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Professor Patrick Cavanagh says "V8," the moniker a team of which he was part coined for an area of the brain they identified, sounds like an appropriate name for a "juice or a motor or something."
But following a system of nomenclature in which areas of the brain responsible for vision are named V1, V2, V3 and so forth in order of their discovery, the researchers were obliged to name the new area of the visual system they identified after the tomato-based juice.
"Kind of a funny name," Cavanagh admitted.
Cavanagh was one member of a team headed by Nouchine Hadjikhani, a research fellow at Harvard-affiliated Mass. General Hospital, that pinpointed the function of the new brain region, which they believe to be responsible for color vision. Their results were published in the July edition of Nature Neuroscience.
Cavanagh explained the discovery with a historical analogy. What the previous researchers had done, he said, was "like finding North America and calling it China."
"This isn't China," he said, "It's V8."
Thirty years of color research
The story of how the brain region came to be named after a vegetable juice has its roots in over thirty years of research on how the brain processes color.
When your eye sees an object, the image is first processed by your retina, then by a lower brain area, and then by the cerebral cortex. The image first goes to the least specialized region of the cortex, known as V1. As information is subject to more processing, it goes to higher and more specialized areas of the visual cortex designated as V2, V3 and so forth.
English scientist S. A. Zeki thought he had identified the region of the brain used to recognize color in the 1970s. Working with macaque monkeys, Zeki found that there was one region of the brain, V4, responsible for color and another, V5, respon- This theory predicted some bizarre disorders,which were soon identified in his clinic. A woman was found who was terrified of crossingthe street because she could not perceive motion.She would see cars in one place and then find themsuddenly pop up in another but she did not seethem move. She was found to have a lesion in V5 but not tobe deficient in any other respect. There was also the famous case of a artist whoselectively lost the ability to see color after anaccident. He had a lesion in V4 only. The relationship between the vision disordersand the brain abnormalities lent credence toZeki's theory that certain areas of the brain areresponsible for specific functions like motion andcolor perception. But as time went on, Hadjikhani, explained, itbecame clear that "no one really knew where thecolor processor was situated in the brain." Datacast doubt on whether even the macaque colorprocessor was really located in region V4. Last year, Alan Cowey and his colleagues atOxford identified an area in the macaque justbehind V4 that seemed to be responsible for colorvision. Now Hadjikhani and her team believe they havelocated an analogous area in humans--V8. They obtained their data by showing subjectsmoving wheels of color while monitoring whichareas of their brain the colors activated. The researchers employed a technique calledfunctional magnetic resonance imaging, which looksat the tiny magnetic changes that result fromaltered levels of blood flowing in the brain. To back up their data they studied the areas ofthe brain activated by color afterimages, theillusory images of complementary colors thatpeople experience after staring at a certain colorfor a long time. In a result that Hadjikhani described as"cool," they were able to demonstrate that V8 wasalso activated during color after images. But Zeki and his colleagues are up in arms.They have submitted a letter to NatureNeuroscience arguing against the findings. Atissue--in what Cavanagh described as a case of"physiological infighting"--are the true locationsof V4 and V8, and what their functions are. "Zeki is almost certainly wrong," Cavanaghsaid. "Pioneering and fundamental, but wrong." Like a Black and White Movie The discovery has already had some practicalimplications, helping to explain the symptomsexperienced by people who lose their color visionin accidents. Many people--almost 8 to 10 percent of the malepopulation--are born without normal color vision.This form of color blindness is due to defects inthe retina. But it is a far smaller number ofpeople--probably about 20 or so in the entirehistory of neuroscience--who have lost their colorvision due to lesions caused by accidents. Thesepeople are known as spinal achromats. Toachromats, the world looks like a black and whitemovie. In a separate paper published alongside theHadjikhani findings in Nature Neuroscience,Cavanagh reported that this condition is a resultof a lesion in V8. The paper focused on the degree to whichinformation about color is separated frominformation about motion and brightness that isalso processed in the brain. The researchers foundthat achromats were able to distinguish the motionof certain color stimuli just as those without thedisorder. This indicated that the pathway from the retinato the motion analysis areas was independent ofthe color areas damaged by the disorder
This theory predicted some bizarre disorders,which were soon identified in his clinic.
A woman was found who was terrified of crossingthe street because she could not perceive motion.She would see cars in one place and then find themsuddenly pop up in another but she did not seethem move.
She was found to have a lesion in V5 but not tobe deficient in any other respect.
There was also the famous case of a artist whoselectively lost the ability to see color after anaccident. He had a lesion in V4 only.
The relationship between the vision disordersand the brain abnormalities lent credence toZeki's theory that certain areas of the brain areresponsible for specific functions like motion andcolor perception.
But as time went on, Hadjikhani, explained, itbecame clear that "no one really knew where thecolor processor was situated in the brain." Datacast doubt on whether even the macaque colorprocessor was really located in region V4.
Last year, Alan Cowey and his colleagues atOxford identified an area in the macaque justbehind V4 that seemed to be responsible for colorvision.
Now Hadjikhani and her team believe they havelocated an analogous area in humans--V8.
They obtained their data by showing subjectsmoving wheels of color while monitoring whichareas of their brain the colors activated.
The researchers employed a technique calledfunctional magnetic resonance imaging, which looksat the tiny magnetic changes that result fromaltered levels of blood flowing in the brain.
To back up their data they studied the areas ofthe brain activated by color afterimages, theillusory images of complementary colors thatpeople experience after staring at a certain colorfor a long time.
In a result that Hadjikhani described as"cool," they were able to demonstrate that V8 wasalso activated during color after images.
But Zeki and his colleagues are up in arms.They have submitted a letter to NatureNeuroscience arguing against the findings. Atissue--in what Cavanagh described as a case of"physiological infighting"--are the true locationsof V4 and V8, and what their functions are.
"Zeki is almost certainly wrong," Cavanaghsaid. "Pioneering and fundamental, but wrong."
Like a Black and White Movie
The discovery has already had some practicalimplications, helping to explain the symptomsexperienced by people who lose their color visionin accidents.
Many people--almost 8 to 10 percent of the malepopulation--are born without normal color vision.This form of color blindness is due to defects inthe retina.
But it is a far smaller number ofpeople--probably about 20 or so in the entirehistory of neuroscience--who have lost their colorvision due to lesions caused by accidents. Thesepeople are known as spinal achromats. Toachromats, the world looks like a black and whitemovie.
In a separate paper published alongside theHadjikhani findings in Nature Neuroscience,Cavanagh reported that this condition is a resultof a lesion in V8.
The paper focused on the degree to whichinformation about color is separated frominformation about motion and brightness that isalso processed in the brain. The researchers foundthat achromats were able to distinguish the motionof certain color stimuli just as those without thedisorder.
This indicated that the pathway from the retinato the motion analysis areas was independent ofthe color areas damaged by the disorder
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