers. For this reason, the inner two layers are called the magnocellular layers and the outer four layers are called the parvocellular layers.
• The neurons in the dorsal lateral geniculate nucleus send their axons to the primary visual cortex—the region surrounding the calcarine fissure, a horizontal fissure located in the medial and posterior occipital lobe. The primary visual cortex is often called the striate cortex because it contains a dark staining layer (striation) of cells.
• The optical nerves join together at the base of the brain to form the X-shaped optic chiasm. There, axons from ganglion cells serving the inner halves of the retina (the nasal sides) cross through the chiasm and ascend to the dorsal lateral geniculate nucleus of the opposite side of the brain. The axons from the outer halves of the retina remain on the same side of the brain. The lens inverts the image of the world projected on the retina (and similarly reverses left and right). Therefore, because the axons from the nasal halves of the retinas cross to the other side of the brain, each hemisphere receives information from the contralateral half (opposite side) of the visual scene.

Light consists of electromagnetic radiation, similar to radio waves but of different frequency and wavelength. Color can vary in three perceptual dimensions: hue, brightness, and saturation, which correspond, respectively, to the physical dimensions of wavelength, intensity, and purity.

The photoreceptors in the retina—the rods and the cones—detect light. Muscles move the eyes so that images of the environment fall on the retina. Accommodation is accomplished by the ciliary muscles, which change the shape of the lens. Photoreceptors communicate through synapses with bipolar cells, which communicate through synapses with ganglion cells. In addition, horizontal cells and amacrine cells combine messages from adjacent photoreceptors.

When light strikes a molecule of photopigment in a photoreceptor, the retinal molecule detaches from the opsin molecule, a process known as bleaching. This event causes the membrane potential to become more polarized. The change in the membrane potential decreases the release of glutamate and informs the bipolar cell with which the photoreceptors communicate that light has just been detected. As a result of this process, the rate of firing of the ganglion cell changes, and a message is sent through the axons of the optic nerves.

Visual information from the retina reaches the striate cortex surrounding the calcarine fissure after being relayed through the magnocellular and parvocellular layers of the dorsal lateral geniculate nuclei. Several other regions of the brain, including the hypothalamus and the tectum, also receive visual information. These regions help to regulate activity during the day-night cycle, coordinate eye and head movements, control attention to visual stimuli, and regulate the size of the pupils .

• The receptive field of a neuron in the visual system is the part of the visual field that neuron "see"—that is, the part in which light must fall for the neuron to be stimulated.
• Over sixty years ago, Hartline (1938) discovered that the frog retina contained three types of ganglion cells. ON cells responded with an excitatory burst when the retina was illuminated, OFF cells responded when the light was turned off, and ON/OFF cells respond briefly when the light went on and again when it went off.
• The two major categories of ganglion cells (ON and OFF) and the organization of their receptive fields into contrasting center and surround provide useful information to the rest of the visual system.
• Several studies have shown that ON cells and OFF cells do, indeed, signal different kinds of information. Thus, rod bipolar cells must all be of the ON type.
• The second characteristic of the receptive fields of ganglion cells—their center surround organization—enhances our ability to detect the outlines of objects even when the contrast between the object and the background is low.

• Although monochromatic (black-and –white) is perfectly adequate for most purposes, color vision gives us, for example, the ability to distinguish ripe fruit.

• Proposed that the eye detected different colors because it contained three types of receptors, each sensitive to a single hue. Trichromatic (three-color) theory.
• Ewald Hering, opponent colors. Humans have long regarded yellow, blue, red, and green as primary colors. Colors can be described as mixtures of these primary colors. The trichromatic system cannot explain why yellow is included in this group. Again, these facts are not explained by the trichromatic theory. As well shall see in the following section, the visual system uses both trichromatic and opponent-color systems to encode information related to color.

• Physiological investigations of retinal photoreceptors in higher primates have found that Young was right: Three different types of photoreceptors (three different types of cones) are responsible for color vision. Investigators have studied how well light of different wavelengths is absorbed by individual photoreceptors, determining the amount of light of different wavelengths that is absorbed by the photopigment. These characteristics are controlled by the particular opsin a photoreceptor contains; different opsins absorb particular wavelengths more readily.
• The peak sensitivities of the three types of cones are approximately 420 nm (blue-violet), 530 nm (green), and 560 nm (yellow green). For convenience, the short-, medium-, and long-wavelength cones are traditionally called "blue", "green", and "red" cones, respectively.
• Genetic defects in color vision appear to result from anomalies in one or more of the three types of cones. People with protanopia confuse red and green. They see the world in shades of yellow and blue; both. People with deuteranopia ("second-color defect") also confuse red and green and also have normal visual acuity. Their "green" cones appear to be filled with "red" con opsin.
• Tritanopia ("third-color defect") is rare, affecting fewer than 1 in 10,000 people. This disorder involves a faulty gene that is not located on an X chromosome; thus, it is equally prevalent in males and females. People with trintanopia have difficulty with hues of short wavelengths and see the world in greens and reds.
• For example, red light excites "red" cones, which causes the excitation of red-green ganglion cells. Green light excites "green" cones, which causes the inhibition of red-green cells. But consider the effect of mediate between red and green, it will stimulate both "red" and "green" cones about equally. Yellow-blue ganglion cells are excited by both "red" and "green" cones, so their rate of firing increases. However, red-green ganglion cells are excited by red and inhibited by green, so their firing rate does not change.

• Recordings of the electrical activity of single neurons in the retina indicate that each ganglion cell receives information from photoreceptors-just one in the fovea and many more in the periphery. The receptive field of most retinal ganglion cell consists of two concentric circles, with the cells becoming excited when light falls in one region and becoming inhibited when it falls in the other. This arrangement enhances the ability of the nervous system to detect contrasts in brightness. ON cells are excited by light objects against dark backgrounds; OFF cells detect dark objects against light backgrounds.
• Color vision occurs as a result of information provided by the three types of cones, each of which is sensitive to light of a certain wavelength : long, medium, or short. The absorption characteristics of the cones are determined by the particular opsin that their photopigment contains. Most forms of defective color vision appear to be caused by alterations in cone opsins. The "red" cones of people with protanopia are filled with "green" cone opsin, and the "green" cones of people with deuteranopia are filled with "red" cone opsin. The retinas of people with tritanopia appear to lack "blue" cones.
• Most color-sensitive ganglion cells respond in an opposing center-surround fashion to the pairs of primary colors: red and green, and blue and yellow. The responses of these neurons are determined by the retinal circuitry connecting them with the photoreceptors.

• The map is distorted; approximately 25 percent of the striate cortex is devoted to the analysis of information from the fovea, which represents a small part of the visual field. They selectively responded to specific features of the visual world. That is, the neural circuitry within the visual cortex combines information from several sources.

• Most neurons in the striate cortex are sensitive to orientation. That is, if a line positioned in the cell’s receptive field and rotated around its center, the cell will respond only when the line is in a particular position.

• Although the early studies by Hubel and Wiesel suggested that neurons in the primary visual cortex detected lines and edges, subsequent research found that they actually responded best to sine-wave gratings.
• Simple cell. An orientation-sensitive neuron in the striate cortex whose receptive field is organized in an opponent fashion.
• Complex cell. A neuron in the visual cortex that responds to the presence of a line segment with a particular orientation located within its receptive field, especially when the line moves perpendicularly to its orientation.
• Sine-wave grating. A series of straight parallel bands varying continuously in brightness according to a sine-wave function, along a line perpendicular to their lengths.
• Spatial frequency. The relative width of the bands in a sine-wave grating, measured in cycles per degree of visual angle.
• Retinal disparity. The fact that points on objects located at different distances from the observer will fall on slightly different locations on the two retina; provides the basis for stereopsis.
• Ocular dominance. The extent to which a particular neuron receives more input from one eye than the other.
• Blindsight. The ability of a person to reach for objects located in his or her "blind" field; occurs after damage restricted to the primary visual cortex.

• The striate cortex consists of six layers and several sublayers. Visual information is received from the magnocellular and parvocellular layers of the dorsal lateral geniculate nucleus. The magnocellular system is more primitive, color-blind, and sensitive to movement, depth, and small differences in brightness; the parvocellular system is more recent, color-sensitive, and able to discriminate finer details.
• The striate cortex is organized into modules, each surrounding a pair of CO blobs, which are revealed by a stain for cytochrome oxidase, an enzyme found in mitochondria. Each half of a module receives information from one eye; but because information is shared, most of the neurons respond to input from both eyes. The neurons in the CO blobs are sensitive to color and to low-frequency sine-wave gratings, whereas those between the blobs are sensitive to sine-wave gratings of higher spatial frequencies, orientation, retinal disparity, and movement.
• Damage to the visual system up to the striate cortex produces blindness in all or part of the visual field. However, damage that is limited to the striate cortex or to the optic radiations leading to them produces a syndrome called blindsight. People with theless point to objects located there and discriminate their size and orientation. They are also sensitive to movement. But although their behavior can be affected by objects in their blind field, they have no conscious awareness of the presence of these objects. Their ability to respond to visual stimuli apparently depends on connections from the superior colliculus and the lateral geniculate nucleus to the visual association cortex.

• Extrastriate cortex. A region of visual association cortex; receives fibers from the striate cortex and from the superior colliculi and projects to the inferior temporal cortex.
• Color constancy. The relatively constant appearance of the colors of objects viewed under verying lighting conditions.

• Achromatopsia. Inability to discriminate among different hues; caused by damage to the visual association cortex.
• Visual agnosia. Deficits in visual perception in the absence of blindness; caused by brain damage.
• Apperceptive visual agnosia. Failure to perceive objects, even though visual acuity is relatively normal.
• Prosopagnosia. Failure to recognize particular people by the sight of their faces.
• Balint’s syndrome. A syndrome caused by bilateral damage to the parieto-occiptial region; includes optic ataxia, ocular apraxia, and simultaagnosia.

• The visual cortex consists of the striate cortex, the extrastriate cortex (also called the prestriate or circumstriate cortex), and the visual association cortex of the inferior temporal lobe and the pesterior parietal lobe. The visual cortex has at least twenty-five different subregions, arranged in a hierarchical fashion. The extrastriate cortex receives information from the striate cortex and from the superior colliculus. The color-sensitive cells in the CO blobs in the striate cortex send information to area V4 of the extrastriate cortex. Damage to the human extrastriate cortex (presumably, damage to area V$) can cause achromatopsia, a loss of color vision.
• The visual cortex is organized into two streams. The ventral stream, which ends with the inferior temporal cortex, is involved with the perception of objects. Lesions of this region disrupt visual object perception. Also, single neurons in the inferior temporal cortex respond best to complex stimuli and continue to do so even if the object is moved to a different location, changed in size, placed against a different background, or partially hidden. The dorsal stream, which ends with the posterior parietal cortex, is involved with perception of location, movement, and control of eye and hand movements. Damage to area V5 or to the posterior parietal cortex disrupts an animal’s ability to perceive movement or the spatial location of objects.
• PET studies indicate that specific regions of the cortex are involved in perception of form, movement, and color, and these studies will undoubtedly enable us to discover to correspondences between the anatomy of the human visual system and that of laboratory animals. Studies with humans who have sustained damage to the visual association cortex have discovered two basic forms of visual agnosia. Apperceptive visual agnosia involves difficulty in perceiving the shapes of objects, even though the fine details can often be detected. Prosopagnosia, failure to recognize faces, has traditionally been regarded as a separate disorder, but it probably represents a mild form of apperceptive visual agnosia. The second basic form of visual agnosia, associative visual agnosia, is characterized by relatively good object perception (shown by the fact that the patients can copy drawings of objects) but the inability to recognize what is perceived. This disorder is probably caused by damage to axons that connect the visual association cortex with regions of the brain that are important for verbalization and thinking in words. Some patients with this disorder can describe or mime actions appropriate to the objects that they see but cannot recognize.
• Damage to the human visual association cortex corresponding to area V5 disrupts perception of movement. Sometimes people with visual agnosia caused by damage to the ventral system can still perceive the meanings of actions or recognize friends by the way they walk, which indicates that the dorsal stream of their visual cortex is largely intact. Balint’s syndrome, which is caused by bilateral damage to the parieto-occipital region (the dorsal stream), includes the symptoms of optic ataxia, ocular apraxia, and simultanagnosia.