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Sense and Lens

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When those born blind get their vision, they have difficulty correlating the real to the ‘felt’. T.V. Jayan on the outcome of a project for visually challenged children in rural India.

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The participants were asked to feel a building block and then match the object felt with two blocks, one square and the other circular.

Blind children from India’s hinterland have found themselves a place in history by helping researchers resolve a profound and long-standing problem that perplexed philosophers and neuroscientists for over three centuries.

Posed for the first time in 1688 by Irish scientist and politician William Molyneux, the question is elegantly simple: can a person who has been blind from birth but gained sight in adulthood visually discriminate between objects that were previously identifiable only by touch?

The answer seems to be a definite “no”. That’s the conclusion of a team of Indian and American scientists after their studies involving blind children in rural India whose eyesight was restored surgically. In other words, a person’s ability to learn the correspondence between how an object looks and how it feels is not innate; it needs to be learnt. The study appeared yesterday in Nature Neuroscience.


The five children, aged between eight and 17, who participated in the study are part of a project launched by Pawan Sinha, a brain and cognitive sciences professor at the Massachusetts Institute of Technology (MIT), the US.

The Molyneux question has been the subject of much debate in philosophy and neuroscience over the past three centuries, says MIT’s Richard Held, the first author of the paper. It’s important for two reasons, he says. Philosophically speaking, it touches upon the core of the “nature versus nurture” debate. It also addresses a deep scientific question: do the various senses of a living organism share an innate common space?

Though efforts to answer the question began not long after it was first posed, it had thus far remained unresolved. The primary reason for this is that in the West, a majority of curable congenital blindness cases are detected in infancy and treated as early as possible. But the scientists working with Project Prakash — which Sinha launched in 2004 — however, had an opportunity to take a fresh look at the problem. They had been working with children with vision disabilities in rural India as part of the humanitarian venture. The country is said to have the highest number of blind children in the world — more than one million.

Most cases of blindness in India are caused by vitamin A deficiency, cataracts, retinal or optical dystrophies, or microphthalmos (poorly developed eyes). About half the cases are treatable or preventable, but many never receive medical care, especially in rural areas.

Under the project, the scientists have so far screened more than 20,000 children in some of the most backward villages in Uttar Pradesh, Haryana, Rajasthan and Madhya Pradesh. “Over 700 children have been treated for conditions ranging from severe refractive error to congenital blindness,” says Sinha, a co-author of the study. The medical care was provided at New Delhi’s eye hospital, Shroff’s Charity Eye Hospital, a project partner.

For their study, the scientists chose five children who were blind from birth owing to a congenital cataract or an opaque cornea. After surgery — a cataract removal or a corneal transplant — the participants were asked to feel a building block and then match the object felt with one or two blocks (of two different shapes — one square and the other circular). The children were unable to match the blocks they felt with what they only saw. Significantly, their performance improved substantially five days later, although they didn’t receive any kind of training.

This rapid improvement was surprising, says Yuri Ostrovsky, another MIT researcher associated with the study. He points out that many visual tasks, such as face perception, can take six to 12 months to learn after sight is restored. “The outcome has been a surprise — one that has important implications for theories regarding how the brain learns to acquire a coherent account of the complex environment,” Held told KnowHow.

Sinha, who holds a BTech from the Indian Institute of Technology, Delhi, says the project has been an eye opener in more ways than one. It served a dual purpose: providing sight to blind children and advancing fundamental science. This, along with earlier findings from Project Prakash, shows that the human brain retains an impressive ability to launch programmes of visual learning well after the normal period of their deployment has passed.

“It has helped clear several myths regarding vision. Most eye doctors hesitate to treat older patients because they believe the brain is incapable of learning to see after age six or seven,” Sinha told KnowHow. “Our work has broken this dogma.”

The results of the study are significant for basic neuroscience as well as paediatric ophthalmology and implementation of later-stage blindness treatment programmes.

Here’s hoping there will be light for all.
You may click to see :Those Who Once Were Blind Can Learn To See, Study Shows

Source: The Telegraph ( Kolkata, India)

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High on Calories

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Obese people are not able to regulate high-calorie food intake because of changes in their brain.
If your overweight children binge eat, blame it on their flawed brain circuitry. Scientists have now found that despite the desire to cut their food intake, obese individuals will not be able resist junk food, which is very high in calories. That’s because their persistent eating behaviour has precipitated changes in the brain similar to that found in heavy smokers and drug addicts. The study appeared yesterday in the journal Nature Neuroscience.

After spending years studying brain changes associated with drug abuse and smoking, Paul Kenny — a neurobiologist at the Scripps Research Institute in Florida, the US — recently turned his attention to obesity. He and his graduate student, Pal Johnson, wanted to understand the strong yet not-so-easy-to-fathom link between obesity and depleted levels of dopamine or D2, a brain chemical associated with feelings of pleasure.

Scientists in the past had observed that obese individuals have reduced levels of dopamine, but weren’t sure if it was triggered by obesity. It was also known that food intake was associated with dopamine release and the degree of pleasure from eating correlates with the amount of chemical released. Evidence has shown that in comparison to lean people, obese individuals have fewer dopamine receptors in the brain. And people with fewer dopamine receptors need to take in more of a rewarding substance — such as food or drugs — to get an effect that others get with a lesser amount. But the underlying mechanisms are poorly understood.

“What we have achieved is proven in our experiments with laboratory rats that obesity can elicit these brain changes,” Kenny told KnowHow over the telephone.

For this, the Florida scientists embarked upon a series of meticulously planned experiments. In the first, they offered rats — which were grouped into three categories — different menus. While the first group had access solely to less-appetising but healthier chow, the other two were offered a choice of high-calorie food such as bacon, sausage, cake and chocolate in addition to chow, but for varying durations. Some rats had access to the rich fare for just one hour, while the other group could gorge on it most part of the day. The animals were fed this way for 40 days. All of them were wired to record even the slightest change in their D2 levels.

The rats in the first set — which were fed only chow — maintained their weight, while those belonging to the second set — which had restricted access to rich food — exhibited insignificant increase in their body weight. On the contrary, the third group — which had unlimited access to calorie-rich food — gained weight rapidly. These animals were found to be gobbling up twice as much as the other two groups. As the days wore on, their dopamine levels plummeted, requiring them to consume higher quantities of high-fat food to get the feeling of satiation. This is quite like the case of a smoker who has to puff away more cigarettes to get the same high that he or she earlier got with one. Or a drug addict who has to continuously increase the dose for getting a kick.

A second set of experiments with the rats showed that this blunting of the reward sensitivity does not return for a good two weeks even after the high-calorie food was withdrawn.

A true addict, whether rat or human, will compulsively consume the addictive substance even when it is clearly detrimental to health. In the third experiment the scientists tested this hypothesis. To do this, the team trained the rats to expect painful foot shocks upon seeing a light signal. Although the normal rats stopped eating even the most delicious junk food when the light came on, the obese ones used to a high-calorie diet simply ignored the cue and kept feeding.

Anoop Misra, head of internal medicine at Fortis Hospitals in New Delhi, says this explains why obese people find it difficult to modulate their junk food eating habits.

“The US scientists’ experiment has substantiated many assumptions associated with obesity and dopamine levels in the brain fairly well,” says Nihal Thomas, an endocrinologist at the Christian Medical College, Vellore. “The exercise and methodology followed are exquisite.” The findings may help develop drugs that may target dopamine receptors to treat obesity, he observes.

Source : The Telegraph (Kolkata, India)

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How Scratching Curbs the Itch?

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Itching brings with it that ever-increasing urge to scratch, which always works wonders, but not much is known about the physiological  mechanisms behind this phenomenon.

Now scientists have watched spinal nerves transmit that relief signal to the brain in monkeys, a possible step toward finding new treatments for persistent itching in people. & see

Nerve cells play a key role in itching

More than 50 conditions can cause serious itching, including AIDS, Hodgkin’s disease and the side effects of chronic pain treatment, said Glenn Giesler, a neuroscientist at the University of Minnesota in Minneapolis. Some terminal cancer patients even cut back on pain medication just to reduce the itch, he said.

Scratching can lead to serious skin damage and infections in people with chronic itch, he said. So scientists want to find ways for such people to relieve their distress “without tearing up their skin,” he said.

While medications can relieve some kinds of itch, other cases resist current treatments.

Nobody knows just how scratching relieves itch. But the federally funded monkey study, reported Monday on the website of the journal Nature Neuroscience by Giesler and colleagues, takes a step in unraveling the mystery.

The scientists focused on a kind of spinal nerve that transmits the “itch” signal to the brain. The researchers sedated long-tailed macaques for the experiment and placed recording electrodes on their spinal nerves. They injected a chemical into a leg to produce itching. The nerves fired electrical signals in response. Then the researchers scratched the leg with a hand-held metal device that simulates three monkey fingers. The firing rate dropped — the apparent signature of the “relief” signal. In contrast, when researchers scratched the leg without causing an itch first, the firing rate jumped. So the nerves somehow “know” to react much differently if there’s an itch to be relieved than if there isn’t.

Sources: The Times Of India

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Why desire drives us wild

A new brain study has pointed out why most mammals experience moments of overwhelming desire – be it for food, sex or other things – that can be followed by seemingly magical feelings of satisfaction. But the find suggests we are often likely to be left wanting rather than satisfied.

According to a study recently published in the Journal of Neuroscience, wanting and liking are separate urges in the brain that are controlled by different circuits.

When these urges occur in sync, the impact on the brain is very powerful.

But there’s a catch. Mammal brains appear to have fewer mechanisms for pleasure than they do for desire.

“Our results suggest we all are inherently susceptible to wanting more than we’ll actually enjoy, at least in certain situations,”co-author Kent Berridge told Discovery News.

Berridge, a University of Michigan psychology researcher, added, “If separable brain circuits exist for liking and wanting, then a person who had selective activation of the wanting circuit would want more without liking more.”

Such want/like dissociations can lead to addictions with drugs, sex, food, gambling and more, the researchers believe. Some people also appear to be prone to experiencing the out-of-sync phases.

For the study, Berridge and colleague Kyle Smith used a painless microinjection technique to deliver droplets of an opioid drug into a pleasure hotspot within the brains of rats.

The drug caused the rats to want to eat three times their normal amount of food – in this case, sugar – while liking it twice as much as usual.

The scientists measured the “like” degree in rats by studying their facial expressions and behaviours while they ate. These included lip and paw licking.

The researchers then turned off a rat pleasure circuit by microinjecting an opioid suppressant into another part of the rodent’s brain. The rats reacted by still wanting sugar, but exhibited no extra signs of liking it.

Finally, the scientists used a technique called Fos mapping, which shows activated portions of the brain based on colour changes due to proteins that affect certain neural circuits.

This, and the other experiments, revealed the separate want and like “hedonic hotspots”in two areas deep within the brain. Rats, humans and other mammals share these same regions and related circuitry, so rat desire can be comparable to human desire.

Source:The Times Of India