We now know that 24 hours without sleep, or a week of sleeping four or five hours a night induces an impairment equivalent to a blood alcohol level of .1 percent. We would never say, ‘This person is a great worker! He’s drunk all the time!’ yet we continue to celebrate people who sacrifice sleep for work.

Brain Mapping
A new map, a decade in the works, shows structures of the brain in far greater detail than ever before, providing neuroscientists with a guide to its immense complexity.
Neuroscientists have made remarkable progress in recent years toward understanding how the brain works. And in coming years, Europe’s Human Brain Project will attempt to create a computational simulation of the human brain, while the U.S. BRAIN Initiative will try to create a wide-ranging picture of brain activity. These ambitious projects will greatly benefit from a new resource: detailed and comprehensive maps of the brain’s structure and its different regions.
As part of the Human Brain Project, an international team of researchers led by German and Canadian scientists has produced a three-dimensional atlas of the brain that has 50 times the resolution of previous such maps. The atlas, which took a decade to complete, required slicing a brain into thousands of thin sections and digitally stitching them back together with the help of supercomputers. Able to show details as small as 20 micrometers, roughly the size of many human cells, it is a major step forward in understanding the brain’s three-dimensional anatomy.
To guide the brain’s digital reconstruction, researchers led by Katrin Amunts at the Jülich Research Centre in Germany initially used an MRI machine to image the postmortem brain of a 65-year-old woman. The brain was then cut into ultrathin slices. The scientists stained the sections and then imaged them one by one on a flatbed scanner. Alan Evans and his coworkers at the Montreal Neurological Institute organized the 7,404 resulting images into a data set about a terabyte in size. Slicing had bent, ripped, and torn the tissue, so Evans had to correct these defects in the images. He also aligned each one to its original position in the brain. The result is mesmerizing: a brain model that you can swim through, zooming in or out to see the arrangement of cells and tissues.
At the start of the 20th century, a German neuroanatomist named Korbinian Brodmann parceled the human cortex into nearly 50 different areas by looking at the structure and organization of sections of brain under a microscope. “That has been pretty much the reference framework that we’ve used for 100 years,” Evans says. Now he and his coworkers are redoing ­Brodmann’s work as they map the borders between brain regions. The result may show something more like 100 to 200 distinct areas, providing scientists with a far more accurate road map for studying the brain’s different functions.
“We would like to have in the future a reference brain that shows true cellular resolution,” says Amunts—about one or two micrometers, as opposed to 20. That’s a daunting goal, for several reasons. One is computational: Evans says such a map of the brain might contain several petabytes of data, which computers today can’t easily navigate in real time, though he’s optimistic that they will be able to in the future. Another problem is physical: a brain can be sliced only so thin.
Advances could come from new techniques that allow scientists to see the arrangement of cells and nerve fibers inside intact brain tissue at very high resolution. Amunts is developing one such technique, which uses polarized light to reconstruct three-­dimensional structures of nerve fibers in brain tissue. And a technique called Clarity, developed in the lab of Karl Deisseroth, a neuroscientist and bioengineer at Stanford University, allows scientists to directly see the structures of neurons and circuitry in an intact brain. The brain, like any other tissue, is usually opaque because the fats in its cells block light. Clarity melts the lipids away, replacing them with a gel-like substance that leaves other structures intact and visible. Though Clarity can be used on a whole mouse brain, the human brain is too big to be studied fully intact with the existing version of the technology. But Deisseroth says the technique can already be used on blocks of human brain tissue thousands of times larger than a thin brain section, making 3-D reconstruction easier and less error prone. And Evans says that while Clarity and polarized-light imaging currently give fantastic resolution to pieces of brain, “in the future we hope that this can be expanded to include a whole human brain.”

Brain Mapping

A new map, a decade in the works, shows structures of the brain in far greater detail than ever before, providing neuroscientists with a guide to its immense complexity.

Neuroscientists have made remarkable progress in recent years toward understanding how the brain works. And in coming years, Europe’s Human Brain Project will attempt to create a computational simulation of the human brain, while the U.S. BRAIN Initiative will try to create a wide-ranging picture of brain activity. These ambitious projects will greatly benefit from a new resource: detailed and comprehensive maps of the brain’s structure and its different regions.

As part of the Human Brain Project, an international team of researchers led by German and Canadian scientists has produced a three-dimensional atlas of the brain that has 50 times the resolution of previous such maps. The atlas, which took a decade to complete, required slicing a brain into thousands of thin sections and digitally stitching them back together with the help of supercomputers. Able to show details as small as 20 micrometers, roughly the size of many human cells, it is a major step forward in understanding the brain’s three-dimensional anatomy.

To guide the brain’s digital reconstruction, researchers led by Katrin Amunts at the Jülich Research Centre in Germany initially used an MRI machine to image the postmortem brain of a 65-year-old woman. The brain was then cut into ultrathin slices. The scientists stained the sections and then imaged them one by one on a flatbed scanner. Alan Evans and his coworkers at the Montreal Neurological Institute organized the 7,404 resulting images into a data set about a terabyte in size. Slicing had bent, ripped, and torn the tissue, so Evans had to correct these defects in the images. He also aligned each one to its original position in the brain. The result is mesmerizing: a brain model that you can swim through, zooming in or out to see the arrangement of cells and tissues.

At the start of the 20th century, a German neuroanatomist named Korbinian Brodmann parceled the human cortex into nearly 50 different areas by looking at the structure and organization of sections of brain under a microscope. “That has been pretty much the reference framework that we’ve used for 100 years,” Evans says. Now he and his coworkers are redoing ­Brodmann’s work as they map the borders between brain regions. The result may show something more like 100 to 200 distinct areas, providing scientists with a far more accurate road map for studying the brain’s different functions.

“We would like to have in the future a reference brain that shows true cellular resolution,” says Amunts—about one or two micrometers, as opposed to 20. That’s a daunting goal, for several reasons. One is computational: Evans says such a map of the brain might contain several petabytes of data, which computers today can’t easily navigate in real time, though he’s optimistic that they will be able to in the future. Another problem is physical: a brain can be sliced only so thin.

Advances could come from new techniques that allow scientists to see the arrangement of cells and nerve fibers inside intact brain tissue at very high resolution. Amunts is developing one such technique, which uses polarized light to reconstruct three-­dimensional structures of nerve fibers in brain tissue. And a technique called Clarity, developed in the lab of Karl Deisseroth, a neuroscientist and bioengineer at Stanford University, allows scientists to directly see the structures of neurons and circuitry in an intact brain. The brain, like any other tissue, is usually opaque because the fats in its cells block light. Clarity melts the lipids away, replacing them with a gel-like substance that leaves other structures intact and visible. Though Clarity can be used on a whole mouse brain, the human brain is too big to be studied fully intact with the existing version of the technology. But Deisseroth says the technique can already be used on blocks of human brain tissue thousands of times larger than a thin brain section, making 3-D reconstruction easier and less error prone. And Evans says that while Clarity and polarized-light imaging currently give fantastic resolution to pieces of brain, “in the future we hope that this can be expanded to include a whole human brain.”

The attention given to the side of the head which has received the injury, in connection with a specific reference to the side of the body nervously affected, is in itself evidence that in this case the ancient surgeon was already beginning observations on the localization of functions in the brain.

 James Henry Breasted (via neuromorphogenesis)
To quash depression, some brain cells must push through the stress
The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat.

But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples’ immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with — and ultimately triumphing over — stress.

A group of neuroscientists at Mount Sinai’s Icahn School of Medicine in New York focused on the dopaminergic cells in the brain’s ventral tegmentum, a key node in the brain’s reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive.

It would logically follow, then, that if you don’t want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right?

Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain’s reward system.

The researchers wondered whether inducing similar hyperactivity in mice prone to depression — effectively pushing these cells to signal even faster and harder — might help bolster them against succumbing to passivity and defeat when under stress? Using antidepressant medication, viruses and lights that turn circuits on and off, they found that it could. By activating the chemical processes that induced the same level of hyperactivity seen in the ventral tegmenta of resilient mice, they made depression-prone mice more hardy and happy in the face of stress.

The results suggest something profound about the brain and depression: that in the healthy and psychologically resilient, stress induces its own chemical countermeasures, fostering a sort of psychological equilibrium. Someday medications might employ strategies that help promote such equilibrium to head off depression before it starts, as well as to treat it once it has set in.

To quash depression, some brain cells must push through the stress

The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat.

But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples’ immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with — and ultimately triumphing over — stress.

A group of neuroscientists at Mount Sinai’s Icahn School of Medicine in New York focused on the dopaminergic cells in the brain’s ventral tegmentum, a key node in the brain’s reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive.

It would logically follow, then, that if you don’t want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right?

Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain’s reward system.

The researchers wondered whether inducing similar hyperactivity in mice prone to depression — effectively pushing these cells to signal even faster and harder — might help bolster them against succumbing to passivity and defeat when under stress? Using antidepressant medication, viruses and lights that turn circuits on and off, they found that it could. By activating the chemical processes that induced the same level of hyperactivity seen in the ventral tegmenta of resilient mice, they made depression-prone mice more hardy and happy in the face of stress.

The results suggest something profound about the brain and depression: that in the healthy and psychologically resilient, stress induces its own chemical countermeasures, fostering a sort of psychological equilibrium. Someday medications might employ strategies that help promote such equilibrium to head off depression before it starts, as well as to treat it once it has set in.

(Source: Los Angeles Times)

Memory Accuracy and Strength Can Be Manipulated During Sleep

The sense of smell might seem intuitive, almost something you take for granted. But researchers from NYU Langone Medical Center have found that memory of specific odors depends on the ability of the brain to learn, process and recall accurately and effectively during slow-wave sleep — a deep sleep characterized by slow brain waves.

The sense of smell is one of the first things to fail in neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, and schizophrenia. Indeed, down the road, if more can be learned from better understanding of how the brain processes odors, researchers believe it could lead to novel therapies that target specific neurons in the brain, perhaps enhancing memory consolidation and memory accuracy.

Reporting in the Journal of Neuroscience online April 9, researchers in the lab of Donald A. Wilson, PhD, a professor in the departments of Child and Adolescent Psychiatry and Neuroscience and Physiology at NYU Langone, and a research scientist at the NYU-affiliated Nathan Kline Institute for Psychiatric Research, showed in experiments with rats that odor memory was strengthened when odors sensed the previous day were replayed during sleep. Memories deepened more when odor reinforcement occurred during sleep than when rats were awake.

When the memory of a specific odor learned when the rats were awake was replayed during slow-wave sleep, they achieved a stronger memory for that odor the next day, compared to rats that received no replay, or only received replay when they were awake.

However, when the research team exposed the rats to replay during sleep of an odor pattern that they had not previously learned, the rats had false memories to many different odors. When the research team pharmacologically prevented neurons from communicating to each other during slow-wave sleep, the accuracy of memory of the odor was also impaired.

The rats were initially trained to recognize odors through conditioning. Using electrodes in the olfactory bulb, a part of the brain responsible for perceiving smells, the researchers stimulated different smell perceptions, according to precise patterns of electrical stimulation. Then, by replaying the patterns electrically, they were able to test the effects of slow-wave sleep manipulation.

Replay of learned electrical odors during slow-wave sleep enhanced the memory for those odors. When the learned smells were replayed while the rats were awake, the strength of the memory decreased. Finally, when a false pattern that the rat never learned was incorporated, the rats could not discriminate the smell accurately from the learned odor.

“Our findings confirm the importance of brain activity during sleep for both memory strength and accuracy,” says Dr. Wilson, the study’s senior author. “What we think is happening is that during slow-wave sleep, neurons in the brain communicate with each other, and in doing so, strengthen their connections, permitting storage of specific information.”

Is Parkinson’s an Autoimmune Disease?
This is a new, and likely controversial, idea in Parkinson’s disease; but if true, it could lead to new ways to prevent neuronal death in Parkinson’s that resemble treatments for autoimmune diseases,” said the study’s senior author, David Sulzer, PhD, professor of neurobiology in the departments of psychiatry, neurology, and pharmacology at Columbia University College of Physicians & Surgeons.
The new hypothesis about Parkinson’s emerges from other findings in the study that overturn a deep-seated assumption about neurons and the immune system.
For decades, neurobiologists have thought that neurons are protected from attacks from the immune system, in part, because they do not display antigens on their cell surfaces. Most cells, if infected by virus or bacteria, will display bits of the microbe (antigens) on their outer surface. When the immune system recognizes the foreign antigens, T cells attack and kill the cells. Because scientists thought that neurons did not display antigens, they also thought that the neurons were exempt from T-cell attacks.
“That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system,” Dr. Sulzer says. “But, unexpectedly, we found that some types of neurons can display antigens.”
Cells display antigens with special proteins called MHCs. Using postmortem brain tissue donated to the Columbia Brain Bank by healthy donors, Dr. Sulzer and his postdoc Carolina Cebrián, PhD, first noticed—to their surprise—that MHC-1 proteins were present in two types of neurons. These two types of neurons—one of which is dopamine neurons in a brain region called the substantia nigra—degenerate during Parkinson’s disease.
To see if living neurons use MHC-1 to display antigens (and not for some other purpose), Drs. Sulzer and Cebrián conducted in vitro experiments with mouse neurons and human neurons created from embryonic stem cells. The studies showed that under certain circumstances—including conditions known to occur in Parkinson’s—the neurons use MHC-1 to display antigens. Among the different types of neurons tested, the two types affected in Parkinson’s were far more responsive than other neurons to signals that triggered antigen display.
The researchers then confirmed that T cells recognized and attacked neurons displaying specific antigens.
The results raise the possibility that Parkinson’s is partly an autoimmune disease, Dr. Sulzer says, but more research is needed to confirm the idea.
“Right now, we’ve showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons,” Dr. Sulzer says, “but we still need to determine whether this is actually happening in people. We need to show that there are certain T cells in Parkinson’s patients that can attack their neurons.”
If the immune system does kill neurons in Parkinson’s disease, Dr. Sulzer cautions that it is not the only thing going awry in the disease. “This idea may explain the final step,” he says. “We don’t know if preventing the death of neurons at this point will leave people with sick cells and no change in their symptoms, or not.”

Is Parkinson’s an Autoimmune Disease?

This is a new, and likely controversial, idea in Parkinson’s disease; but if true, it could lead to new ways to prevent neuronal death in Parkinson’s that resemble treatments for autoimmune diseases,” said the study’s senior author, David Sulzer, PhD, professor of neurobiology in the departments of psychiatry, neurology, and pharmacology at Columbia University College of Physicians & Surgeons.

The new hypothesis about Parkinson’s emerges from other findings in the study that overturn a deep-seated assumption about neurons and the immune system.

For decades, neurobiologists have thought that neurons are protected from attacks from the immune system, in part, because they do not display antigens on their cell surfaces. Most cells, if infected by virus or bacteria, will display bits of the microbe (antigens) on their outer surface. When the immune system recognizes the foreign antigens, T cells attack and kill the cells. Because scientists thought that neurons did not display antigens, they also thought that the neurons were exempt from T-cell attacks.

“That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system,” Dr. Sulzer says. “But, unexpectedly, we found that some types of neurons can display antigens.”

Cells display antigens with special proteins called MHCs. Using postmortem brain tissue donated to the Columbia Brain Bank by healthy donors, Dr. Sulzer and his postdoc Carolina Cebrián, PhD, first noticed—to their surprise—that MHC-1 proteins were present in two types of neurons. These two types of neurons—one of which is dopamine neurons in a brain region called the substantia nigra—degenerate during Parkinson’s disease.

To see if living neurons use MHC-1 to display antigens (and not for some other purpose), Drs. Sulzer and Cebrián conducted in vitro experiments with mouse neurons and human neurons created from embryonic stem cells. The studies showed that under certain circumstances—including conditions known to occur in Parkinson’s—the neurons use MHC-1 to display antigens. Among the different types of neurons tested, the two types affected in Parkinson’s were far more responsive than other neurons to signals that triggered antigen display.

The researchers then confirmed that T cells recognized and attacked neurons displaying specific antigens.

The results raise the possibility that Parkinson’s is partly an autoimmune disease, Dr. Sulzer says, but more research is needed to confirm the idea.

“Right now, we’ve showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons,” Dr. Sulzer says, “but we still need to determine whether this is actually happening in people. We need to show that there are certain T cells in Parkinson’s patients that can attack their neurons.”

If the immune system does kill neurons in Parkinson’s disease, Dr. Sulzer cautions that it is not the only thing going awry in the disease. “This idea may explain the final step,” he says. “We don’t know if preventing the death of neurons at this point will leave people with sick cells and no change in their symptoms, or not.”

neuromorphogenesis:

Language and Your Brain

For centuries, researchers have studied the brain to find exactly where mechanisms for producing and interpreting language reside. Theories abound on how humans acquire new languages and how our developing brains learn to process languages.

By Voxy.

Drug Abuse and Your Body

Drugs impact every organ in the body. In this easy to read graphic, we demonstrate the impact of the most commonly abused drugs on the body’s organs and its systems.

Many people who use drugs, even if they are prescribed, are unaware of how a drug impacts the normal functioning of the body. Whether it is tranquilizers, steroids, or marijuana you can see the organs affected and read about the drug induced changes that occur within each of the body’s systems.

By Recovery Connections.

(Source: neuromorphogenesis)

The attention given to the side of the head which has received the injury, in connection with a specific reference to the side of the body nervously affected, is in itself evidence that in this case the ancient surgeon was already beginning observations on the localization of functions in the brain.

 James Henry Breasted

(Source: neuromorphogenesis)

Neurons in the Brain Tune into Different Frequencies for Different Spatial Memory Tasks

Your brain transmits information about your current location and memories of past locations over the same neural pathways using different frequencies of a rhythmic electrical activity called gamma waves, report neuroscientists at The University of Texas at Austin.

The research, published in the journal Neuron on April 17, may provide insight into the cognitive and memory disruptions seen in diseases such as schizophrenia and Alzheimer’s, in which gamma waves are disturbed.

Previous research has shown that the same brain region is activated whether we’re storing memories of a new place or recalling past places we’ve been.

“Many of us leave our cars in a parking garage on a daily basis. Every morning, we create a memory of where we parked our car, which we retrieve in the evening when we pick it up,” said Laura Colgin, assistant professor of neuroscience and member of the Center for Learning and Memory in The University of Texas at Austin’s College of Natural Sciences. “How then do our brains distinguish between current location and the memory of a location? Our new findings suggest a mechanism for distinguishing these different representations.”

Memory involving location is stored in an area of the brain called the hippocampus. The neurons in the hippocampus that store spatial memories (such as the location where you parked your car) are called place cells. The same set of place cells are activated both when a new memory of a location is stored and, later, when the memory of that location is recalled or retrieved.

When the hippocampus forms a new spatial memory, it receives sensory information about your current location from a brain region called the entorhinal cortex. When the hippocampus recalls a past location, it retrieves the stored spatial memory from a subregion of the hippocampus called CA3.

The entorhinal cortex and CA3 transmit these different types of information using different frequencies of gamma waves. The entorhinal cortex uses fast gamma waves, which have a frequency of about 80 Hz (about the same frequency as a bass E note played on a piano). In contrast, CA3 sends its signals on slow gamma waves, which have a frequency of about 40 Hz.

Colgin and her colleagues hypothesized that fast gamma waves promote encoding of recent experiences, while slow gamma waves support memory retrieval.

They tested these hypotheses by recording gamma waves in the hippocampus, together with electrical signals from place cells, in rats navigating through a simple environment. They found that place cells represented the rat’s current location when cells were active on fast gamma waves. When cells were active on slow gamma waves, place cells represented locations in the direction that the rat was heading.

“These findings suggest that fast gamma waves promote current memory encoding, such as the memory of where we just parked,” said Colgin. “However, when we need to remember where we are going, like when finding our parked car later in the day, the hippocampus tunes into slow gamma waves.”

Because gamma waves are seen in many areas of the brain besides the hippocampus, Colgin’s findings may generalize beyond spatial memory. The ability for neurons to tune into different frequencies of gamma waves provides a way for the brain to traffic different types of information across the same neuronal circuits.

Colgin said one of the next steps in her team’s research will be to apply technologies that induce different types of gamma waves in rats performing memory tasks. She imagines that they will be able to improve new memory encoding by inducing fast gamma waves. Conversely, she expects that inducing slow gamma waves will be detrimental to the encoding of new memories. Those slow gamma waves should trigger old memories, which would interfere with new learning.

Canadian student has “out of body experiences” whenever she wants
After attending a lecture on “out of body experiences,” a 24-year-old student from the University of Ottawa approached her professor saying, “I thought everybody could do that.” She can apparently do this at will — making her the first person with this condition to be studied.
The resulting paper, which now appears in Frontiers in Human Neuroscience, describes the condition as something of an illusion, where a person’s ability to track their body’s position in space and time has somehow become externalized. In this extraordinary case, the university student claims she can do this whenever she wants — to induce the feeling that she can experience her body moving outside the boundaries of her physical body, while remaining aware of her unmoving physical body.
So, if you’re a neuroscientist studying this particular person, what do you do? You put her in a brain scanner, of course. Writing in ABC News, Gillian Mohney explains more:

[Claude] Messier and his co-author interviewed the student and had her undergo an MRI to see if her brain activity might shed light on her unusual ability.
Messier said the girl first noticed her ability when she was a child and had a hard time going to sleep during naps. To pass the time she would “float” above her body.
"I feel myself moving, or, more accurately, can make myself feel as if I am moving. I know perfectly well that I am not actually moving," the student told the researchers. "In fact, I am hyper-sensitive to my body at that point, because I am concentrating so hard on the sensation of moving…For example, if I ‘spin’ for long enough, I get dizzy."
Messier said at some point the student’s brain showed similar activity to that of a high-level athlete who can vividly imagine themselves winning a competition. One difference, however, was that her brain activity was focused on one side, and the athletes usually show activity on both brain hemispheres.
Messier said more study was needed, but he said that this discovery could mean many more people have this ability but find it “unremarkable.” The discovery could be similar to how synesthesia, a mix of multiple senses, was discovered in a wider population.
Alternately, the ability could be something that everyone is able to do as an infant or child, but lose as they get older.

Wild stuff. Typically, this condition happens as the result of an injury, psychological illness, lesions on the brain, or from a drug that induces the illusion. The researchers speculate that this ability might be present in infancy but that it’s lost without regular practice. They also hypothesize that it’s more prevalent in young people… and that it’s a skill that might be developed.

Canadian student has “out of body experiences” whenever she wants

After attending a lecture on “out of body experiences,” a 24-year-old student from the University of Ottawa approached her professor saying, “I thought everybody could do that.” She can apparently do this at will — making her the first person with this condition to be studied.

The resulting paper, which now appears in Frontiers in Human Neuroscience, describes the condition as something of an illusion, where a person’s ability to track their body’s position in space and time has somehow become externalized. In this extraordinary case, the university student claims she can do this whenever she wants — to induce the feeling that she can experience her body moving outside the boundaries of her physical body, while remaining aware of her unmoving physical body.

So, if you’re a neuroscientist studying this particular person, what do you do? You put her in a brain scanner, of course. Writing in ABC News, Gillian Mohney explains more:

[Claude] Messier and his co-author interviewed the student and had her undergo an MRI to see if her brain activity might shed light on her unusual ability.

Messier said the girl first noticed her ability when she was a child and had a hard time going to sleep during naps. To pass the time she would “float” above her body.

"I feel myself moving, or, more accurately, can make myself feel as if I am moving. I know perfectly well that I am not actually moving," the student told the researchers. "In fact, I am hyper-sensitive to my body at that point, because I am concentrating so hard on the sensation of moving…For example, if I ‘spin’ for long enough, I get dizzy."

Messier said at some point the student’s brain showed similar activity to that of a high-level athlete who can vividly imagine themselves winning a competition. One difference, however, was that her brain activity was focused on one side, and the athletes usually show activity on both brain hemispheres.

Messier said more study was needed, but he said that this discovery could mean many more people have this ability but find it “unremarkable.” The discovery could be similar to how synesthesia, a mix of multiple senses, was discovered in a wider population.

Alternately, the ability could be something that everyone is able to do as an infant or child, but lose as they get older.

Wild stuff. Typically, this condition happens as the result of an injury, psychological illness, lesions on the brain, or from a drug that induces the illusion. The researchers speculate that this ability might be present in infancy but that it’s lost without regular practice. They also hypothesize that it’s more prevalent in young people… and that it’s a skill that might be developed.

Know the brain, and its axons, by the clothes they wear

It is widely know that the grey matter of the brain is grey because it is dense with cell bodies and capillaries. The white matter is almost entirely composed of lipid-based myelin, but there is also a little room in the grey matter for a few select axons to be at least partially myelinated. A group of well known researchers, mostly from Harvard and MIT, decided to look for possible patterns in the myelin found in cortical grey matter. Their Science published findings suggest that this dynamic balance struck up by each axon, somewhere between zero and full myelination, does not tip to the benefit of action potential speed alone. Instead, it follows a more subtle give and take between different kinds cells.

In looking down the length of an axon, longitudinally that is, each segment of myelin is separated by a node. The thickness of the myelin coat varies significantly from node to node. Presumably then, so does the speed and reliability of the spike propagated in that segment. The researchers suggest however, that it is more the phase and offset of these nodes that matters. The distance to first node in particular is important because it is here that the spike shape is first initiaillized. As Doug Fields points out in a perspective that accompanies the paper, spike shape (usually inconsequential in computational models) has important functional implications including the amount of transmitter released, the refractory period and the spike frequency.

Within the cortical grey, it is now known that the bare initial segment of the axon isirresistible to other cells. Their synaptic overtures are regularly accepted and also reciprocated by the axon’s own transmitter release from bare, noncanonical release sites. The researchers found that the length of the myelin-free axon initial segment had a graded distribution with the more superficially located pyramidal cells in the mouse cortex having longer “open” axon. In layer II/III bare stretches up to o 55 µm were evident.

The technology that makes it possible to reconstruct serial sections of brain is perhaps the most advanced—and certainly the most industrialized—in neuroscience. It is precisely the same technique used in the recent Brainbow II studies, which incidentally have also yielded some the most celebrated images in science. But I must say, reader, if you are not blown away by the above mentioned details on myelination, you are not alone. That you are still here indicates that you expect something more.

So forgive me, rightfully esteemed authors, if I suggest you have an opportunity here perhaps not yet missed, but rapidly growing stale. Ken, Sebastian, Jeff—Doug, where is the missing myelin mechanics? In the name of all that is Holy, myelination requires a breaking of symmetry, namely it has to wrap in one direction. We have asked previously, in detail, how this constraint is applied in whole brain and nerve, going down an axon, going to immediately adjacent axons, and also to the multiple arms of any one oligodendrocyte.

As myelin undergoes phase transitions in development, does its 3D tubular mesh align like slow motion lipid spin glasses? Is direction imposed individually at each turn, or in bulk transition, perhaps reflective of temperature dependent crystal or magnetic domain formation? More speculatively, can firing axons, simultaneously pulsing mechanically in the radial direction, rectify their continuous cellular substructure into miniscule torques which aid and abet myelination? How does bulk myelination vary across the bilaterally symetric halves of the brain, across the callosum, and down the altogether unique myelin of the nerves units of the body? Now that we clearly have the technology, lets answer these questions and begin to piece this brain together ground up.

The power of the screw and the drill, known to any machinist, is not lost here. The authors own recent incredible work attests to that. They reference their previous discovery of helical substructure in stacked endoplasmic reticulum sheets connected through unique membrane motiffs. Might neurons themselves be chiral, or at least their axons or apical dendrite have a preferred hand? If it is now possible to image effervescent cell organelles, centriolar-defined coordinate systems, the windings of microtubule arrays even down to the tiny symmetry-breaking protein hooks which preferentially adorn them in axons vs dendrtites, certainly we can now construct geometry on larger scales of the brain.

Even Recreational Marijuana May Be Linked To Brain Changes

Adding to earlier evidence that marijuana may be linked to lasting neurological changes, a new study in the Journal of Neuroscience today finds that even casual pot smoking may have an effect on the size and structure of certain brain regions. The new research reports that for each additional joint a person smokes per week, the greater the odds of structural changes to areas involved in motivation, reward, and emotion. Though it seems like the country has embraced pot as a relatively harmless option in recent years, the authors of the study say that their findings suggest otherwise, especially for young people whose brains are still developing.

“This study raises a strong challenge to the idea that casual marijuana use isn’t associated with bad consequences,” said study author Hans Breiter, psychiatry and behavioral sciences professor at Northwestern University Feinberg School of Medicine and psychiatrist at Northwestern Memorial Hospital. “Some of these people only used marijuana to get high once or twice a week. People think a little recreational use shouldn’t cause a problem, if someone is doing OK with work or school. Our data directly says this is not the case.”

In the new study, the team looked at the brains of people 18-25 years old, some of whom smoked pot recreationally and some who did not. None of the participants showed any signs of being addicted to the drug.

Using different brain imaging techniques, the researchers were able to measure the volume, shape, and grey matter density of two key structures: the nucleus accumbens and the amygdala. The nucleus accumbens is involved in the reward circuit, including pleasure-seeking and motivation, and it’s strongly linked to addiction. The amygdala is involved in emotion, particularly in fear, anxiety, and the stress response, and in drug craving.

The team found that both brain structures varied in multiple ways, according to the number of joints per week the participants smoked – in other words, the more joints smoked, the more brain changes were evident. The nucleus accumbens was especially likely to show alterations in shape and density, and to be larger, as a function of joints per week.

“These are core, fundamental structures of the brain,” said study author Anne Blood, director of the Mood and Motor Control Laboratory at Massachusetts General Hospital and psychiatry professor at Harvard Medical School. “They form the basis for how you assess positive and negative features about things in the environment and make decisions about them.”

What’s interesting about the study is that it suggests that even sometimes-smokers show changes in the brain. What’s not clear is whether there were differences in the pot smokers’ behavior or cognitive function. But the authors suggest that the brain changes seen here may be a sort of precursor to addiction: Earlier studies in animals have shown that the active ingredient in pot, tetrahydrocannabinol (THC), may affect neural connectivity, which could be an early sign of a bourgeoning addiction.

“It may be that we’re seeing a type of drug learning in the brain,” said author Jodi Gilman, at Massachusetts General Center for Addiction Medicine. “We think when people are in the process of becoming addicted, their brains form these new connections.”

Although a majority of people in the country support legalization of marijuana, not everyone is so convinced. Last year, Breiter’s team showed that everyday pot smoking in teenagers was, even two years after stopping, linked to brain abnormalities and to poorer working memory. “With the findings of these two papers,” Breiter said, “I’ve developed a severe worry about whether we should be allowing anybody under age 30 to use pot unless they have a terminal illness and need it for pain.”

Capgras and Fregoli Delusions

When people hear the words “psychiatric disorder,” they often think of depression, bipolar disorder, or schizophrenia. However, there are other psychiatric disorders that are not well-known, but are fascinating nonetheless. 

Have you ever thought that a close friend or family member, perhaps even your significant other, had been replaced by an imposter, a pretender? On the other end of the spectrum, perhaps you’ve thought that everybody around you was actually the same person assuming different disguises and playing different roles. If so, you may have an obscure psychological disorder.

Capgras Delusion

People suffering from this disorder believe that some of the people around them are imposters. They believe that familiar people and even pets have been replaced by imposters. They recognize the face of their family members or beloved pets, but they believe the real person has been replaced by an imposter. It is unknown exactly what causes Capgras Delusion, but it has been seen in people who suffer from other psychiatric disorders or have experienced a head trauma. It has been suggested that sufferers of Capgras Delusion have lost the connection between the area of the brain that recognize faces and the area that supplies an emotional response to the faces seen. Though the person recognizes the face as that of their wife, sister, or dog, they no longer have the emotional response usually connected to that face. Because of the lack of emotion, they may believe that the person cannot be who they think they are because if they were, the sufferer would have an emotional response to them. One sufferer of Capgras Delusion is profiled here on YouTube. Treatment for Capgras Delusion includes individual therapy that involves reframing and reality testing as well as antipsychotics and other drugs.

Fregoli Syndrome

This is similar to Capgras Delusion, but involves the sufferer believing that those around them are actually other people in disguise. When they see their wife, for example, they believe she is actually their doctor or some other person they know. This is named after Leopoldo Fregoli, who was an Italian actor known for his ability to quickly change appearance during stage performances. It was first described in 1927 in a paper in which the authors discussed a 27-year-old woman who was living in London. She believed she was being followed and persecuted by two actors she saw at the theatre often. She felt these people were taking the form of others she knew or had previously met. In a more recent case, the sufferer was a 21-year-old man who was schizophrenic. He believed that his daily facial cream attracted female students. He met a young woman on Facebook and wanted to have a relationship with her, but she was not interested. The man then developed the belief that when he was contacted by other women on Facebook, they were not who they appeared to be, but rather they were the first young woman in disguise. The man believed that this young woman was applying the same cream to her face to transform her appearance. Causes of Fregoli Syndrome are not entirely known, but it has been found in people taking the drug Levodopa. This is used to treat Parkinson’s Disease and dopamine responsive dystonia. Traumatic brain injuries are another possible cause. Treatment usually includes antipsychotic drugs. In some cases, antidepressants and anticonvulsants are prescribed.

Causes:

Traumatic brain injury

Injury to the right frontal and left temporo-parietal areas can cause Fregoli syndrome. Research by Feinberg, et al. has shown that significant deficits in executive and memory functions follow shortly after damage in the right frontal or left temporoparietal areas. Tests performed on patients that have suffered from a brain injury revealed that basic attention ability and visuomotor processing speed are typically normal. However, these patients made many errors when they were called to participate in detailed attention tasks. Selective attention tests involving auditory targets were also performed, and brain-injured patients had many errors; this meant that they were deficient in their response regulation and inhibition.

Fusiform gyrus

Current research has shown that lesions in the right temporal lobe and the fusiform gyrus may contribute to DMSs. MRIs of patients exemplifying Fregoli symptoms have shown parahippocampal and hippocampal damage in the anterior fusiform gyrus, as well as the middle and inferior of the right temporal gyri. The inferior and medial of the right temporal gyri are the storage locations for long-term memory in retrieving information on visual recognition, specifically of faces; thus, damage to these intricate connections could be one of the leading factors in face misidentification disorders.

Recently, a face-specific area in the fusiform gyrus has been discovered and is close to the anterior fusiform gyrus. MRI studies performed by Hudson, et al. have shown lesions in the anterior fusiform gyrus, which is close to the face specific area (ventral fusiform cortex), may also be associated with Fregoli syndrome and other DMSs. Such damage may cause disruption in long-term visual memory and lead to improper associations of human faces.

On another note, our brains interpret visual scenes in two pathways: one is via the Parietal lobe-occipital dorsal pathway (visual spatial material is analyzed here), and the other is via the temporal-occipital ventral pathway (recognizes objects and faces). Thus, lesions in either structures or disruption of delicate connections may produce DMSs.

Abnormal P300

Delusional misidentification syndrome is thought to occur due to a dissociation between identification and recognition processes. The integration of information for further processing is referred to as working memory (WM). The P300 (P stands for positive voltage potential and the 300 for the 300-millisecond poststimulus) is an index of WM and is used during a WM test in DMS patients. In comparison to normal patients, DMS patients generally exhibit an attenuated amplitude of P300 at many abductions. These patients also exhibit prolonged latencies of P300 at all abductions. These implications suggest that DMSs are accompanied by abnormal WM, specifically affecting the prefrontal cortex (both outside and inside).

Sources: 1 2 3 4

How memories stick together
Scientists at the Salk Institute have created a new model of memory that explains how neurons retain select memories a few hours after an event.
This new framework provides a more complete picture of how memory works, which can inform research into disorders liked Parkinson’s, Alzheimer’s, post-traumatic stress and learning disabilities.
"Previous models of memory were based on fast activity patterns," says Terrence Sejnowski, holder of Salk’s Francis Crick Chair and a Howard Hughes Medical Institute Investigator. “Our new model of memory makes it possible to integrate experiences over hours rather than moments.”
Over the past few decades, neuroscientists have revealed much about how long-term memories are stored. For significant events—for example, being bit by a dog—a number of proteins are quickly made in activated brain cells to create the new memories. Some of these proteins linger for a few hours at specific places on specific neurons before breaking down.
This series of biochemical events allow us to remember important details about that event—such as, in the case of the dog bite, which dog, where it was located and so on.
One problem scientists have had with modeling memory storage is explaining why only selective details and not everything in that 1-2 hour window is strongly remembered. By incorporating data from previous literature, Sejnowski and first author Cian O’Donnell, a Salk postdoctoral researcher, developed a model that bridges findings from both molecular and systems observations of memory to explain how this 1-2 hour memory window works. The work is detailed in the latest issue of Neuron.
Using computational modeling, O’Donnell and Sejnowski show that, despite the proteins being available to a number of neurons in a given circuit, memories are retained when subsequent events activate the same neurons as the original event. The scientists found that the spatial positioning of proteins at both specific neurons and at specific areas around these neurons predicts which memories are recorded. This spatial patterning framework successfully predicts memory retention as a mathematical function of time and location overlap.
"One thing this study does is link what’s happing in memory formation at the cellular level to the systems level," says O’Donnell. "That the time window is important was already established; we worked out how the content could also determine whether memories were remembered or not. We prove that a set of ideas are consistent and sufficient to explain something in the real world."
The new model also provides a potential framework for understanding how generalizations from memories are processed during dreams.
While much is still unknown about sleep, research suggests that important memories from the day are often cycled through the brain, shuttled from temporary storage in the hippocampus to more long-term storage in the cortex. Researchers observed most of this memory formation in non-dreaming sleep. Little is known about if and how memory packaging or consolidation is done during dreams. However, O’Donnell and Sejnowski’s model suggests that some memory retention does happen during dreams.
"During sleep there’s a reorganizing of memory—you strengthen some memories and lose ones you don’t need anymore," says O’Donnell. "In addition, people learn abstractions as they sleep, but there was no idea how generalization processes happen at a neural level."
By applying their theoretical findings on overlap activity within the 1-2 hour window, they came up with a theoretical model for how the memory abstraction process might work during sleep.
Image: The hippocampus is a region of the brain largely responsible for memory formation. Courtesy of the Salk Institute for Biological Studies.

How memories stick together

Scientists at the Salk Institute have created a new model of memory that explains how neurons retain select memories a few hours after an event.

This new framework provides a more complete picture of how memory works, which can inform research into disorders liked Parkinson’s, Alzheimer’s, post-traumatic stress and learning disabilities.

"Previous models of memory were based on fast activity patterns," says Terrence Sejnowski, holder of Salk’s Francis Crick Chair and a Howard Hughes Medical Institute Investigator. “Our new model of memory makes it possible to integrate experiences over hours rather than moments.”

Over the past few decades, neuroscientists have revealed much about how long-term memories are stored. For significant events—for example, being bit by a dog—a number of proteins are quickly made in activated brain cells to create the new memories. Some of these proteins linger for a few hours at specific places on specific neurons before breaking down.

This series of biochemical events allow us to remember important details about that event—such as, in the case of the dog bite, which dog, where it was located and so on.

One problem scientists have had with modeling memory storage is explaining why only selective details and not everything in that 1-2 hour window is strongly remembered. By incorporating data from previous literature, Sejnowski and first author Cian O’Donnell, a Salk postdoctoral researcher, developed a model that bridges findings from both molecular and systems observations of memory to explain how this 1-2 hour memory window works. The work is detailed in the latest issue of Neuron.

Using computational modeling, O’Donnell and Sejnowski show that, despite the proteins being available to a number of neurons in a given circuit, memories are retained when subsequent events activate the same neurons as the original event. The scientists found that the spatial positioning of proteins at both specific neurons and at specific areas around these neurons predicts which memories are recorded. This spatial patterning framework successfully predicts memory retention as a mathematical function of time and location overlap.

"One thing this study does is link what’s happing in memory formation at the cellular level to the systems level," says O’Donnell. "That the time window is important was already established; we worked out how the content could also determine whether memories were remembered or not. We prove that a set of ideas are consistent and sufficient to explain something in the real world."

The new model also provides a potential framework for understanding how generalizations from memories are processed during dreams.

While much is still unknown about sleep, research suggests that important memories from the day are often cycled through the brain, shuttled from temporary storage in the hippocampus to more long-term storage in the cortex. Researchers observed most of this memory formation in non-dreaming sleep. Little is known about if and how memory packaging or consolidation is done during dreams. However, O’Donnell and Sejnowski’s model suggests that some memory retention does happen during dreams.

"During sleep there’s a reorganizing of memory—you strengthen some memories and lose ones you don’t need anymore," says O’Donnell. "In addition, people learn abstractions as they sleep, but there was no idea how generalization processes happen at a neural level."

By applying their theoretical findings on overlap activity within the 1-2 hour window, they came up with a theoretical model for how the memory abstraction process might work during sleep.

Image: The hippocampus is a region of the brain largely responsible for memory formation. Courtesy of the Salk Institute for Biological Studies.