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Showing posts with label scientists say. Show all posts
Showing posts with label scientists say. Show all posts

Sunday, October 20, 2013

Method of recording brain activity could lead to 'mind-reading' devices, scientists say 10-19

Method of recording brain activity could lead to 'mind-reading' devices, scientists say

BY BRUCE GOLDMAN


Josef Parvizi
A brain region activated when people are asked to perform mathematical calculations in an experimental setting is similarly activated when they use numbers — or even imprecise quantitative terms, such as “more than”— in everyday conversation, according to a study by Stanford University School of Medicine scientists.


Using a novel method, the researchers collected the first solid evidence that the pattern of brain activity seen in someone performing a mathematical exercise under experimentally controlled conditions is very similar to that observed when the person engages in quantitative thought in the course of daily life. 

“We’re now able to eavesdrop on the brain in real life,” said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford’s Human Intracranial Cognitive Electrophysiology Program  . Parvizi is the senior author of the study, published Oct. 15 in Nature Communications. The study’s lead authors are postdoctoral scholar Mohammad Dastjerdi, MD, PhD, and graduate student Muge Ozker.

The finding could lead to “mind-reading” applications that, for example, would allow a patient who is rendered mute by a stroke to communicate via passive thinking. Conceivably, it could also lead to more dystopian outcomes: chip implants that spy on or even control people’s thoughts.


“This is exciting, and a little scary,” said 
Henry Greely, JD, the Deane F. and Kate Edelman Johnson Professor of Law and steering committee chair of the Stanford Center for Biomedical Ethics  , who played no role in the study but is familiar with its contents and described himself as “very impressed” by the findings. “It demonstrates, first, that we can see when someone’s dealing with numbers and, second, that we may conceivably someday be able to manipulate the brain to affect how someone deals with numbers.”


The researchers monitored electrical activity in a region of the brain called the intraparietal sulcus, known to be important in attention and eye and hand motion. Previous studies have hinted that some nerve-cell clusters in this area are also involved in numerosity, the mathematical equivalent of literacy. 

However, the techniques that previous studies have used, such as functional magnetic resonance imaging, are limited in their ability to study brain activity in real-life settings and to pinpoint the precise timing of nerve cells’ firing patterns. These studies have focused on testing just one specific function in one specific brain region, and have tried to eliminate or otherwise account for every possible confounding factor. In addition, the experimental subjects would have to lie more or less motionless inside a dark, tubular chamber whose silence would be punctuated by constant, loud, mechanical, banging noises while images flashed on a computer screen.

“This is not real life,” said Parvizi. “You’re not in your room, having a cup of tea and experiencing life’s events spontaneously.” A profoundly important question, he said, is: “How does a population of nerve cells that has been shown experimentally to be important in a particular function work in real life?” 

His team  ’s method, called intracranial recording, provided exquisite anatomical and temporal precision and allowed the scientists to monitor brain activity when people were immersed in real-life situations. Parvizi and his associates tapped into the brains of three volunteers who were being evaluated for possible surgical treatment of their recurring, drug-resistant epileptic seizures.

The procedure involves temporarily removing a portion of a patient’s skull and positioning packets of electrodes against the exposed brain surface. For up to a week, patients remain hooked up to the monitoring apparatus while the electrodes pick up electrical activity within the brain. This monitoring continues uninterrupted for patients’ entire hospital stay, capturing their inevitable repeated seizures and enabling neurologists to determine the exact spot in each patient’s brain where the seizures are originating.

During this whole time, patients remain tethered to the monitoring apparatus and mostly confined to their beds. But otherwise, except for the typical intrusions of a hospital setting, they are comfortable, free of pain and free to eat, drink, think, talk to friends and family in person or on the phone, or watch videos.

The electrodes implanted in patients’ heads are like wiretaps, each eavesdropping on a population of several hundred thousand nerve cells and reporting back to a computer.

In the study, participants’ actions were also monitored by video cameras throughout their stay. This allowed the researchers later to correlate patients’ voluntary activities in a real-life setting with nerve-cell behavior in the monitored brain region. 

As part of the study, volunteers answered true/false questions that popped up on a laptop screen, one after another. Some questions required calculation — for instance, is it true or false that 2+4=5? — while others demanded what scientists call episodic memory — true or false: I had coffee at breakfast this morning. In other instances, patients were simply asked to stare at the crosshairs at the center of an otherwise blank screen to capture the brain’s so-called “resting state.”

Consistent with other studies, Parvizi’s team found that electrical activity in a particular group of nerve cells in the intraparietal sulcus spiked when, and only when, volunteers were performing calculations.

Afterward, Parvizi and his colleagues analyzed each volunteer’s daily electrode record, identified many spikes in intraparietal-sulcus activity that occurred outside experimental settings, and turned to the recorded video footage to see exactly what the volunteer had been doing when such spikes occurred.

They found that when a patient mentioned a number — or even a quantitative reference, such as “some more,” “many” or “bigger than the other one” — there was a spike of electrical activity in the same nerve-cell population of the intraparietal sulcus that was activated when the patient was doing calculations under experimental conditions. 

That was an unexpected finding. “We found that this region is activated not only when reading numbers or thinking about them, but also when patients were referring more obliquely to quantities,” said Parvizi.

“These nerve cells are not firing chaotically,” he said. “They’re very specialized, active only when the subject starts thinking about numbers. When the subject is reminiscing, laughing or talking, they’re not activated.” Thus, it was possible to know, simply by consulting the electronic record of participants’ brain activity, whether they were engaged in quantitative thought during nonexperimental conditions.

Any fears of impending mind control are, at a minimum, premature, said Greely. “Practically speaking, it’s not the simplest thing in the world to go around implanting electrodes in people’s brains. It will not be done tomorrow, or easily, or surreptitiously.”

Parvizi agreed. “We’re still in early days with this,” he said. “If this is a baseball game, we’re not even in the first inning. We just got a ticket to enter the stadium.”

Saturday, September 14, 2013

'Love hormone' may play wider role in social interaction than previously thought, scientists say 09-14



'Love hormone' may play wider role in social interaction than previously thought, scientists say

BY BRUCE GOLDMAN



Robert Malenka and Gul Dolen  found that the hormne known as oxytocin plays a stronger role in social bonding than previously thought.

Researchers at the Stanford University School of Medicine have shown that oxytocin — often referred to as "the love hormone" because of its importance in the formation and maintenance of strong mother-child and sexual attachments — is involved in a broader range of social interactions than previously understood.

The discovery may have implications for neurological disorders such as autism, as well as for scientific conceptions of our evolutionary heritage.   

Scientists estimate that the advent of social living preceded the emergence of pair living by 35 million years. The new study suggests that oxytocin's role in one-on-one bonding probably evolved from an existing, broader affinity for group living.

Oxytocin is the focus of intense scrutiny for its apparent roles in establishing trust between people, and has been administered to children with autism spectrum disorders in clinical trials. The new study, published Sept. 12 in Nature, pinpoints a unique way in which oxytocin alters activity in a part of the brain that is crucial to experiencing the pleasant sensation neuroscientists call "reward." The findings not only provide validity for ongoing trials of oxytocin in autistic patients, but also suggest possible new treatments for neuropsychiatric conditions in which social activity is impaired.

"People with autism-spectrum disorders may not experience the normal reward the rest of us all get from being with our friends," said Robert Malenka, MD, PhD, the study's senior author. "For them, social interactions can be downright painful. So we asked, what in the brain makes you enjoy hanging out with your buddies?"

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Some genetic evidence suggests the awkward social interaction that is a hallmark of autism-spectrum disorders may be at least in part oxytocin-related. Certain variations in the gene that encodes the oxytocin receptor — a cell-surface protein that senses the substance's presence — are associated with increased autism risk.

Malenka, the Nancy Friend Pritzker Professor in Psychiatry and Behavioral Sciences, has spent the better part of two decades studying the reward system — a network of interconnected brain regions responsible for our sensation of pleasure in response to a variety of activities such as finding or eating food when we're hungry, sleeping when we're tired, having sex or acquiring a mate, or, in a pathological twist, taking addictive drugs. The reward system has evolved to reinforce behaviors that promote our survival, he said.

For this study, Malenka and lead author Gül Dölen, MD, PhD, a postdoctoral scholar in his group with over 10 years of autism-research expertise, teamed up to untangle the complicated neurophysiological underpinnings of oxytocin's role in social interactions. They focused on biochemical events taking place in a brain region called the nucleus accumbens, known for its centrality to the reward system.

In the 1970s, biologists learned that in prairie voles, which mate for life, the nucleus accumbens is replete with oxytocin receptors. Disrupting the binding of oxytocin to these receptors impaired prairie voles' monogamous behavior. In many other species that are not monogamous by nature, such as mountain voles and common mice, the nucleus accumbens appeared to lack those receptors.

"From this observation sprang a dogma that pair bonding is a special type of social behavior tied to the presence of oxytocin receptors in the nucleus accumbens. But what's driving the more common group behaviors that all mammals engage in — cooperation, altruism or just playing around — remained mysterious, since these oxytocin receptors were supposedly absent in the nucleus accumbens of most social animals," said Dölen.

The new discovery shows that mice do indeed have oxytocin receptors at a key location in the nucleus accumbens and, importantly, that blocking oxytocin's activity there significantly diminishes these animals' appetite for socializing. Dölen, Malenka and their Stanford colleagues also identified, for the first time, the nerve tract that secretes oxytocin in the region, and they pinpointed the effects of oxytocin release on other nerve tracts projecting to this area.

Mice can squeak, but they can't talk, Malenka noted. "You can't ask a mouse, 'Hey, did hanging out with your buddies a while ago make you happier?'" So, to explore the social-interaction effects of oxytocin activity in the nucleus accumbens, the investigators used a standard measure called the conditioned place preference test.

"It's very simple," Malenka said. "You like to hang out in places where you had fun, and avoid places where you didn't. We give the mice a 'house' made of two rooms separated by a door they can walk through at any time. But first, we let them spend 24 hours in one room with their littermates, followed by 24 hours in the other room all by themselves. On the third day we put the two rooms together to make the house, give them complete freedom to go back and forth through the door and log the amount of time they spend in each room."

Mice normally prefer to spend time in the room that reminds them of the good times they enjoyed in the company of their buddies. But that preference vanished when oxytocin activity in their nucleus accumbens was blocked. Interestingly, only social activity appeared to be affected. There was no difference, for example, in the mice's general propensity to move around. And when the researchers trained the mice to prefer one room over the other by giving them cocaine (which mice love) only when they went into one room, blocking oxytocin activity didn't stop the mice from picking the cocaine den.

In an extensive series of sophisticated, highly technical experiments, Dölen, Malenka and their teammates located the oxytocin receptors in the murine nucleus accumbens. These receptors lie not on nucleus accumbens nerve cells that carry signals forward to numerous other reward-system nodes but, instead, at the tips of nerve cells forming a tract from a brain region called the dorsal Raphe, which projects to the nucleus accumbens. The dorsal Raphe secretes another important substance, serotonin, triggering changes in nucleus accumbens activity. In fact, popular antidepressants such as Prozac, Paxil and Zoloft belong to a class of drugs called serotonin-reuptake inhibitors that increase available amounts of serotonin in brain regions, including the nucleus accumbens.

As the Stanford team found, oxytocin acting at the nucleus accumbens wasn't simply squirted into general circulation, as hormones typically are, but was secreted at this spot by another nerve tract originating in the hypothalamus, a multifunction midbrain structure. Oxytocin released by this tract binds to receptors on the dorsal Raphe projections to the nucleus accumbens, in turn liberating serotonin in this key node of the brain's reward circuitry. The serotonin causes changes in the activity of yet other nerve tracts terminating at the nucleus accumbens, ultimately resulting in altered nucleus accumbens activity — and a happy feeling.

"There are at least 14 different subtypes of serotonin receptor," said Dölen. "We've identified one in particular as being important for social reward. Drugs that selectively act on this receptor aren't clinically available yet, but our study may encourage researchers to start looking at drugs that target it for the treatment of diseases such as autism, where social interactions are impaired."

Malenka and Dölen said they think their findings in mice are highly likely to generalize to humans because the brain's reward circuitry has been so carefully conserved over the course of hundreds of millions of years of evolution. This extensive cross-species similarity probably stems from pleasure's absolutely essential role in reinforcing behavior likely to boost an individual's chance of survival and procreation.

The study was funded by the Simons Foundation Autism Research Initiative   and the Walter and Idun Berry Foundation. Additional Stanford co-authors were technician Ayeh Darvishzadeh and former undergraduate Kee Wui Huang, now a neuroscience graduate student at Harvard University.

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