Chapter III
THE VISUAL PERCEIVING PROCESS IN OUR BRAIN
The main goal in writing this chapter is to show that the visual world around us as perceived by our visual system is processed in four quadrants.
Figure 1. Our visual brain (inclusive the eyes) processes the visual field in four quadrants (After Gray, 1980 p.979, fig 7.109)
Right hemifield in upper and lower quadrants and left hemifield in upper and lower quadrants. This approach is somewhat different from what I found in textbooks and articles. I can divide these articles in two categories:
We have to realize that there is a clear physical division in our brain for the visual processing. We have a vertical division in left and right halves of the brain as well as a horizontal division in a lower and an upper part. The division of the latter parts is seen at the back of our brain and is called the calcarine fissure. The processing of far and near space is processed in higher visual areas. Far space mainly in the left lower part (ventral), the near spaces more in the upper right part (dorsal).
But first of all we describe the different parts of our brain that are processing the signals from the outside world for the construction of an image of this world around us.
2. The eye: the mirror of our soul
"The eye through its physiology is another key to understand the inner mysteries"
"Redness, like beauty is in the eye of the beholder" (Brou et. al, 1986)
The pupil is the opening that allows the light to enter the eye and reach the receptors at the back of our eye. It appears dark because the receptors are absorbing the entering light. The pupil can change in size adjusting for different light levels, but also by emotional factors. Dilatation and constriction of the pupils reflect not only changes in light intensity but also ongoing mental activity. When people are solving a mathematical the pupil size becomes larger till the solution has been found.
Figure 2. Changes of pupil size are traced in a subject doing three mental-arithmetic problems. Filled dots indicate the moment the problem is posed, the pupil dilates until the problems are solved (open circles) (After Hess, 1975).
What is happening when the specific electromagnetic waves are detected by our receptors at the back of our eyes on the retina? It is unbelievable how nature has produced such delicate machinery. The best microchips in the world will not soon be equal in complexity to this most compressed part of our brain.
(Remember the eyes are part of the brain protruding through the skull and the only visible parts of our brain). The retina is as thin as a piece of paper (1/2 mm)! The receptors which originally were orientated towards the incoming light. During the evolution the originally towards light orientated receptors were turned 180 degrees.
Most of the visible light never reaches the retina, it is absorbed by the cornea, lens and the humors (fluid). The cornea and the lens not only focus the image on the retina but also invert it. There are also other non-neural changes as the effect on the pupil size on the number of photons entering the eye as spherical and chromatic aberrations bending some of the wavelengths more sharply than other wavelengths. So if one is focussing on a green part of an object the blue parts may be slightly blurry and hazy (Hoyenga and Hoyenga, 1987).
By older people the eye fluid becomes cloudy and short waves (blue) are more absorbed and a greater percentage of rays in the red part of the spectrum will reach the retina. I will see the sunset more reddish than my grandson will.
Only 10% of the light that is hitting our eyes are absorbed by our receptors, especially energy in the short-wavelength of the spectrum.
Figure 3. Only 10% of the light of 5oo nanometres that strikes the cornea gets absorbed by the visual receptors. (Hoyenga and Hoyenga,1987)
There are two types of receptors: the cones (3 million per eye) and rods (110 million per eye). The cones are more abundant in the center and more specialized to catch wavelengths in the blue, red and green. The rods are more orientated in the periphery and have a rhodopsin as a pigment and are 1000 times more sensitive for light. Under nighttime lighting only rods contribute to vision. You can prove it yourself that dim light is processed mainly in the periphery of your eye. Look at night at a bright star. Fix on this star search your peripheral vision for a dim star. Then move your eyes to look at the dim star. You will find that the faint star disappears when it is imagined on the central retina but reappears when you look with your peripheral retina to the side of it.
Figure 4. The density of the rod and cone receptors in relation to the location on the retina. The temporal visual field (nasal retina) has more rods than the nasal hemifield. (After Hoyenga and Hoyenga, 1987)
During daylight the cones do the bulk of the work. The genes for the cone pigments and rhodopsin probably arose from an ancestral gene. The blue pigment came first and was followed by a green and red pigment. New World monkeys have only two cone pigments (blue and green) whereas Old World monkeys and humans have three cone pigments: blue green and red. We were able to detect in the green forest the red fruits! Dogs have only two pigments and can not make a difference between red and green. (Carnivores do not need this distinction apparently). Shrimps have 10 color pigments.
They need to recognize other shrimps in fight. Before the fight they show colored markings with complex arrangements on their elbows. In this way they cannot fight the wrong opponent (Epstein, 1989)
Figure 5. Evolutionary relations of human pigments (After Stryer, 1988).
Animals can even adopt their pigments to the changing environment. Eels in fresh water use red and blue pigments. When they go for pairing to the Sargasso Sea they replace their red pigment by a second type of blue pigment. The amount of receptors differs considerably between animals: humans 200.000 per square millimeter, a sparrow 400.000 and a buzzard 1.000.000.
Our cones have a circular arrangement, identical to animals living in the woods. Animals living in open space like lions have a stripe-like arrangement of their cone receptors. There is also a difference how the eyes are placed in the head. We have the eyes as a predator, whereas prey animals have their eyes at both sides of the head. The first way allows to catch better the prey and the second way to look better around to see the predator.
Figure 6. The visual field for a predator (human being) and a prey (birds and fish) (After Nathan, 1988)
3. The astonishing receptor pigment in the rods: rhodopsin
The transformation of the electromagnetic waves in neuronal signals is produced through a cascade of very complicated processes in the three layers of the retina. It is far beyond my imagination to really capture what is happening in my eyes when the smallest quantity of light particles – a photon- hit my eyes. I will only single out only one event: that is the moment that the photon reaches the outer component of a rod receptor. It shows me how little I am conscious of all what happens when signals from the world outside reach my body, in this case the retina of my eyes. In the dark the rod receptor is filled with a salty fluid that has an electrical potential; it is what is called depolarized when the membrane has become less negative. This depolarization produces at the end of the receptor a release of a chemical substance to the neighboring cells (neurotransmitter): the transformation of an electric signal into a chemical signal. This effect is produced by a constant influx of millions of sodium ions per second. This movement of positive charge across the membrane is called the dark current. When a light photon hits the receptor the positive charge become more negative. This is called hyperpolarization. Contrary to what we logically would expect inhibition is creating light signals in our brain! The diminishing of the voltage brings about a number of processes in the other layers. A protein 11-cis retinal located in the protein rhodopsin in the retina receptor changes in form after being hit by one photon. The energy of light straightens out the bend in the chain of carbon atoms. The photon has been converted in atomic motion!
Figure 7. The protein 11 cis retinal changes in form after being hit by photon of light. (After Stryer, 1988)
Through a very complicated chemical process it closes a million Na+ ions channels per second of the membrane receptor. In 300 milliseconds the electric current in the rod diminishes with 1 volt. This process of transduction is as old as 700 million years. This lowering of voltage creates a wave of complicated signals through a series of specialized cells in the retina. 1 million nerves per eye (the optic nerve) guide signals to other parts of the brain, where finally an image of the world around us is created.
The following column shows the cascade of events that takes place in the receptor cell of an eye, when only one photon hits the receptor.
1 rhodopsin molecule absorbs one photon
500 tranducin molecules are activated
500 phosphodiesterase molecule are activated
10 cyclic GMP molecules are hydrolyzed
250 Na΅ channels close
10Na΅ions per second are prevented from entering the cell for a period of 1 second
rod cell membrane is hyperpolarizes by 1 mV
Figure 8. The closure of the gap, that prevents sodium ions to enter in the rod. The rod will then by hyperpolarized by 1mV.
As we have just mentioned, light has provoked a very interesting effect. Light has inhibited the receptor cells to diminish the release of their neurotransmitter (glutamate). One of the most surprising things of the working in the human body is that by inhibiting to inhibit it is made possible that a signal can be transmitted. It is called disinhibition and is one of the major organizing principles in the nervous system function. There are a great number of inhibitory neurons acting like reins that serve to keep the neuronal horses from running away. Through inhibiting the inhibitory neurons to fire it is made it possible for other neurons to transmit signals. We can also make a comparison with the working of DNA in our cells. Every cell is capable to make all sorts of cells but it must been prohibit to use all his potentials. In order to program the making of a specific cell the inhibition must be released. When the inhibition does not work accurately the cell is making cells that are not wanted by the organism: the birth of a cancer cell. So inhibition is the safeguard for a sound working of our body. Another comparison is that policemen are surrounding a human being in order to prevent him to give expression to all his emotions. Only by prohibiting one or two policemen allow the human being to express his emotions in a non-destructive way.
Disinhibition is the keyword for a sound functioning of body and mind.
4. The processing in the retina, after the receptor cells have been hit by the electromagnetic vibrations, is a highly impressive event
In the retina of a thickness of half a millimeter we have not only the million receptors but also a very complicated web of a great number of cells. Horizontal, bipolar, interplexiform, amacrine and ganglion cells. Every cell named has a different role in the visual processing. For example there are 30 different sorts of amacrine cells. It is beyond the scope of the article to go in detail about the functioning of the cells. After studying the complex network I have become more and more impressed by the way nature has made it for us possible to perceive and to transform the electromagnetic waves reaching our eye into an image of the world around us..
The receptors (rods and cones) do not normally generate action potentials. Slight changes in the membrane potential determine the amount of neurotransmitter released. In the dark the photoreceptor is depolarized and continually releases a chemical transmitter (glutamate) to the bipolar cell. Information from the receptor cells goes to two types of bipolar cells. Each photoreceptor has two synaptic contacts with horizontal cells and bipolar cells. Horizontal cells cause bipolar cells to be affected by receptors to which they are not directly connected. Thanks to these cells a bipolar cell can be indirectly connected with several receptors. They play a great role in creating a center and surround of the ganglion cells. (The receptive field). The nature of the horizontal cells is inhibitory. They give hyperpolarizing responses to light irrelevant in respective to wavelength. Horizontal cells integrate light from a larger area than do cones. The workings of the horizontal cells are crucial to creation of sharp contrasts. In the dark these horizontal cells are exited by the receptors. They emit an inhibitory neurotransmitter (GABA) that is hyperpolarizing neighboring cones. When light is projected on the center receptive bipolar and ganglion cells things change drastically. The release of neurotransmitters by the receptors is reduced by the hyperpolarizing event of the receptor due to the light. This means that the horizontal cells are not anymore prohibiting the neighboring cones. This means that the horizontal cells make the darkness in the neighboring cells darker resulting in a greater contrast between light and dark. Again we see that the inhibitor is inhibited to inhibit! Without horizontal cells there would be no opponent surround in the receptive fields of bipolar, amacrine and ganglion cells. Bipolar and ganglion cells would either be depolarized or hyperpolarized by light.
There are two types of bipolar cells. One type of bipolar cell is the off cell that in dark is depolarized and the other the on cell that is hyperpolarized. When the photoreceptors are stimulated with light this will change the potentials of the bipolar cells. The hyperpolarization of the bipolar cells is not any more prohibited and can transmit the signals to the ganglion cells. The off cells are prohibited on their turn.
Rod bipolar cells have no direct communication with ganglion cells. The amacrine cells are transmitting signals from the rod receptor cells to the ganglion cells. These amacrine cells are lacking axons. They are modulators. They adjust retinal activity to specific visual environments that is the varying spectral composition of the sunlight during the day.
Amacrine cells may decrease any response to constantly present light. Activating amacrine cells may inhibit all output of the retina. Also they have to equilibrate the different illumination reflecting from the ground and directly from the sky. The upper and lower retina is therefore especially equipped to execute this delicate task. Recent studies have revealed differences in density of ganglion cells and different cell types between the lower an upper retina. (Previc 1990, Chalupa and White 1990).
Figure 9. The connections of rods and cones with the ganglion cells. Only two receptors of the 212 million receptors of the eyes are shown (After Kandel and Schwartz , 1985).
Finally 1.5 million ganglion cells per eye receive the signals from 106 million receptors. They are sending their axons into the optic nerve. As bipolar cells we have two types of ganglion cells with either an ON or an OFF center. These are further subdivided in two major types of ganglion cells the large Magno-ganglion cell and the smaller Parvo-type ganglion cell. M-cells only constitutes 10% of the ganglion cell population, P-cells constitute most of the rest. The M-cells are particularly important for the detection of the stimulus movement while the P-cells are more sensitive to stimulus form and fine detail. The P-type cells are sensitive to differences in wavelengths of light. Perceived color is based on the relative activity of ganglion cells whose receptive field centers receive input from red, green and blue cones. When red cones are satiated their opponent green will come into action and the same for blue cones versus yellow cones. The same holds true for the opponents light versus dark. After playing in the whole evening on a green snooker table coming into the dark night the sky will have a reddish color.
Figure 10. Connections between three types (long, medium and short wavelength) of cones with bipolar cells (Kalat, 1992)
The processing of the signals from the world around us are processed in two parallel streams of information each for one eye. They remain segregated at the first synaptic relay in the lateral geniculate nucleus (LGN) of the thalamus. Also the M- and P-cells remain separated in the LGN.
5. From the retina nerve fibers are sent all over the place in our brain
"
First evidence that cerebral cortex is composed of separate areas came from a study of part of the visual cortex more than two centuries away". (Tootell 1996)"By studying the visual cortex, you learn that the job of perception is not one job but many. And these jobs get parceled out. Different regions -- different retinotopic maps -- specialize. Moreover, they don't send their results to one central processing area; they send their results all over the place. Everything is connected to everything else, and the connections run back and forth.(…)There's nothing problematic with this decentralization, by the way. It's just what we should expect. Indeed, the reason I particularly delight in the visual cortex is that it rubs your nose so firmly in the unacceptability of the traditional, centralized vision of consciousness. (…) The key insight about vision and the brain is not that there are, say, hand-eye coordination circuits -- though there are, of course. It's that there are lots of these systems, which use the eyes in one way or another. The wrong approach is to try to simplify that truth into a conception of the eyes as simple receivers of some input which will subsequently get packaged and sent to some place to get appreciated. That's a fundamental error -- albeit an extremely attractive, seductive error. Simply confronting what we now know about the functional neuroanatomy of the visual cortex seems to me the first step in forcing us out of these bad conceptual habits" (D.Dennett, 1999).
"..we can see how the brain takes the picture apart, but we do not understand how it puts it together"(Crick 1994).
"Each pathway performs its functions somewhat independently of the others, although in some unknown way the brain combines the information"(Kalat, 1992).
The left part of our visual field is projected to the temporal part of the right eye and the nasal part of the left eye. The optic nerves transmitting the nasal part of our eyes are crossing over from one half to the other half whereas the temporal parts are staying inside the same half. This arrangement has great consequences. Each part of the brain is exclusive processing one part of the visual field.
This means that not only our brain is split in two halves but also the processing of the visual field. But it is not all. The processing of the upper part of our visual field is done with the lower part of the retina and the lower part by the upper part. This implicates that we have not only a separation in left and right visual field but also in lower and upper part. Thus each half of the visual field is processing in four separate channels. What is the reason we are not seeing this division into 4 quadrants? In the brain we have 200 million nerves connecting the left and right half of our brain as well as nerves in higher parts of the visual processing areas connecting signals from our lower and upper visual field signals (dorsal and ventral pathways).
Nerve signals coming from the retina are guided along 1 million nerves going to different parts in the brain. For humans the most important area where they are projected is a nucleus of the thalamus: lateral geniculate nucleus (LGN). More than 100.000 nerves per eye are going to a subcortical structure, the superior colliculus (SC). These nuclei are important for attention and the initiating of saccades.
The geniculostriate pathway is a new evolutionary development. It is only fully developed in mammals. In other vertebrates vision is mediated by input through the retinotectal pathway to the superior colliculus. The retinotectal pathway has more crossed fibers from the contralateral eye and the temporal hemiretina (nasal hemifield) has a smaller direct input to the superior colliculus. The superior colliculus has a greater representation of the temporal visual field than of the nasal hemifield Conduction of crossed fibers is quicker than through uncrossed fibers.
The reflex orienting of covert attention is more efficiently summoned by signals in the temporal hemifield. The retinotectal pathway plays a role in blindsight. Patients with the destruction of the retinostriate pathway can saccade to targets they cannot see , this input is guided via the retino tectal pathway, with an advantage for the temporal hemivisual field. (Rafal, 1991)
They also can integrate various sensory impulses. The SC has seven layers. The upper three are receiving signals directly from the retina. The SC is always trying to get the object in the center of the visual field. The deeper layers guide eye movements.
The SC can take over some visual capacities even if the primary visual cortex is damaged. This is called blindsight (Weiskrantz, 1989).
How was blindsight discovered? Daniel was a patient by whom the right visual cortex had been removed, that is his vision of the left visual field. Six weeks after surgery the doctor held out his hand in Daniel left blinded field, Daniel touched it!.
Another part of the thalamus, the pulvinar, is important to segregate irrelevant from relevant information. The nerves going to the hypothalamus, the suprachiasmatic nucleus, are intended to keep our biological clock ticking.
Figure 11. The Sprague effect. Damaging another part of the brain can restore damage of the orienting behavior. (After Stein, 1993.)
A very strange defect is the so-called Sprague effect. The right part of the visual cortex of a cat was destroyed, as a result the cat lost interest in the left visual field. Then the left SC was destroyed. A very strange thing happened. The cat was again interested in the left visual hemifield.
How is this possible? A lesion followed by a second lesion can restore the deficit. The explanation is quite simple. The SC is dependent on the exciting influence of the cortex of the same hemisphere. This input is balanced by the inhibitory input of the contralateral substantia nigra transmitted by nerves going from one hemisphere to the other, in this case from the left to the right hemisphere. When the right cortex is destroyed the inhibitory input is prohibiting the right SC. By destroying the left SC the right SC does not get the inhibitory input of the left SC and is able to regain its influence on the orienting response versus the left visual field.
The optic nerves from both eyes are combined to form the optic chiasm. The axons originating from the nasal retina cross over from one side to the other. This is the moment where we have the split between the left and right visual field. All the information about the left visual field is directed to the right side of the brain. The visual field is not only split by a vertical line in a right and left field, but also by a horizontal line the upper and lower visual field. Actually four different channels are projecting the retinal information to the all the brain areas involved in the visual processing. Interesting to see what can happen when the retinofugal projection of the optic chiasm is split down the middle. Only the crossing fibers from the nasal part are cut. The peripheral vision will be lost in both eyes. This is the reason that David could kill Goliath. The greatness of Goliath was caused by a swollen pituitary gland of the hypothalamus. The chiasm butts against the stalk of this pituitary gland. So Goliath lost sight of the approaching David and David could kill Goliath easily throwing a stone against his skull. (M.F.Bear et al.).
Figure 12. Goliath death by David is due to the damage to his peripheral vision.
6.The thalamus is the conductor of the brain orchestra sending his orders to other parts of the brain
The lateral geniculate nucleus (LGN) of the thalamus has six layers. Each layer receives only information from one eye. The horizontal meridian is tilted 90 degrees. The right eye axons are connected with layer 2,3 and 5 of the LGN in the right hemisphere and the left eye axons with layer 1,4 and 6. The lower layers 1 and 2 have large cells and are therefore called magnocellular layers whereas layers 3,4,5 and 6 have small cells and are called the parvocellular layers. The lower two layers (magno) are not concerned with color whereas the uppers four (parvo) are concerned with color vision. Each neuron in the LGN receives input from only a few retinal ganglion cells. The receptive fields of the LGN resemble strongly those of the retina. There is a slightly enhancement in the LGN cells between the surround and the center. The central part is more emphasized in the LGN than in the retina. In the LGN there is also a very strong input of the excitatory synapses from the visual cortex to the LGN, even more axons than from the LGN to the visual cortex. In addition to the neurons in the six principal layers of the LGN there are also numerous tiny neurons that lie just ventral to each eye. Cells in these koniocellular layers receive input from the retina and produce an output to the visual cortex. They could have a function in saccadic suppression via circuits involving the superior colliculus and the striate cortex (Hendry and Yoshioka, 1994).
Link 1: more on the functions of the thalamus
7.Most of the orders from the thalamus are processed in the back of our brain
"The temporal progression of activities of V1 neurons reflects the gradual involvement of V1 in successively higher levels of computations. This happens by intracortical and feedback connections. V1 is not just a module for computing local feature, but possibly serves a high resolution buffer or visual computer to perform all computations that integrate global information with spatial precision" (Lee et. al., 1998).
From the LGN the nerve fibers are going to the primary visual cortex.. These axons are called the optic radiation. Fibers representing the inferior parts of the retina swing in a broad arc over the temporal lobe reaching the occipital pole of the visual cortex. This group of fibers is called the Meyer's loop. When there are unilateral lesions of the temporal lobe they can effect the superior quadrant of the contralateral visual field.
The visual cortex at the back of the brain is called the striate cortex or V1. It is only 2 mm thick! In all articles the visual cortex is represented in an exaggerated proportion. It would be better if a picture with the right dimensions would accompany these images. It will help us to realize what a miracle is lodged within our skull. The primary visual cortex is as thick as the letter a in this text. The total cortex is only a sheet of 40 x 40 cm. The length of the internal connections of the nerve fibers is 80.000 km. An article of Cherniak (1992) is pointing towards this exaggeration of the dimensions of our brain.
"An idea that human cognitive resources are virtually without limit turns up at all levels of mind/brain science. This tacit unbounded-resource assumption has paradoxical consequences in neuroscience, particularly involving the quantitative incoherence of some key anatomical studies of cortical connectivity resources: cortical sheet area, synaptic density there, and giant axonic arborizations in visual cortex. This inattention to quantitative consistency checking in neuroanatomy appears to stem from, as a notable instance, something of the nonspatial character of the Cartesian concept of mind being extended to the brain as physical structure".
There are nine distinct layers of neurons in the primary visual cortex. There is a division of labor as we have seen in the LGN. The division between magna and parvo is still maintained. In layer 4 they are arranged as pancakes. Also is kept the separation between left and right eye.
Axons from LGN mainly go to layer IVC. Magno to IVC alpha and parvo to layer IV beta. It contains two overlapping retinotopic maps. The eyes are also segregated. The left and right eye is represented in a series of alternating bands, like stripe of a zebra. These patches are 0.5 mm wide.
Any part of layer IVC (with a thickness of 0.5 mm and a dimension of 1 mm x 1 mm) would contain a full complement of segregated inputs from both magno- and parvocellular LGN layers from both left and right eyes. The first time where the eyes are going to mix is in layers IVB and II. In layer 3 there is a division of inputs from the LGN, one with blobs (color and luminance) and one with interblobs (motion, spatial orientation). The output from M layers is relayed to layer IVB of V1 and also divided in two components. One component feeds the orientation -plus direction -selective cells of layer IVB and is therefore concerned with motion, while the other feeds the orientation-selective cells of the same layer and is therefore concerned with form.
A point in space can be processed by one cortical module. A cortical module of 2 x 2 mm consists of two sets of ocular dominance column in layer IV (binocular view), 16 blobs in layer III (color) cells between the blobs with a complete sampling of all 180 degrees of possible orientations.
Figure 13. A cortical module in the primary visual cortex. (After Bear, et. al. 1996.)
8. Pathways emanating from V1 of both hemispheres to higher visual areas
From the visual cortex there are four different pathways directed to higher brain areas.
In addition to the major pathways from V1 to temporal lobe there are other smaller bypass routes, pathways from V1 to V4 and from V2 to TEO. They can provide coarse graded information to arrive rapidly in the temporal lobe. This advanced information about the current stimulus might aid in constructing the initial representation with fine graded information arriving later to fill in important details. Latencies of 80 ms where recorded along these bypasses (Nakamura et. al., 1993).
From each hemisphere there are two mutually exclusive and hierarchically projecting pathways from V1 to the higher visual areas.
It is good to realize that now the separation of eyes is mixed, the separation of the horizontal meridian of the visual field in upper and lower part becomes more manifest. The vertical meridian of the visual field has been clear since the optic chiasm, by the processing of the signals from each hemifield in the left and right halves of the brain. As we have seen the separation of the eyes has been maintained in the LGN and in the layer IVC of the V1.
There are striking differences in the composition of the upper and lower part of the retina. This distinction becomes even clearer in the processing in the dorsal and ventral streams.
The distinction between parvo and magno becomes less clear and they are interacting with each other. Already in V1 there are connections between the later IVB (input from magno layers of the LGN ) with layers 2 and 3 (who got their input from the parvo layers of the LGN). In the visual area V2 adjacent to V1 there are is a system of horizontally coursing fibers. Also we see connections between the area V3, V4 and V5. Then there is an important system of back projections from the higher visual area to V2 and V1. These could serve to unite signals derived from M and P layers. It is important to realize that the superior temporal sulcus has massive connections to the parietal cortex. The temporal cortex receives signals not only from the P system but also from the M system as well.
Bauer and Dow (1989) recorded that upper layers of V1 were tend to show either orientation or color selectivity, while lower layer cells tend to show movement sensitivity output lower layers to SC pons and middle temporal visual area. This suggests a functional dichotomy between the supragranular system involved in fixational eye movements and pattern vision and an infragranular system activate primarily by optical flow fields during ambulation.
9. The functional properties of the higher visual brain areas
V2 has a retinal map of the opposite half of the visual field. The map is split into two parts, corresponding to the upper and lower parts of the contralateral half of the visual field. The V2 neurons are, like V1, interested in processing properties as orientation, movement, disparity and color. But is also different because all the neurons receive input from both eyes! The architecture consists of a set of dark stripes and is separated from each other by lightly strips (after a staining process). The dark stripes are thick and thin. This differs from the V1, the receptive fields of V2 are greater than in V1, but less precise!
V3 has a retinal representation, which is a mirror image of its representation in area V2. The representation of the horizontal meridian forms the boundary with V2, whereas the vertical meridian is at the anterior border of V3. Like V2 the area V3 can be subdivided into a dorsal and ventral part each representing a different retinal quadrant. The cells are not responsive to color but to lines with a specific orientation. They are processing signals related to form without color.
V4 receives input from the central (foveal) representation in V1 and the most input from V2. It is the area that is specializing for the processing of color.
They contain cells that are orientation selective as well as wavelength selective to varying degrees.
The eye has evolved to see the world in unchanging colors regardless of the always unpredictable shifting and uneven illumination. This all is computed mainly in the area V4.
V4 receives parvocellular as well as magnocellular signals (Ferrera et al. 1994).
V5 lies more anterior to the V4 complex. It receives direct input from V1.
All its cells are sensitive to motion and over 90% are directionally sensitive. They respond to motion of a visual stimulus. None of the cells are concerned with color.
Barbur et al. (1993) show that V5 (the motion center) was active in a patient without parallel activation of area V1, implying that the visual input can reach V5 without passing through V1. Such input is sufficient for both discrimination and the conscious awareness of the visual stimulus. V1 does not have a monopoly in mediating conscious vision and that other areas, even when isolated from it, can have direct access and contribute to that conscious experience
V6 has an unconventional retinal map. It has to do with the space representation of the brain.
Figure 14. Estimated density of ascending projections among the visual areas in macaque occipital cortex. Cortical areas are shown in proportion to their actual sizes and the thickness of lines connecting them is proportional to the numbers of fibers in the pathways (After Colby, 1991)
From all this we are realizing more how the division of work acts in the brain. Although there is a lot of crosstalk between the visual areas, feed-forward and feedback systems etc. It is amazing to see how the retinal image of the world around us is torn into thousand pieces and elaborated by all sorts of different cells in our brain. The big question is however: how is the brain putting all these pieces together to form a coherent image of the world around us.
Recently Galarera and Hestrin (1999) are suggesting that encoding of information in the cortex be thought to depend on synchronous firing of cortical neurons. Inhibitory neurons are playing an important role in the synergetic behavior. They are thinking that electrical synapses establish a network of fast-spiking cells in the neocortex, which may play a key role in coordinating cortical activity.