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Your up-to-date guide to research in: Vol. 2 Issue 4 May 1997 NEUROSCIENCE

Vision research
Is seeing believing?
The Greek philosopher Euclid believed that sight resulted from light owing out of the eye to feel the world around us.We now know that quite the opposite is the case: like a camera, the eye adjusts and brings into focus light from the outside world onto a lm, the retina, at the back of the eye. However, the retina is far more sophisticated than photographic lm, and the nal picture is developed in a different structure the brain. Researchers are currently investigating how the retina encodes visual information, and how the visual cortex creates for us a meaningful perception of our world.

goldsh rods onto the end of blunt electrodes to measure the tiny electrical uctuations that occur when photoreceptors are illuminated. In the dark, an energy-rich substance called cGMP (cyclic guanosine monophosphate) clamps cGMP open sodium channels in the rods outer segment. Na+ channels closed Na+ channels open Sodium ions ow Na+ through these channels into the cell to generate the dark current; the rod is therefore K+ depolarized at rest. When photoreceptors glutamate capture the light, the cascade of events that follows lowers cGMP current from single levels, sodium channels rod on snap shut, and a off light compensatory current in the inner segment hyperpolarizes the cell. The eye continually ickers to ensure Light thus switches off the dark current. that the centre of our visual eld falls on Photoreceptors release a steady stream the fovea for ne examination. of glutamate that excites the bipolar cells below. As light turns down the dark current, A trick of the light Paradoxically, this stream is restricted, and bipolar cells photoreceptors are more excitable in the quieten. Note that neither photoreceptors dark; light reduces this excitability. The nor bipolar cells re action potentials; level of heightened excitability of the ganglion cells do. The bunch of axons photoreceptors the dark current keeps from ganglion cells form the optic nerve them primed for action. How does this that acts like a cable transmitting visual work? Researchers painstakingly sucked images from eye to brain in the form of

Catching the light About 125 million rods and 7 million cones are evenly scattered over the human retina except at the fovea the region on the retina where visual acuity (crispness) is greatest where there are only cones. Visual acuity is dictated, in part, by the degree of blending (convergence) of signals from the photoreceptors. In general, signals from 15 to 45 rods, but only ve to 20 cones, are averaged to form a single output. At the fovea, the output from a single cone remains unaltered. Greater averaging at the periphery of vision explains why you see little detail out of the corner of your eye.

electrical signals. When you move from a dim room into bright daylight you are initially blinded. As an unavoidable limitation of having a set dark current, photoreceptors

rod cone direction of light

horizontal cell bipolar cell amacrine cell

to optic nerve

ganglion cell

are quickly saturated by bright light. To restore sensitivity, cones can switch on a dark current even when illuminated this is called light adaptation. Calcium ions are vital for this process: in the dark, calcium keeps a check on the level of cGMP In the light, the calcium level drops, and the cGMP level can rise to reopen the sodium channels. The rejuvenated dark current restores the cones responsiveness to further changes in illumination.

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Also covered in this issue: the visual brain; principles of vision; visual development; a bionic eye

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Visual principles The visual system works on the basis of contrast, and is sensitive to differences rather than absolute measures of the intensity or colour of light. This principle applies throughout the visual pathway from the retina to the visual cortex. Ganglion cells are responsive to activity within a small circular area of the retina called its receptive eld. In on-centre cells, a spot of light shining on the centre of the receptive eld causes the ganglion

on-centre cell

off -centre cell

light

of a cone is similar, irrespective of the colour of the impinging wavelength of light. Colour is thus designated at some other stage of visual processing. The ganglion cells carry out the rst stage of colour analysis. Colour-sensitive ganglion cells respond best to spots of light surrounded by a ring of a contrasting colour, for example, red with a green surround, or blue with a yellow (a mix of green and red) surround. Once again, contrast is important. Another special property of colour vision colour constancy is generated in the cortex. For example, a red apple looks red whether sitting in the sun (white light), in candlelight (yellow light) or under a UV lamp (blue light). Objects retain their colour regardless of the impinging light. While we still dont know exactly how the brain achieves this feat, contrasts are likely to be important. From eye to brain About a million optic bres emerge from the retina. Fibres from the left and right visual elds remain segregated until they reach the cortex where information from the same visual eld of both eyes comes together. The rst relay station is the lateral geniculate nucleus (LGN) in the thalamus. Visual information from neighbouring up regions of the retina remain neighbours

in the LGN, and the retinal map is kept intact. Some of the optic bres branch off to the superior colliculus, the control centre for the ocular muscles which directs our gaze, in particular to moving objects. The colliculus also receives input from the ears and so we automatically turn to look for the source of a sound.

Two eyes but only one world


Our perception of a threedimensional world is dependent, at least in part, on having a pair of eyes. Our eyes are set at slightly different levels, so each eye receives a slightly different view of the object. The discrepancy between views enables the brain to estimate the depth of the object. The closer the object to your face, the greater the discrepancy between the two visual images and the more solid the object; the same object placed at a distance will seem atter. Specialized cells in the primary cortex, responsive to input from both eyes, probably play a role.

cell to re, while light shining on the surround reduces its activity. In off-centre cells, a spot of light directed at the centre of the eld reduces ring while ring is increased by a doughnut-shaped beam of light. In both cell types, diffuse light shone over the entire eld produces no effect the effects cancel each other out. Contrasting receptive elds are dependent on the convergence of signals from photoreceptors. This blending of signals is carried out by specialized neuronal bridges called interneurons the horizontal and amacrine cells. A multicoloured world Colour vision not only improves the aesthetics of the world but also the quality of vision. Detecting differences in the wavelengths of light helps us visualize their ner details, especially where the contrast in light intensity at different points is small, such as in very bright light. However, the electrical output

Visual development Vision is not fully developed in newborn animals, even in human infants. There is a critical period in our development during which the visual cortex must be exercised for normal sight to develop. Researchers covered one eye of a new born kitten. When the eye was uncovered three months later, the kitten remained blind in that eye. Closing the eye of an adult cat, by contrast, did not blind it.

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Cortical interpretations Scientists are still puzzling over

their constituent lines and shapes, which simple and complex cells can detect. Are some cortical cells capable of responding to sophisticated features like faces? If this was the case then we might expect that, with neuron loss through ageing or brain damage, some of us would become blind to certain objects; obviously, this situation does not occur. However, doctors have reported a peculiar condition called prosopagnosia. These patients can see but cant recognize even the most familiar faces. The cortex may possess more specialized neurons than we think.

how the brain extracts meaning from the millions of visual inputs that ood it each instant. Are cells in the cortex tuned to recognize specic objects, or is a more general process at work? Researchers were initially perplexed as to why spots of light excited retinal cells but left cortical neurons silent. Cortical cells will, however, respond to more sophisticated forms of illumination. Simple cortical cells re at the sight of light held at different angles; complex cells re for moving edges of light. The outlines of most objects can be broken down into

Eyes right About 300 000 people are currently registered blind or partially sighted (in the UK). We have much to learn about underlying causes of optical diseases. Visual disorders are, however, important areas of current research activity. Retinitis pigmentosa is the most common inherited form of blindness (See LabNotes Genetics Issue 1). The rst symptoms are nightblindness, but gradually the persons peripheral vision decays, and eventually they become blind. The tell-tale signs are a build-up of pigment on the retina, and a loss of rods and cones. Researchers have discovered that there is a fault in the rhodopsin pigment in a number of families suffering from retinitis pigmentosa. Perhaps the pigment over-reacted to light, and once switched on could not be switched off, ultimately killing the cells. Transgenic mice were created in which the normal rhodopsin was replaced by the faulty version. The mutant mice were blind even though the mutant rhodospin behaved normally. Researchers now suspect that there is a build-up of rhodopsin, perhaps explaining the dark pigmentation that disrupts the function of rods. Other transgenic mice might help solve the puzzle, and possibly be useful in explaining other retinal diseases.

A bionic eye? For those that have lost their sight later in life after the brain has learnt to see retinal transplants might compensate for damaged retinal cells. One approach is to transplant fetal retinal cells into the adult. Fetal cells are ideal for transplantation as they are invisible to the hosts immune system and so wont be rejected. Furthermore, they can still divide and so repopulate the retina, and replace damaged or missing photoreceptors; function may also be restored. The technique is still in its infancy and is still highly controversial, but trials on patients have begun. Alternatively, a bionic eye an electronic implant may get round the ethical concerns of using living tissue, but will only work if the ganglion cells are still functional. Tiny retinal implants are built from around 25 electrodes only a 1100 of a millimetre thick and linked to a miniature solar panel. When the panels absorb light,

electrical currents are generated in the electrodes. These stimulate the ganglion cells, sitting directly below, to send a signal to the brain, thus bypassing damaged retinal cells.

So far, the implants have been tested in experimental animals and in one human volunteer. With the implant in place, the patient could locate a spot of light. Visual resolution could be improved if more electrodes were used, perhaps sufcient for the wearer to read text again.

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Vision a new perspective


We have all been fooled by visual illusions. Perception is not simply what we see, but how the brain interprets this. Even Professor Semir Zeki, an expert on visual processing who works at University College London, says he has to stop and think about that fact that we see not with our eyes but with our heads. His work has centred on getting a handle on how the visual cortex recreates our outer world for us. Historically, vision has been thought to be a passive process. Light falls on the retina and is converted into electrical signals which then pass to the primary visual cortex V1. This made sense of the data we had at the time, that damage to parts of the visual cortex V1 destroyed sight in the corresponding visual eld. The task of perception, making sense of all this information, was left to the surrounding area. well, are these parallel processes really working in synchrony at all? The group therefore devised a computer game to test human volunteers as to whether or not our different visual processing pathways do, indeed, keep the same pace. The test was wonderfully simple: volunteers were asked to determine the colour of the upward-moving box generated on a computer screen. The task is a little tricky as the box changes colour while it moves up and down (red to green, or vice versa). The researchers were surprised at the result. Volunteers were much better at correctly identifying the colour rather than direction of motion of the boxes. Other experiments were devised to compare and contrast other visual elements such as colour and motion. Dr Zeki and colleagues nally came to the conclusion that parallel processing does not occur in synchrony at all. The brain extracts the colour information of an image, before it extracts its form and this, in turn, before its motion.
Wellcome Trust Medical Photographic Library

Professor Semir Zeki


remains). A neighbouring region, V3, responded to form rather than colour, while moving images triggered activity in V5. Damage in area V5 results in the rather bizarre condition called akinetopsia in which moving objects become invisible: for example, a person will see a stationary car, but not its approach. It became clear that the concept of the unitary visual system was far too simplistic. A number of processing systems work in parallel to make sense of what we see. Why does the brain need to process visual information in this way? We see to acquire knowledge about the world, for our survival. However, we only pick out certain components of our visual landscape, so every instant we discard a lot of visual information to capture the most essential parts. It therefore makes sense to have separate systems that can extract specic sorts of information colour, form and motion from our environment. Recently, Dr Zeki and his colleagues began to suspect that there are even more subtleties to the brains processing powers. When you look at a person, you see them in perfect register, i.e. you see their shape, colour and movement all at the same time. The brain must be able to recombine all these separate components in perfect time so as to accurately recreate the original. However, a search for a cortical region that can carry out such a task proved fruitless. We asked ourselves,

It was primarily Dr Zekis work that turned this concept on its head. Using modern imaging techniques in humans such as PET (see LabNotes Neuroscience Issue 1), as well as recording the brain activity generated in experimental animals in response to different types of visual stimuli, the researchers found that distinct and discrete cortical regions were activated by different elements of the stimuli. For example, colours excited an area called V4. In agreement, people who have suffered damage to V4 say from a stroke are completely colour blind and see the world in dirty shades of grey (this is quite different to retinal colour blindness in which some colour appreciation

Dr Zekis results directly challenge existing beliefs about visual processing. His work raises yet more difcult questions. For example, how does the brain recombine these out-of-step, visual components to recreate an accurate picture of the outside world? Dr Zeki has come to the conclusion that perhaps a cortical mixing pot for all these separate visual elements does not exist. Instead, the different pathways remain independent, but constantly talk to one another. And how do they do this? Such questions will continue to keep visual researchers busy for many years to come.

Topics coming up in future issues: mental health; brain and behaviour; brain development