mucholderthen:

Illustration
the visible spectrum as part of the electromagnetic spectrum
(Credit:  Abrisa Glass & Coatings, 2005)

X-rays, light, and radio waves are examples of electromagnetic waves.

Light is what we call the part of the electromagnetic spectrum that we can detect with our eyes. The cone photoreceptors in our eyes have evolved so that they are most sensitive at different regions of the visible spectrum. This forms the basis for our sensation of color 

At the blue end of the visible spectrum, the wavelength of light is shorter — about 400 nanometers.

A nanometer is 1 billionth of a meter, or 1 × 10−9 meter.  The abbreviation for nanometer is ‘nm’.

At the red end of the spectrum, the wavelength of light is longer — about 700 nm.

Cone photoreceptors have evolved into three different types. Each one is most sensitive to a different region of the visible spectrum. One type responds best to shorter wavelengths; another responds best to wavelengths towards the middle of the spectrum; and the third type responds best to longer wavelengths.

The different cone photoreceptors are not sharply tuned to a particular color, however. So a short-wavelength cone photoreceptor can still respond to longer-wavelength light that falls on it. It is more likely to respond to shorter wavelength light, but it is still possible for it to respond to mid- and long-wavelength light.

The signals from the three different types of cones are combined in the retina and in the brain, eventually giving rise to the sensation of color.

[ via Mixing Light ]

neuromorphogenesis:

Here’s the Real Reason Why Virtual Reality Doesn’t Work Yet

It’s another blow for immersive virtual reality. University of California researchers have shown that even people with perfect eyesight navigate the world by relying on a lot more than what they see. Here’s why VR won’t really work until we go beyond visual cues and fancy treadmills.

Inside our brain’s hippocampus we have what are called place cells. These specialized cells help us build a “cognitive map” of our surroundings — mental representations which allow us to orientate ourselves in our spatial environment.

These neurons have been observed to fire like crazy whenever a rat has to go about the task of figuring out where it is in the world. And if the rat in an entirely new location altogether, it has to create a new cognitive map from scratch.

But once this map has been created, rats can quickly figure out where they are should they return to that location.

Scientists have theorized that rats don’t require much sensory information to build these maps, figuring that distant visual images, the ability to move themselves around, and maybe some proprioceptive orientation is all that’s required to do the trick. But as the new study by Pascal Ravassard and colleagues has shown, that’s not enough — and not enough by a mile.

To reach this conclusion, Pascal Ravassard and colleagues experimented with rats placed in a virtual reality environment. Indeed, VR is becoming a popular tool amongst some scientists. For example, researchers have interacted with rats by becoming virtual rats themselves, and they’ve gotten monkeys to feel virtual objects by using a brain implant.

But as this experiment showed, getting a rat’s brain to respond to a VR environment in the same way it responds to the real world is not so easy.

For the study, the researchers tried to create two apparently identical worlds, one real (RW) and one virtual (VR). Each environment consisted of a linear track in the center of a square room with distinct visual cues on each of the four walls. These cues were nearly identical in both environments, but the rats’ bodies were fixed in VR — thus minimizing (or even eliminating) other important spatial cues, like balance. So, the only incoming environmental data during VR exposure were the visual cues and self-motion.

After attaching tetrodes to measure the neural activity of six rats, the researchers had them run the track in both the RW and VR environments. When looking at the results, it was clear that the VR environment was not exciting the place cells as per usual. In VR, place cells showed 20% activity as compared to 45% in RW — more than twice as much.

So, vision and self-motion will spark a little bit of place cell activity, but balance and other sensory cues are what’s fully required to properly encode a rat’s — and likely a human’s — position. Moreover, the researchers speculate that other cues — like smell, sound, and textures — are what’s needed to help the rats properly self-locate themselves. But looking at the scans, the researchers realized that the only spatial encoding that was being done in VR was distance.

It’s clear from the study, therefore, that a variety of sensory clues must interact and compete in the brain for us to construct a robust cognitive map.

neuromorphogenesis:

The woman who can’t recognise her face

Name: Heather Sellers
Condition: Prosopagnosia

“I’ve been in a crowded elevator with mirrors all around, and a woman will move and I’ll go to get out the way and then realise: ‘oh that woman is me’.”

Heather Sellers has prosopagnosia, more commonly known as face blindness. “I can’t remember any image of the human face. It’s simply not special to me,” she says. “I don’t process them like I do a car or a dog. It’s not a visual problem, it’s a perception problem.”

Heather knew from a young age that something was different about the way she navigated her world, but her condition wasn’t diagnosed until she was in her 30s. “I always knew something was wrong – it was impossible for me to trust my perceptions of the world. I was diagnosed as anxious. My parents thought I was crazy.”

The condition is estimated to affect around 2.5 per cent of the population, and it’s common for those who have it not to realise that anything is wrong. “In many ways it’s a subtle disorder,” says Heather. “It’s easy for your brain to compensate because there are so many other things you can use to identify a person: hair colour, gait or certain clothes. But meet that person out of context and it’s socially devastating.”

As a child, she was once separated from her mum at a grocery store. Store staff reunited the pair, but it was confusing for Heather, since she didn’t initially recognise her mother. “But I didn’t know that I wasn’t recognising her.”

Chaos explained

Heather was 36 when she stumbled across the phrase face blindness in a psychology textbook. “When I saw those two words I knew instantly that was exactly what I had – that explained all the chaos.”

She found her way to Harvard neuroscientist Brad Duchaine who diagnosed her as having one of the three worst cases of the disorder that he had ever seen.

So what’s it like to not recognise anyone you know? Heather says the biggest difficulty with the disorder is recognising people who she is close to – the people that are most important to recognise. In the school where she teaches English she is fine, because she recognises people by their clothes or hair and asks her students to wear name badges.

But it can be harder in social settings. Once she went up to the wrong person at a party and put her arm around him thinking he was her partner. And at college men would phone her angry that she had walked straight past them after they had had a date. “At the time I was thinking ‘I didn’t see you, why is everyone making my life so difficult?’”

It’s not just other people Heather doesn’t recognise – she can’t identify her own face either. “A few times I have been in a crowded elevator with mirrors all around and a woman will move, and I will go to get out the way and then realise ‘oh that woman is me’.” She also finds it unsettling to see photos and not recognise herself in them.

Face processing

To try and understand the condition, Duchaine and his colleagues recorded brain activity while 12 people with prosopagnosia looked at famous and non-famous faces. The team found that part of the brain responsible for stored visual memory was activated in six people when they saw the famous faces.

But another component of brain activity thought to represent a later stage of face processing wasn’t triggered. “Some part of their brain was recognising the face,” says Duchaine, but the brain was failing to pass this information into higher-level consciousness (Brain, doi.org/fzmqgz).

“There may be training where we give people feedback and say ‘look you recognise that face even though you’re not aware of it’,” says Duchaine.

Now Zaira Cattaneo at the University of Milano-Bicocca in Italy and colleagues have identified the specific brain areas that allow us to recognise our friends. The team used transcranial magnetic stimulation to block two vital aspects of face processing in people without prosopagnosia. Targeting the left prefrontal cortex blocked the ability to distinguish individual features like the nose and eyes, and blocking the right prefrontal cortex impaired the ability to distinguish the location of those features from one another (NeuroImage, doi.org/mff).

“We made performance worse,” says Cattaneo. “We want to make it better.” Now the team are trying to activate these areas of the brain. “The aim is to enhance face recognition abilities by directly modulating excitability in the prefrontal cortices,” says Cattaneo.

Would Heather want a cure, should one be found? “I can’t imagine what you see when you see a face, and it’s scary,” she says. “I go back and forth on what I’d do. I’ve done so much work in figuring out how to chart my world, I’d need to do a whole new rewrite. But it would be fascinating.”

neuromorphogenesis:

Want to slow mental decay? Play a video game

Study shows mental agility game slows cognitive decline in older people

There may be a way for older people to prevent natural aging of their minds, and it could be as simple as playing a video game.

That’s according to a studyfrom the University of Iowa, which found that people aged 50 and older who played just ten hours of a game priming their mental processing speed and skills delayed declines by as many as seven years in a range of cognitive skills.

“We know that we can stop this decline and actually restore cognitive processing speed to people,” says Fredric Wolinsky, professor in the UI College of Public Health and lead author on the paper published May 1in the journal PLOS One. “So, if we know that, shouldn’t we be helping people? It’s fairly easy, and anyone can go get the training game and play it.”

The study comes amidst a burst of research examining why, as we age, our minds gradually lose “executive function,” generally considered mission control for critical mental activities, such as memory, attention, perception, and problem solving. Studies show loss of executive function occurs as people reach middle age; other studies say our cognitive decline begins as soon as 28 years of age. Either way, our mental capacities do diminish, and medical and public health experts are keen to understand why in an effort to stem the inexorable tide as much as possible.

Wolinsky and colleagues separated 681 generally healthy medical patients in Iowa into four groups—each further separated into those 50 to 64 years of age and those over age 65. One group was given computerized crossword puzzles, while three other groups were exposed to a video game called “Road Tour,” (since renamed “Double Decision”), marketed by Posit Science Corp. Briefly, the exercise revolves around identifying a type of vehicle (displayed fleetingly on a license plate) and then reidentifying the vehicle type and matching it with a road sign displayed from a circular array of possibilities, all but one of them false icons. The player must succeed at least three out of every four tries to advance to the next level, which speeds up the vehicle identification and adds more distractions, up to 47 in all.

The goal, naturally, is to increase the user’s mental speed and agility at identifying the vehicle symbol and picking out the road sign from the constellation of distractors (which are rabbits, by the way).

“The game starts off with an assessment to determine your current speed of processing. Whatever it is, the training can help you get about 70 percent faster,” says Wolinsky, who has no financial stake in the brain-fitness game.

The groups that played the game at least 10 hours, either at home or in a lab at the university, gained, and retained, at least three years of cognitive improvement when tested after one year, according to a formula developed by the researchers. A group that got four additional hours of training with the game did even better, improving their cognitive abilities by four years, according to the study.

“We not only prevented the decline; we actually sped them up,” Wolinsky says.

Improving people’s processing speed is considered important for a host of reasons. One widely accepted benefit is widening a person’s field of view. “As we get older, our visual field collapses on us,” Wolinsky explains. “We get tunnel vision. It’s a normal functioning of aging. This helps to explain why most accidents happen at intersections because older folks are looking straight ahead and are less aware of peripherals.”

Recognizing this, the National Institutes of Health in the late 1990s commissioned the largest cognitive training study of its kind, called ACTIVE. The national, multi-site trial, in which Wolinsky was involved, showed the elderly’s memory, reasoning, and visual processing speed could be improved with interventions, thus slowing the aging of their minds. But the ACTIVE study had its limitations: Among them, the control group didn’t get any training and the primary goal was to assess the effects on seniors’ field-of-view vision.

Wolinsky’s team added an active control group—those doing the crossword puzzles. The researchers found those who played the “Road Tour” game also scored far better than the crossword puzzle group on tests involving executive function beyond field-of-view vision, such as concentration, nimbleness with shifting from one mental task to another, and the speed at which new information is processed. The improvement ranged from 1.5 years to nearly seven years in cognitive improvement, the study found.

“It’s the ‘use it or lose it’ phenomenon— with a twist,” Wolinsky says. “Age-related cognitive decline is real, it’s happening, and it starts earlier and then continues steadily. Here, the exercise designed by neuroscientists delivered significant gains that generalized to daily life.”

Image:University of Iowa researchers say playing video games that challenge mental processing speed and skills can prevent mental decline by as many as seven years. The study tested elderly people playing a game called “Road Tour.”

neuromorphogenesis:

A Sense of Where You Are

In 1988, two determined psychology students sat in the office of an internationally renowned neuroscientist in Oslo and explained to him why they had to study with him.

Unfortunately, the researcher, Per Oskar Andersen, was hesitant, May-Britt Moser said as she and her husband, Edvard I. Moser, now themselves internationally recognized neuroscientists, recalled the conversation recently. He was researching physiology and they were interested in the intersection of behavior and physiology. But, she said, they wouldn’t take no for an answer.

“We sat there for hours. He really couldn’t get us out of his office,” Dr. May-Britt Moser said.

“Both of us come from nonacademic families and nonacademic places,” Edvard said. “The places where we grew up, there was no one with any university education, no one to ask. There was no recipe on how to do these things.”

“And how to act politely,” May-Britt interjected.

“It was just a way to get to the point where we wanted to be. But seen now, when I know the way people normally do it,” he said, smiling at the memory of his younger self, “I’m quite impressed.”

So, apparently, was Dr. Andersen. In the end, he yielded to the Mosers’ combination of furious curiosity and unwavering determination and took them on as graduate students.

They have impressed more than a few people since. In 2005, they and their colleagues reported the discovery of cells in rats’ brains that function as a kind of built-in navigation system that is at the very heart of how animals know where they are, where they are going and where they have been. They called them grid cells.

“I admire their work tremendously,” said Eric Kandel, the Nobel laureate neuroscientist who heads the Kavli Institute for Brain Science at Columbia and who has followed the Mosers’ careers since they were graduate students.

John O’Keefe of University College London, who in the 1970s identified the so-called place cells in the brain that register specific places, like the corner deli or grandma’s house, and who was one of the Mosers’ mentors, said that the discovery of the grid cells was “incredibly significant.”

The workings of the grid cells show that in the brain “you are constantly creating a map of the outside world,” said Cori Bargmann, of Rockefeller University, who is one of the two leaders of a committee set up to plan the National Institutes of Health’s contribution to President Obama’s recently announced neuroscience initiative.

Often, the workings of billions of neurons that produce our thoughts are opaque. But electrical recordings of signals emitted by grid cells show a map “with a framework and coordinates that are completely intuitive,” Dr. Bargmann said. And to find such a straightforward system is, in its own way, “just mind-boggling.” What is the brain doing being so mysteriously unmysterious?

The implications of the discovery are both practical and profound. The cells have been proved to exist in primates, and scientists think they will be found in all mammals, including humans. The area in the brain that contains the grid cell navigation system is often damaged early in Alzheimer’s disease, and one of the frequent early symptoms of Alzheimer’s patients is that they get lost. The Mosers do not work on humans, but any clues to understanding how memory and cognitive ability are lost are important.

On the most profound level, Dr. O’Keefe, the Mosers and others speculate that the way the brain records and remembers movement in space may be the basis of all memory. This idea resonates with the memory palaces of the Renaissance, imagined buildings that used spatial cues as memory aids. The technique dates to the ancient Greeks. In this regard, neuroscience may be catching up with intuition.

A Welcome Ambush

Edvard, 51, and May-Britt Moser, 50, now direct the Kavli Institute for Systems Neuroscience and the Centre for the Biology of Memory at the Norwegian University of Science and Technology here in Trondheim. They have a steady stream of findings coming from their lab, and a slew of awards, the latest of which, the Perl-U.N.C. Neuroscience Prize, they received April 16 at the University of North Carolina.

But they did not grow up in a center of academic ferment or intellectual competition. They were born and raised on islands off the coast of Norway a couple of hundred miles north of Bergen, part of an area known as Norway’s Bible Belt. They went to the same high school, but didn’t really get to know each other until they met again at the University of Oslo in the 1980s.

May-Britt, who grew up on a farm, remembers an environment in which drinking, card playing and dancing were all frowned upon. When she called home from Oslo announcing that she had been to a bar and had her first beer, her mother said, “And what’s next?”

The Mosers married in 1985 while still undergraduates. By the time they had finished their doctorates, in 1995, they had two daughters, but they were ready to see the world, to train in laboratories outside Norway. And they did spend time in England, with Dr. O’Keefe, and in Scotland, with Richard Morris at the University of Edinburgh.

But the Mosers’ travels were cut short when they were ambushed by a job offer too good to refuse, from the university in Trondheim, where they have been ever since.

“Without knowing it, we actually negotiated,” May-Britt said, “because we were not interested if we only got one job, and we got two jobs. And we were not interested if we did not get the equipment we needed, and they gave us that.” Suddenly, without having really planned it, they had their own lab.

Of course, nothing happens suddenly in research. They began in what Dr. May-Britt Moser described as a bomb shelter, and gradually, over time, built up their program. Similarly, they did not set out looking in the part of the brain where they ended up.

They began recording the activity of cells in the hippocampus, with electrodes implanted in the brains of rats as they roamed an enclosed area. This is still a main method, and the rats are intriguing to watch, pursuing little bits of chocolate cereal on the floor of an enclosure, seemingly oblivious to the implants attached to their skulls.

A Black Box

The Mosers wanted to find how information was flowing to the place cells, whether it was going from one area of the hippocampus to another. But even after they inactivated sections of this brain area, the place cells still functioned. So it seemed that information was flowing in from the nearby brain area, the entorhinal cortex.

They started looking there, and in their early work they were helped by Menno Witter, then in Amsterdam, now at Trondheim, in the delicate task of guiding the electrodes to the right spot.

“We didn’t immediately find the grid cells,” Dr. Edvard Moser said. At first they noticed cells that would emit a signal every time a rat went to a particular spot, and they thought that perhaps this was something like the place cells in the hippocampus that are tied to locations in the outside world. But gradually they learned that what they were seeing was a cell that tracked the rat’s movement in the same way, no matter where the rat was. The cell was not responding to some external mark, it was keeping track of how the rat moved. And when they gave the rats enough room, a very regular pattern emerged.

“The first thing was that we thought there was something wrong with the equipment,” Dr. Edvard Moser said.

“I thought, ‘Is this a bug?’ ” Dr. May-Britt Moser said.

After a 2005 paper in Nature, in which they reported the discovery and named the cells, other labs confirmed the findings and more discoveries followed, in their lab and elsewhere.

It is now clear that the grid cells, in combination with cells that sense head direction and others that sense borders or boundaries — both originally identified in other parts of the brain by other labs — form a kind of dead-reckoning navigation system in the brain that maps movement.

Information flows from this part of the brain to the hippocampus, and then back. Exactly how the grid informs the place cells, and vice versa, is not known.

What scientists have now are two ends of a system with a black box in the middle that is not fully understood. At one end are place cells. At the other are grid cells. As to what exactly happens in between, and how the grid cells form in the first place, Dr. Edvard Moser said, “That’s still a 10-, a 20-year research problem.”

Or, as Dr. O’Keefe put it, “We are still in the pre-Newtonian phase of neuroscience.”

The Mosers remain something of an anomaly. Not only are they off the beaten academic track, but they are a married couple who work together on the same scientific problems at the same institution at the highest levels of science, a true rarity.

They do have different spheres in their new, state-of-the-art lab. May-Britt is more hands-on with the experiments and the design, and Edvard is more involved in mathematical analysis and interpretation of the results.

“We have a common project and a common goal,” he wrote in response to an e-mailed question, “and we both intensely burn for it. And we depend on each other for succeeding.”

He continued, “Most couples manage to cooperate on child raising — for us, our brain project is our third child, so nothing different, really.”

neuromorphogenesis:

Rare, Lethal Childhood Disease Tracked to Specific Protein

For the first time, a defective protein that plays a specific role in degrading intermediate filaments (IF), one of three classes of filaments that form the structure of nerve cells, has been discovered by an international team of researchers. 

Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, the research discusses how the defective protein, gigaxonin, was first identified in children with a rare and untreatable genetic disease known as giant axonal neuropathy (GAN). 

The knowledge of gigaxonin’s specific role explains why a failure in protein degradation would lead to massive aggregations of IF in the neuronal cells of GAN children, said Mahammad, who works in the laboratory of Robert Goldman, PhD,chair of cell and molecular biology. 

Mahammad and other members of the Goldman Laboratory collaborated with Puneet Opal, MD, PhD, associate Professor in the Ken and Ruth Davee Department of Neurology and cell and molecular biology, along with researchers in the laboratory of Pascale Bomont at the INSERM neurological institute in Montpelier, France, and the laboratory of Jean-Pierre Julien at the Université Laval in Quebec, Canada. 

The GAN gene was first identified in 2000 by the Bomont Laboratory, reporting that it encoded for the protein gigaxonin. Based on sequence homology, gigaxonin is involved in the normal turnover of proteins by the well-studied ubiquitin-proteasome system. But it wasn’t clear why a failure in protein degradation would lead to massive aggregations of IF in a patient’s neuronal cells. 

Because it is not possible to study nerve cells experimentally from patients, Mahammad and collaborators instead used fibroblasts from skin biopsies of children with GAN because previous studies have revealed that other classes of IF are also altered in GAN patients. In particular, the IF vimentin expressed in fibroblasts of children with GAN also forms abnormally large aggregates. These cells can readily be obtained from skin biopsies and grown in lab cultures. 

When the researchers introduced the gigaxonin gene into both control and patient fibroblasts, the results were dramatic. In the fibroblasts cultured from GAN patients, the complex network of vimentin filaments and abnormal aggregates disappeared. The vimentin filaments in the control cells also disappeared following the overexpression of the gigaxonin protein. Boosting gigaxonin to higher levels in normal cultured nerve cells also led to a degradation of neuronal forms of IF. However, the cytoskeleton’s two other major systems, microtubules and actin filaments, were not affected by this treatment. 

These findings point to a central role for gigaxonin in regulating the normal turnover of IF proteins. When gigaxonin is defective, neurofilaments, the specific type of IF located in nerve cells, pile up to form aggregates that eventually disrupts the normal functioning of neurons in GAN. 

Gigaxonin is the first factor to be identified that plays a specific role in the degradation of several types of IF proteins, including neurofilaments, according to Mahammad. This discovery may have implications for more common types of neurodegenerative diseases that are also characterized by large accumulations of IF proteins, including Alzheimer’s disease, Parkinson’s disease, dementia with Lewy bodies, Charcot-Marie-Tooth disease, neuronal intermediate filament inclusion disease, and diabetic neuropathy. 

GAN is an extremely rare genetic disorder that strikes both the central and peripheral nervous systems of children. The leading GAN disease foundation, Hannah’s Hope Fund, currently knows of 31 cases worldwide, 19 in the United States alone. But its rarity doesn’t dull its severity in children. Although, there are no symptoms at birth, by age three the first signs of muscle weakness usually appear and progress slowly but steadily. With increasing difficulty in walking and coordinating hand movements, children with GAN are often wheelchair-bound by age 10. Over time, they become dependent on feeding and breathing tubes; only a few will survive into young adulthood. The pathological markers for GAN are swollen (thus “giant”) axons, filled with abnormal aggregates rich in neurofilaments. 

Image: In the fibroblasts derived from the skin biopsies of giant axonal neuropathy (GAN) patients, the vimentin intermediate filaments (green) form large abnormal aggregates (indicated by arrow). In some cases these abnormal aggregates are larger than the nucleus (blue). Presented by postdoctoral fellow Saleemulla Mahammad, PhD, at the American Society for Cell Biology Annual Meeting, new research discusses how the defective protein, gigaxonin, was first identified in children with the rare and untreatable genetic disease known as GAN.

scienceisbeauty:

The connectivity of fiber tracks in alumnus Chris Gaiteri’s brain based on an imaging technique he created - a self-portrait of sorts.

Art in Science on Display at W&L’s Kamen Gallery (Washington and Lee University).

neuromorphogenesis:

Do you obsess over your appearance? Your brain might be wired abnormally

Body dysmorphic disorder is a disabling but often misunderstood psychiatric condition in which people perceive themselves to be disfigured and ugly, even though they look normal to others. New research at UCLA shows that these individuals have abnormalities in the underlying connections in their brains.

Dr. Jamie Feusner, the study’s senior author and a UCLA associate professor of psychiatry, and his colleagues report that individuals with BDD have, in essence, global “bad wiring” in their brains — that is, there are abnormal network-wiring patterns across the brain as a whole.

And in line with earlier UCLA research showing that people with BDD process visual information abnormally, the study discovered abnormal connections between regions of the brain involved in visual and emotional processing.

The findings, published in the May edition of the journal Neuropsychopharmacology, suggest that these patterns in the brain may relate to impaired information processing.

“We found a strong correlation between low efficiency of connections across the whole brain and the severity of BDD,” Feusner said. “The less efficient patients’ brain connections, the worse the symptoms, particularly for compulsive behaviors, such as checking mirrors.”

People suffering from BDD tend to fixate on minute details, such as a single blemish on their face or body, rather than viewing themselves in their entirety. They become so distressed with their appearance that they often can’t lead normal lives, are fearful of leaving their homes and occasionally even commit suicide. Patients frequently have to be hospitalized. BDD affects approximately 2 percent of the population and is more prevalent than schizophrenia or bipolar disorder. Despite its prevalence and severity, scientists know relatively little about the neurobiology of BDD.

In the current study, Feusner and his colleagues performed brain scans of 14 adults diagnosed with BDD and 16 healthy controls. The goal of the study was to map the brain’s connections to examine how the white-matter networks are organized. White matter is made up of nerve cells that carry impulses from one part of the brain to another.

To do this, they used a sensitive form of brain imaging called diffusion tensor imaging, or DTI. DTI is a variant of magnetic resonance imaging that can measure the structural integrity of the brain’s white matter. From these scans, they were able to create whole brain “maps” of reconstructed white-matter tracks. Next, they used a form of advanced analysis called graph theory to characterize the patterns of connections throughout the brains of people with BDD and then compared them with those of healthy controls.

The researchers found people with BDD had a pattern of abnormally high network “clustering” across the entire brain. This suggests that these individuals may have imbalances in how they process “local” or detailed information. The researchers also discovered specific abnormal connections between areas involved in processing visual input and those involved in recognizing emotions.

“How their brain regions are connected in order to communicate about what they see and how they feel is disturbed,” said Feusner, who also directs the Adult Obsessive-Compulsive Disorder Program and the Body Dysmorphic Disorder Research Program at UCLA.

“Their brains seem to be fine-tuned to be very sensitive to process minute details, but this pattern may not allow their brains to be well-synchronized across regions with different functions,” he said. “This could affect how they perceive their physical appearance and may also result in them getting caught up in the details of other thoughts and cognitive processes.”

The study, Feusner noted, advances the understanding of BDD by providing evidence that the “hard wiring” of patients’ brain networks is abnormal.

“These abnormal brain networks could relate to how they perceive, feel and behave,” he said. “This is significant because it could possibly lead to us being able to identify early on if someone is predisposed to developing this problem.”

Image: Side view of the brain showing network connections in healthy controls (left) and BDD (right). The BDD brains have, on average, greater local connections for each region. In the figure, the size of each region (represented by blue spheres) corresponds to the clustering coefficient magnitude, a measure of how strongly interconnected neighboring nodes are to each other. (Courtesy of UCLA)

neuromorphogenesis:

Neural codes for memory implants

The ability to short-circuit debilitating tremors in disease states with implantable stimulators is nothing short of remarkable. The same can be said for cochlear prosthetics which restore hearing, and more recently, retinal implants which give some rudimentary light-sensing capability to the blind. The logical extension of these sensorimotor restorative devices converges upon something a bit more extravagant—a purely cognitive implant—namely, the memory prosthetic. At the present time, there is only one researcher that has consistently demonstrated command of the technologies which would make such a device possible. Ted Berger, and his group from the University of Southern California, have recently extended their initial efforts to develop hippocampal memory devices in mice, to create full frontal cortex implants for primates. Berger published the initial results of these studies last September, in the Journal of Neural Engineering. This June, he will be a featured speaker at the Global Futures 2045 International Congress in New York, which will spot several visionaries in neuroscience and AI. Before he runs away with the show, it important to take a closer look at the exact methods he is using, and also the assumptions about possible neural codes upon which they are built.

Efforts to restore memory loss due to Alzheimer’s disease have led to implantation of pacemaker-like stimulators in the fornix of patients. The fornix is the major output tract of the hippocampus, which is in turn just one among several components that must be counted among mammalian memory systems. In primates, the relative expansion of cortical structures, and hence their importance, has led Berger to develop a device which could work within this structure. The general strategy is to “decode” neuron activity in the superficial layers of the cortex, which presumably make essential functional connections to the deeper layer neurons, and stimulate those deeper neurons in a way that mimics how they would normally respond to superficial layer input in the healthy state.

While that scheme certainly does not capture all the essential behavior of a given region of cortex, it is as good a place to start as any. The deep layer neurons are the ones that project out of the cortex to parts beyond. Their activity therefore represents, at least in theory, a summary of what is going on within that particular region. The approach has been to simultaneously record the activity of both the upper and lower layer neurons to build up a data set of their activity. Mathematical methods are then used to “decode” not only the activity of the upper layers, but also represent the responses of the deeper layer neurons to that activity.

These decoding algorithms come from a field of mathematics known as nonlinear systems analysis. They were originally developed, or at least refined, during the Cold War era to track and target incoming missiles by extracting signals from noisy radar data. For the above mentioned prosthesis for the blind, these methods were simplified so that they could be used in a more practical way to represent the activity of a large group of cells in the retina. Berger’s collaborator at USC, Vasilis Marmarelis, is a pioneer in the application of these kinds of signal processing techniques to biological systems. When it comes to implementing these methods compactly in silicon VLSI chips, USC has also proven to be a place of ample resource for Berger.

Although these signal processing techniques have been called “decoding” algorithms, in actuality, they do not represent any kind of a neural code. They basically treat the system they are modeling as a “black box’ composed only of inputs and outputs. They do not attempt to include any of the underlying physiology of the neurons. The idea of the “neural code” itself is a bit of a misnomer. Berger begins with assumption that the spikes of neurons accurately reflect either sensory input, motor output, or something in between. Depending on the function of the particular cell, spikes assume contextual meaning external to the neurons themselves, and can therefore be cast as the medium of memory.

In reality, spikes also reflect a lot about what is going on inside each neuron—they are the energetic end result of the activity inside the cell. In addition to integrating inputs from each its of neighbors, the output of neurons in the form of spikes bears testimony to the efforts of thousands of mitochondria in the cell competing for every molecule of oxygen and glucose metabolite in their domain. Without that energy, there are no spikes. Neurons do their best to keep things running smoothly, but much of the flexibility and responsiveness comes from this sensitivity to conditions inside and outside the cell. Any attempt to describe a code for a neuron needs to account for the fact that the cell that is doing the coding is a different animal from moment to moment.

Replacing the function of a small patch of cortex is a good start. It may however, be a bit premature to call such a device an actual memory implant. Berger plans to condense all the hardware required to emulate, and stimulate, neurons into a small package that can fit inside the skull, free of any external tethers. He is also looking ahead to work with surgeons who have already implanted hardware in the hippocampus of patients with epilepsy, and apply his techniques there. Thus far, most of the experimental studies have focused on restoring some kind of memory ability to animals that have been challenged with a drug that reduces performance.

For the monkey experiments, cocaine was the agent given to degrade cortical processing. Using cocaine to proxy an effect you hope to restore by localized and layer-specific cortical simulation is obviously not a perfect experiment. Unambiguously measuring the restoration of performance in a specific task for repetitively trained animals is quite a challenge in-and-of itself. Berger and his collaborator, Sam Deadwyler, demonstrated that their device could be used to bring the performance of cocaine intoxicated monkeys in line with normal performance in a delayed matching memory test. Another interpretation of the experiments might just as well be that the device might also make a handy cocaine antidote. Restoring performance is one thing, but augmenting normal performance to a higher level would be a far greater trick.

Journal reference: Journal of Neural Engineering

neuromorphogenesis:

‘Master Gene’ Makes Mouse Brain Look More Human

In the cartoon series named after them, Pinky and the Brain, two laboratory mice genetically enhanced to increase their intelligence plot to take over the world—and fail each time. Perhaps their creators hadn’t tweaked the correct gene. Researchers have now found a genetic mutation that causes mammalian neural tissue to expand and fold. The discovery may help explain why humans evolved more elaborate brains than mice, and it could suggest ways to treat disorders such as autism and epilepsy that arise from abnormal neural development.

In mice and humans alike, the cerebral cortex—the outermost layer of brain tissue associated with high-level functions such as memory and decision-making—starts out as a spherical sheet of tissue made up of only neural stem cells. As these stem cells divide, the cortex increases its surface area, expanding like an inflating balloon, says neuroscientist Victor Borrell of the Institute of Neurosciences of Alicante in Spain. Unlike the small, smooth mouse brain, however, the uppermost layers of tissue in the human brain cram millions of neurons into specialized folds and furrows responsible for complex tasks such as language and thought. Because the human cerebral cortex is generally considered “special,” some scientists have hypothesized that the genes that govern its development of cortical folds and furrows are also unique to humans, Borrell says.

In 2012, scientists got their first hint that a gene called TRNP1 might influence brain development in both mice and humans. The discovery came from a dissertation by Ronny Stahl, who conducted his doctoral research in the lab of co-author Magdalena Götz at Ludwig Maximilian University in Munich, Germany. In studies of neural development in mice, Stahl found that TRNP1 produces a protein that determines whether neural stem cells self-replicate, leading to a balloonlike expansion of cortical surface area, or whether they differentiate into a plethora of intermediate stem cell types and neurons, thickening the cortex and forming more complex brain structures. Based on that discovery, the team hypothesized that varying levels of the gene’s expression in mice and humans might account for the varying levels of cortical thickness and different shapes between the two species.

To test their theory, the researchers investigated what would happen to fetal mouse brains if they interfered withTrnp1 expression using synthetic sequences of genetic material that silenced the gene, a technique called RNA interference. The tiny fetal mouse brains developed cortical folds, the authors report today in Cell. The “most exciting” part of the discovery was that “just by varying how much of this gene is expressed, we are able to have folds in the cortex,” Borrell says. 

The researchers also analyzed samples of human neural tissue from embryos that had been stored by a hospital pathologist. . The team found lower levels of TRNP1 in areas that were destined to form folds, and higher levels in areas that would not have developed them, suggesting that the protein produced by the gene inhibits more complex brain development in humans as well as in mice. Although the developmental stages they analyzed in the human embryos—gestation weeks 8 to 9 and 17 to 18—occur before the folds begin to appear, Borrell says, the varying levels of gene expression provide an “instruction for something to occur.”

The findings go against a common conception that “dumber species will have different genes” for brain development than more intelligent species, Borrell says. He adds that the mechanism could help explain how New World monkeys, with their small, smooth brains, could have evolved from an ancestor with a bigger and more folded brain. “It’s not a linear evolution from small, simple, smooth brains to large, gyrated brains,” he says. The research could also lead to better diagnosis and treatment of diseases such as microcephaly and autism, which arise from a misfolded cortex, he says.

“These are surprising and interesting findings,” says Arnold Kriegstein, a neuroscientist at the University of California, San Francisco. “Clearly this is a model for both human as well as mouse development.” The next step, he says, is to investigate how embryonic mouse brains with induced folds develop as they mature past the fetal stages of development and to look across species to see if the gene has similar effects in other mammals. “It is important to pursue this further,” he says.

neuromorphogenesis:

Is memory just a leaky reconstruction?

We are in the middle of a debate about the status of neuroscience. Against the deceptive allure of neuroimaging and reported sightings of “brain centres” for everything from sarcasm to religious experience, there are stern reassurances that, if we were ever to work out the scientific basis of consciousness, it would be too complicated for us to understand. Is neuroscience really changing the way we comprehend ourselves?

If tracing behaviour and experience to its neural underpinnings really offers a new understanding of humanity, aren’t novelists bound to draw on it in revealing how their characters understand themselves? In one sense, neuro-explanations seem to challenge the mechanisms by which novels work. Neuroscientists warn us that we may have no freewill, no “self” at the helm; their work shows that our memories are leaky reconstructions and that even our visual perception of the world is a system of illusions. How do these messages change what we do, how we feel, how we decide to live? Fiction is a perfect medium for exploring these questions.

A 2009 article by Marco Roth in n+1 magazine pointed out that neuroscience in fiction is often connected with atypical and pathological behaviour. For example, Gary Lambert’s depression in Jonathan Franzen’s The Corrections gives a central role to his screwy neurotransmitters, but we don’t get neuro-explanations for the (debatably) more sane members of the Lambert family. Richard Powers’sThe Echo Maker is more interested in the brain-damaged patient, Mark Schluter, than with the science-inflected self-descriptions of his neuropsychologist, Gerald Weber.

If neuroscientific ideas are really going to prove their worth to novelists, they need to be able to provide satisfactory accounts of ordinary, non‑pathological experience. One novel to attempt that is Ian McEwan’sSaturday, which tells the story of the neurosurgeon Henry Perowne, and his run-ins with the violent, chromosomally-disordered Baxter. Intimate with the workings of the brain, Perowne sees his own experience in terms of the bioelectrical processes that underlie it. Feeling a “sustained, distorting euphoria”, for example, he speculates that “there’s been a chemical accident while he slept – something like a spilled tray of drinks, prompting … a kindly cascade of intracellular events.”

Perowne’s familiarity with neuroscience certainly colours his thoughts about himself, but it’s not clear that it changes his relationships with his own experience and behaviour: it doesn’t make him less trusting of his own memory or visual perception, for example. More importantly, this immersion in neuroscience doesn’t change the story. Setting aside a couple of episodes where Perowne’s medical knowledge is directly exploited, the plot of Saturday would not unfold any differently if he had been ignorant of brain science. Baxter’s wild behaviour ultimately has a genetic rather than a neurological cause. And, when his course of action is violently altered, it is poetry – a recital of Matthew Arnold’s “Dover Beach” – rather than neuroscience that brings it about.

Other novelists are pessimistic about brain science’s capacity to make a difference. In Sebastian Faulks’s A Possible Life, the neuroscientist Elena makes the momentous discovery that the human capacity for self-awareness can be pinned to a particular junction between “Glockner’s Isthmus” (a fictional nexus of selfhood) and “the site of episodic memory”. Yet though feted internationally for her breakthrough, Elena can’t connect her new neuroscientific reality to her own experience – or she won’t let herself. “She knew it to be truthful, valid and endlessly provable, but she didn’t allow the implications to affect the way she lived.”

Faulks’s story seems to be telling us that, even if the scientific message turns out to be simple, being able to reduce quintessentially human mental capacities to neural processes would not add much to our understanding. Perhaps neuroscience will continue to be most useful in accounting for disorder; indeed, perhaps its way of working will be to turn everything into the pathological. Marco Roth’s complaint about the fictional dominance of neuro-dysfunction mirrors a wider trend, evidenced in the recent outcry about the psychiatry manual DSM-V, to see clinical symptoms where once we would have seen ordinary human variation.

Neuro-explanations might simply be too complex for fiction; alternatively, just as genetic explanations seemed less seductive once the human genome was described, so our enthusiasm for the brain might wane as we recognise that much of its work actually translates into the functioning of a disappointingly small number of “core” networks. There is still complexity, but it might be of a more boring kind than that promised by a tally of 86bn neurones.

Fiction exists for its own purposes, and writers and readers will rightly resist attempts to turn it into “evidence” for or against anything. It’s possible that neuroscience is just too new for its ideas to have permeated literary fiction in the way that those other paradigm-changers, Darwinism and psychoanalysis, did. As a novelist, I am interested in exploring characters for whom the networks of the cortex are a real, charged presence. How does this understanding affect what you do when things start happening, when you have to make moral choices? Because of the way it puts subjectivity, character and moral action at its heart, the novel is the ideal crucible for the experiment.

wildcat2030:

Neuroscience: Idle minds

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Neuroscientists are trying to work out why the brain does so much when it seems to be doing nothing at all.

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For volunteers, a brain-scanning experiment can be pretty demanding. Researchers generally ask participants to do something — solve mathematics problems, search a scene for faces or think about their favoured political leaders — while their brains are being imaged.

But over the past few years, some researchers have been adding a bit of down time to their study protocols. While subjects are still lying in the functional magnetic resonance imaging (fMRI) scanners, the researchers ask them to try to empty their minds. The aim is to find out what happens when the brain simply idles. And the answer is: quite a lot.

Some circuits must remain active; they control automatic functions such as breathing and heart rate. But much of the rest of the brain continues to chug away as the mind naturally wanders through grocery lists, rehashes conversations and just generally daydreams. This activity has been dubbed the resting state. And neuroscientists have seen evidence that the networks it engages look a lot like those that are active during tasks.

Resting-state activity is important, if the amount of energy devoted to it is any indication. Blood flow to the brain during rest is typically just 5–10% lower than during task-based experiments1. And studying the brain at rest should help to show how the active brain works. Research on resting-state networks is helping to map the brain’s intrinsic connections by showing, for example, which areas of the brain prefer to talk to which other areas, and how those patterns might differ in disease. (via Neuroscience: Idle minds : Nature News & Comment)

neuromorphogenesis:

How the brain folds to fit

During fetal development of the mammalian brain, the cerebral cortex undergoes a marked expansion in surface area in some species, which is accommodated by folding of the tissue in species with most expanded neuron numbers and surface area. Researchers have now identified a key regulator of this crucial process.

Different regions of the mammalian brain are devoted to the performance of specific tasks. This in turn imposes particular demands on their development and structural organization. In the vertebrate forebrain, for instance, the cerebral cortex – which is responsible for cognitive functions – is remarkably expanded and extensively folded exclusively in mammalian species. The greater the degree of folding and the more furrows present, the larger is the surface area available for reception and processing of neural information. In humans, the exterior of the developing brain remains smooth until about the sixth month of gestation. Only then do superficial folds begin to appear and ultimately dominate the entire brain in humans. Conversely mice, for example, have a much smaller and smooth cerebral cortex.

“The mechanisms that control the expansion and folding of the brain during fetal development have so far been mysterious,” says Professor Magdalena Götz, a professor at the Institute of Physiology at LMU and Director of the Institute for Stem Cell Research at the Helmholtz Center Munich. Götz and her team have now pinpointed a major player involved in the molecular process that drives cortical expansion in the mouse. They were able to show that a novel nuclear protein called Trnp1 triggers the enormous increase in the numbers of nerve cells which forces the cortex to undergo a complex series of folds. Indeed, although the normal mouse brain has a smooth appearance, dynamic regulation of Trnp1 results in activating all necessary processes for the formation of a much enlarged and folded cerebral cortex.

Levels of Trnp1 control expansion and folding
“Trnp1 is critical for the expansion and folding of the cerebral cortex, and its expression level is dynamically controlled during development,” says Götz. In the early embryo, Trnp1 is locally expressed in high concentrations. This promotes the proliferation of self-renewing multipotent neural stem cells and supports tangential expansion of the cerebral cortex. The subsequent fall in levels of Trnp1 is associated with an increase in the numbers of various intermediate progenitors and basal radial glial cells. This results in the ordered formation and migration of a much enlarged number of neurons forming folds in the growing cortex.

The findings are particularly striking because they imply that the same molecule – Trnp1 – controls both the expansion and the folding of the cerebral cortex and is even sufficient to induce folding in a normally smooth cerebral cortex. Trnp1 therefore serves as an ideal starting point from which to dissect the complex network of cellular and molecular interactions that underpin the whole process. Götz and her colleagues are now embarking on the next step in this exciting journey - determination of the molecular function of this novel nuclear protein Trnp1 and how it is regulated. (Cell 2013) göd

psydoctor8:

Adrian Raine on Neurocriminology for the WSJ

The field of neurocriminology—using neuroscience to understand and prevent crime—is revolutionizing our understanding of what drives “bad” behavior.

If early biological and genetic factors beyond the individual’s control make some people more likely to become violent offenders than others, are these individuals fully blameworthy? And if they are not, how should they be punished?

A more profound understanding of the early biological causes of violence can help us take a more empathetic, understanding and merciful approach toward both the victims of violence and the prisoners themselves. It would be a step forward in a process that should express the highest values of our civilization.

Bonus video of Dr. Raine explaining the fMRI images above. Really glad to see his work out there. 

neuromorphogenesis:

The Neuroscience of Calming a Baby

Every parent and caregiver knows from first hand experience that babies calm down when they are picked up, gently rocked, and carried around the room. New research published in the journal Current Biology on April 18, 2013 shows that this is a universal phenomenon. Infants experience an automatic calming reaction when they are being carried, whether they are mouse pups or human babies.

“From humans to mice, mammalian infants become calm and relaxed when they are carried by their mother,” says Kumi Kuroda of the RIKEN Brain Science Institute in Saitama, Japan. Being held in a mother’s arms is the safest place for a baby to be, and the mother can have peace of mind knowing her baby is happy, content, and relaxed. The fact that babies are neurobiologically wired to stop crying when carried is a part of our evolutionary biology that helps our species survive.

This study is the first to show that the infant calming response to carrying is a coordinated set of central, motor, and cardiac regulations that is an evolutionarily preserved aspect of mother-infant interactions, the researchers say. It also helps to have a scientific explanation for the frustration many new parents struggle with… a calm and relaxed infant will often begin crying immediately when he or she is put down. When my daughter was young, swaddling her seemed to create a compact posture and sense of security that triggered an automatic relaxation response when she was put back down and helped break this cycle.

What triggers this calming response?

Kuroda and colleagues at RIKEN determined that the calming response is mediated by the parasympathetic nervous system and a region of the brain called the cerebellum (Latin: little brain). The researchers found that the calming response was dependent on tactile inputs and proprioception. Proprioception is the ability to sense and understand body movements and keep track of your body’s position in space. They also found that the parasympathetic nervous system helped lower heart rate as part of mediating the coordinated response to being carried.

Both human and mouse babies calm down and stop moving immediately after they are carried, and mouse pups stop emitting ultrasonic cries. Mouse pups also adopt the characteristic compact posture, with limbs flexed, seen in other mammals such as cats and lions.

The idea that the familiar calming dynamic was also playing out in mice occurred to Kuroda one day when she was cleaning the cages of her mouse colony in the laboratory. She says, “When I picked the pups up at the back skin very softly and swiftly as mouse mothers did, they immediately stopped moving and became compact. They appeared relaxed, but not totally floppy, and kept the limbs flexed. This calming response in mice appeared similar to me to soothing by maternal carrying in human babies.”

The Role of the Cerebellum in Calmness

The cerebellum is always on guard to protect your body from danger and prepare you for ‘fight-or-flight’ by keeping track of everything going on in your environment. 

Among many other jobs, the cerebellum has a huge responsibility to maintain your safety and physical well being. This takes a lot of brain power and energy. Although the cerebellum is only 10% of brain volume it holds over 50% of your brain’s neurons. Neuroscientists are perplexed by everything that the cerebellum does. This study offers one more valuable clue. 

Scientists have known for years that the cerebellum is directly linked to a feedback loop with the vagus nerve which keeps heart rate slow and gives you grace under pressure. As adults, we can calm ourselves by practicing mindfulness and Loving-Kindness Meditation which puts the cerebellum at peace and creates a parasympathetic response of well being. This appears to be the same response that occurs in infants when they are being carried. 

Interestingly, the only time during the day that the cerebellum is allowed to let down it’s guard and go offline is during REM sleep when your body is paralyzed to prevent you from acting out your dreams. It makes sense that being picked up and carried would send automatic signals that allow the cerebellum to relax and create healthy vagal tone which would lower heart rates in infants.

Conclusion

The researchers believe that these findings could have broad implications for parenting and contribute to preventing child abuse. “This infant response reduces the maternal burden of carrying and is beneficial for both the mother and the infant,” explains Kuroda. She goes on to say, “Such proper understanding of infants would reduce frustration of parents and be beneficial, because unsoothable crying is a major risk factor for child abuse.”

“A scientific understanding of this infant response will save parents from misreading the restart of crying as the intention of the infant to control the parents, as some parenting theories—such as the ‘cry it out’ type of strategy—suggest,” Kuroda says. “Rather, this phenomenon should be interpreted as a natural consequence of the infant sensorimotor systems.” If parents understand that properly, perhaps they will be less frustrated by the crying, Kuroda says. And that puts those children at lower risk of abuse.

The authors conclude that, “Although our study was done on mothers, we believe that this is not specific to moms and can be used by any primary caregiver.”