Re-align trajectory
The secret, the evidence suggests, is that listening to music is an active process: We’re making the music in our heads as the sounds play our brains.

neuromorphogenesis:

Why does the brain remember dreams?

Some people recall a dream every morning, whereas others rarely recall one. A team led by Perrine Ruby, an Inserm Research Fellow at the Lyon Neuroscience Research Center (Inserm/CNRS/Université Claude Bernard Lyon 1), has studied the brain activity of these two types of dreamers in order to understand the differences between them. In a study published in the journal Neuropsychopharmacology, the researchers show that the temporo-parietal junction, an information-processing hub in the brain, is more active in high dream recallers. Increased activity in this brain region might facilitate attention orienting toward external stimuli and promote intrasleep wakefulness, thereby facilitating the encoding of dreams in memory.

The reason for dreaming is still a mystery for the researchers who study the difference between “high dream recallers,” who recall dreams regularly, and “low dream recallers,” who recall dreams rarely. In January 2013 (work published in the journal Cerebral Cortex), the team led by Perrine Ruby, Inserm researcher at the Lyon Neuroscience Research Center, made the following two observations: “high dream recallers” have twice as many time of wakefulness during sleep as “low dream recallers” and their brains are more reactive to auditory stimuli during sleep and wakefulness. This increased brain reactivity may promote awakenings during the night, and may thus facilitate memorisation of dreams during brief periods of wakefulness.

In this new study, the research team sought to identify which areas of the brain differentiate high and low dream recallers. They used Positron Emission Tomography (PET) to measure the spontaneous brain activity of 41 volunteers during wakefulness and sleep. The volunteers were classified into 2 groups: 21 “high dream recallers” who recalled dreams 5.2 mornings  per week in average, and 20 “low dream recallers,” who reported 2 dreams per month in average. High dream recallers, both while awake and while asleep, showed stronger spontaneous brain activity in the medial prefrontal cortex (mPFC) and in the temporo-parietal junction (TPJ), an area of the brain involved in attention orienting toward external stimuli.

The South African neuropsychologist Mark Solms had observed in earlier studies that lesions in these two brain areas led to a cessation of dream recall.  The originality of the French team’s results is to show brain activity differences between high and low dream recallers during sleep and also during wakefulness.

“Our results suggest that high and low dream recallers differ in dream  memorization, but do not exclude that they also differ in dream production. Indeed, it is possible that high dream recallers produce a larger amount of dreaming than low dream recallers” concludes the research team.

neuromorphogenesis:

Human brain reacts to emoticons as real faces
Humans have developed to read :-) in the same way as a human face, but do not have the same connection with (-:

Emoticons such as :-) have become so important to how we communicate online that they are changing the way that our brains work.


They are used to provide clues to the tone of SMS, emails and tweets that can be hard to succinctly describe in words alone. But Dr Owen Churches, from the school of psychology at Flinders University in Adelaide, has found that they have become so important that we now react to them in the same way as we would to a real human face.


When we see a face there is a very specific reaction in certain parts of the brain such as the occipitotemporal cortex. When that image of a face is inverted there is another very specific reaction. This can be tracked using advanced brain scanning techniques.


Churches found that the same reaction occurred when 20 participants in a study were shown emoticons, but only when they were viewed in the traditional, left-to-right format. When they were “inverted”, or flipped to be read right-to-left, the expected reaction was not found.


This showed that humans have now developed to read :-) in the same way as a human face, but do not have the same connection with (-:. The study, published in the Social Neuroscience journal, also included participants being shown real faces and meaningless strings of characters as controls.

neuromorphogenesis:

Human brain reacts to emoticons as real faces

Humans have developed to read :-) in the same way as a human face, but do not have the same connection with (-:

Emoticons such as :-) have become so important to how we communicate online that they are changing the way that our brains work.

They are used to provide clues to the tone of SMS, emails and tweets that can be hard to succinctly describe in words alone. But Dr Owen Churches, from the school of psychology at Flinders University in Adelaide, has found that they have become so important that we now react to them in the same way as we would to a real human face.

When we see a face there is a very specific reaction in certain parts of the brain such as the occipitotemporal cortex. When that image of a face is inverted there is another very specific reaction. This can be tracked using advanced brain scanning techniques.

Churches found that the same reaction occurred when 20 participants in a study were shown emoticons, but only when they were viewed in the traditional, left-to-right format. When they were “inverted”, or flipped to be read right-to-left, the expected reaction was not found.

This showed that humans have now developed to read :-) in the same way as a human face, but do not have the same connection with (-:. The study, published in the Social Neuroscience journal, also included participants being shown real faces and meaningless strings of characters as controls.

➜ A Brain Basis for Musical Hallucinations?

Why do some people hear music that’s not there?

Musical hallucinations are most commonly found in people who have suffered hearing loss or deafness. But why they happen is unknown. In a new paper in Cortex, British neuroscientists Kumar et al claim to have found A brain basis for musical hallucinations

Using magnetoencephalography (MEG), the authors investigate brain activity in a patient, a 66 year old woman who had been hearing phantom ‘piano melodies’ for almost two years, after she had suddenly become partly deaf. She was an amateur keyboard player, and was able to write down the tunes she ‘heard’:musicalhallucinationThe same melody – sometimes a real tune, sometimes ‘made up’ – would repeat for hours at a time, and it could get annoying. However, she had discovered that listening to certain pieces of real music provided temporary relief; the hallucinations would stop during the piece, and only restart after a certain lag-period of several seconds.

Kumar et al made use of this fact to compare brain activity when hallucinations were ‘on’ and ‘off’ – they recorded MEG data before and after playing 15 seconds of Bach, one of the hallucination-blocking composers. Immediately after each Bach burst, hallucinations were low, while 60 seconds later they had returned.

hallucinationsClever… however there’s a serious problem in this procedure: it can’t separate the effects of hallucinations from the effects of stopping listening to real music, nor from the expectation of future real music (the timing of which was predictable).

The obvious solution would have been to also include bursts of some music that didn’t block hallucinations, as a control condition. The patient herself reported that some music didn’t. This would dramatically increase the inferences one could draw from the data. Some MEG data from healthy control participants hearing the same music would also help to establish specificity. This limitation isn’t acknowledged.

Anyway, Kumar et al report increased gamma band activity in the left aSTG area, part of the auditory cortex. They say that

The area that shows higher activity during musical hallucination coincides with an area implicated in the normal perception of melody using fMRI.

However, strangely, the actual Bach music did not produce significant changes in activity in this area, or anywhere else in the brain. Only imaginary music caused real brain waves; Kumar et al say that this has been seen in other studies and

It is not yet understood why phantom percepts are associated with much stronger gamma oscillations, as measured with MEG and electroencephalography (EEG), than those associated with external sensory stimulation; for review see Sedley & Cunningham, 2013 “Do cortical gamma oscillations promote or suppress perception?”

Some other changes in the beta frequency band were found in the motor cortex and posteromedial cortex/precuneus. Neither of these is thought of as a ‘music area’. To be honest, I don’t think these results shed much light on the phenomenon.

The second half of the paper is rather different, providing a theoretical overview of musical hallucination. This section could almost be a paper in itself. The authors argue that

Our hypothesis is that peripheral hearing loss reduces the signal-to-noise ratio of incoming auditory stimuli and the brain responds by decreasing sensory precision or post-synaptic gain…

A recurrent loop of communication is thus established which is no longer informed, or entrained, by precise bottom-up sensory prediction errors… it is constrained only by a need to preserve the internal consistency between hierarchical representations of music.

This reciprocal communication between an area in music perception and area/s involved in higher music cognition (motor cortex and precuneus) with no constraint from the sensory input gives rise to musical hallucinations.

Kumar S, Sedley W, Barnes GR, Teki S, Friston KJ, & Griffiths TD (2013). A brain basis for musical hallucinations. Cortex PMID: 24445167

neuromorphogenesis:

After Death, H.M.’s Brain Uploaded to the Cloud

The most famous neuroscience patient of the modern era died of respiratory failure on December 2, 2008, at 5:05 PM Eastern Time. Not long after, the body of 82-year-old Henry Molaison — known simply as H.M. in hundreds of scientific papers — went on a two-hour ride from his nursing home in Windsor Locks, Connecticut, to Massachusetts General Hospital in Boston. The cadaver spent the next nine hours inside of an MRI machine, getting scanned every which way.

Meanwhile, on the other side of the country, neuroanatomist Jacopo Annese rushed to the San Diego airport and boarded a red-eye flight to Boston. After landing, and pounding a few cups of coffee, he went to the hospital to join neuropathologist Matthew Frosch in the meticulous and high-stakes extraction of H.M.’s brain.

H.M. had one of the most important brains in the world, at least if you ask a neuroscientist. In 1953, at age 27, he underwent experimental brain surgery to treat the terrible seizures that had plagued him since childhood. The seizures quieted after surgeon William Beecher Scoville removed pieces of the temporal lobes above his ears — including, notably, large parts of the hippocampus — but it came at the cost of permanent amnesia. For the rest of his life, H.M. could only hold on to memories of events that happened before his surgery.

Though he couldn’t remember what he had for breakfast, H.M. could learn new motor memory tasks and had normal intelligence, illustrating both the specificity of the hippocampus and the multifaceted nature of memory. All of this we know thanks to decades of work by Suzanne Corkin and her colleagues at McGill University and MIT. As Corkin writes in her fascinating new book Permanent Present Tense*, “Henry’s disability, a tremendous cost to him and his family, became science’s gain.”

H.M. not only participated in hundreds of studies while he was alive, but donated his brain to science. The morning after H.M. died, a groggy and jet-lagged Annese knew that this brain tissue might pay scientific dividends for many decades to come — but only if the extraction went smoothly.

“I had these nightmares about Young Frankenstein — you know, when he drops the brain?” Annese recalls, laughing. “This artifact is so important, and you can create big damage when you’re doing an autopsy if you’re not careful.” Luckily the scientists recovered the brain without making any nicks. So far, so good, Annese told himself.

H.M.’s brain stayed in Boston, suspended upsidedown in a standard formaldehyde buffer, until February. Then Annese took it to California, to his lab at The Brain Observatory at the University of California, San Diego. Over the next 10 months, Annese gradually added sucrose to the buffer, creating a cryoprotectant that would allow the entire brain to be frozen without forming tissue-damaging ice crystals.

On the one-year anniversary of H.M.’s death, Annese’s team froze his entire brain as a single block and began a 53-hour process of cutting it into some 2,400 super-thin slices. “I didn’t sleep for three days,” Annese says. He had a team of students that took shifts to help him — and to make sure he stayed awake. ”There was always one person next to me, and if I looked like I was phasing out or missing a slice, the code word was ‘prosciutto’,” says Annese, who is Italian. “It was probably the most engaging, most exciting thing I’ve ever done.”

Annese’s team live-streamed and Tweeted the entire procedure, and he says some 400,000 people tuned in to watch. In the end, just two slices were damaged while cutting.

A camera mounted above the iced brain took a high-resolution picture of each slice. These images became the basis of a digital, interactive atlas of H.M.’s brain, as Annese and Corkin describe in Nature Communications. The atlas will be made available to any other researcher interested in collaboration, Annese says.

On image 3 the boxes on the picture, you are looking at what was left of H.M.’s hippocampus. Although most emphasis on H.M. has focused on his missing hippocampus, brain-imaging studies have shown since the late 1990s that he actually retained about 50 percent of this region. The new resource confirms this, and also allows researchers to look closely at individual hippocampal cells, providing a fine-grained molecular view that is not possible with brain imaging.

“Imaging can only go so far,” says David Amaral, director of research at the M.I.N.D. Institute at the University of California, Davis, who worked on a 1997 brain-imaging study of H.M.’s brain. “We knew that there was a portion of the hippocampus that was intact. What you can’t see in MRI is whether the neurons are there and what state they’re in. Now that’s come out in this new paper.”

Those hippocampal neurons look fairly normal, which comes as a surprise to Menno Witter, a memory expert at the Kavli Institute for Systems Neuroscience in Trondheim, Norway, who was not involved in the work. That’s because H.M.’s surgery removed not only parts of the hippocampus, but the entire ‘entorhinal cortex,’ a region that connects the hippocampus to the cortex, or outer layers of the brain. In animal models, Witter says, “removal of entorhinal inputs generally lead to striking changes” in the hippocampus. (It could be that these changes did happen in H.M.’s brain, but won’t be obvious until researchers compare it with more control samples, he adds.)

Even without inputs from the entorhinal cortex, it’s possible that H.M.’s remaining hippocampus was partially connected to the brain stem and other, non-cortical areas of the brain. So it could have had a functional role in H.M.’s cognition, Witter says. “What that is, I would find that hard to predict.”

More generally, this new paper and other research on H.M. over the years has gradually shifted from a focus on individual regions, such as the hippocampus, to the interaction of many connected regions. “There is certainly agreement that the hippocampus is critical for episodic memory,” says Rebecca Burwell, a memory researcher at Brown University who was not involved in the work. “But these new findings confirm that understanding brain circuits, in this case the pathways in and out of the hippocampus, is the key to understanding how the brain supports memory and other cognitive processes.”

H.M.’s brain is the most famous of about 60 brains that are currently undergoing Annese’s new freezing-and-cutting procedure, and 300 living people have signed up to donate theirs. Annese hopes that his digital approach will become “a radical new way of brain banking,” where brain tissues are saved from dusty storage rooms and uploaded to a more lasting digital warehouse.

The most fascinating thing about the H.M., and the new H.M. atlas, has to do with the last decade of his life, in which he developed severe dementia. It could have been Alzheimer’s, and researchers are currently searching H.M.’s brain samples for the disease’s signature amyloid-beta plaques. One theory of Alzheimer’s says that the disease begins in the entorhinal cortex. That idea would be called into question if H.M. indeed had the disease.

And even if H.M. didn’t have Alzheimer’s, his dementia still leaves a puzzle for brain researchers. “What will be of interest is what we can make of how intact H.M.’s brain is given that he was undergoing this dementing illness,” Amaral says. “To me, that’s one of the major unanswered questions about Henry. And something else that Henry can teach us.”

neuromorphogenesis:

Study reveals how ecstasy acts on the brain and hints at therapeutic uses

Results of the study at Imperial College London, parts of which were televised in Drugs Live on Channel 4 in 2012, have now been published in the journal Biological Psychiatry.

The findings hint at ways that ecstasy, or MDMA, might be useful in the treatment of anxiety and post-traumatic stress disorder (PTSD).

MDMA has been a popular recreational drug since the 1980s, but there has been little research on which areas of the brain it affects. The new study is the first to use functional magnetic resonance imaging (fMRI) on resting subjects under its influence.

Twenty-five volunteers underwent brain scans on two occasions, one after taking the drug and one after taking a placebo, without knowing which they had been given.

The results show that MDMA decreases activity in the limbic system – a set of structures involved in emotional responses. These effects were stronger in subjects who reported stronger subjective experiences, suggesting that they are related.

Communication between the medial temporal lobe and medial prefrontal cortex, which is involved in emotional control, was reduced. This effect, and the drop in activity in the limbic system, are opposite to patterns seen in patients who suffer from anxiety.

MDMA also increased communication between the amygdala and the hippocampus. Studies on patients with PTSD have found a reduction in communication between these areas.

The project was led by David Nutt, the Edmond J. Safra Professor of Neuropsychopharmacology at Imperial College London, and Professor Val Curran at UCL.

Dr Robin Carhart-Harris from the Department of Medicine at Imperial, who performed the research, said: “We found that MDMA caused reduced blood flow in regions of the brain linked to emotion and memory. These effects may be related to the feelings of euphoria that people experience on the drug.”

Professor Nutt added: “The findings suggest possible clinical uses of MDMA in treating anxiety and PTSD, but we need to be careful about drawing too many conclusions from a study in healthy volunteers. We would have to do studies in patients to see if we find the same effects.”

MDMA has been investigated as an adjunct to psychotherapy in the treatment of PTSD, with a recent pilot study in the US reporting positive preliminary results.

As part of the Imperial study, the volunteers were asked to recall their favourite and worst memories while inside the scanner. They rated their favourite memories as more vivid, emotionally intense and positive after MDMA than placebo, and they rated their worst memories less negatively. This was reflected in the way that parts of the brain were activated more or less strongly under MDMA. These results were published in the International Journal of Neuropsychopharmacology.

Dr Carhart-Harris said: “In healthy volunteers, MDMA seems to lessen the impact of painful memories. This fits with the idea that it could help patients with PTSD revisit their traumatic experiences in psychotherapy without being overwhelmed by negative emotions, but we need to do studies in PTSD patients to see if the drug affects them in the same way.”

neuromorphogenesis:

How Inactivity Changes the Brain
A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a notable new report.
The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.
Until about 20 years ago, most scientists believed that the brain’s structure was fixed by adulthood, that you couldn’t create new brain cells, alter the shape of those that existed or in any other way change your mind physically after adolescence.
But in the years since, neurological studies have established that the brain retains plasticity, or the capacity to be reshaped, throughout our lifetimes. Exercise appears to be particularly adept at remodeling the brain, studies showed.
But little has been known about whether inactivity likewise alters the structure of the brain and, if so, what the consequences might be.
So for a study recently published in The Journal of Comparative Neurology, scientists at Wayne State University School of Medicine and other institutions gathered a dozen rats. They settled half of them in cages with running wheels and let the animals run at will. Rats like running, and these animals were soon covering about three miles a day on their wheels.
The other rats were housed in cages without wheels and remained sedentary.
After almost three months of resting or running, the animals were injected with a special dye that colors certain neurons in the brain. In this case, the scientists wanted to mark neurons in the animals’ rostral ventrolateral medulla, an obscure portion of the brain that controls breathing and other unconscious activities central to our existence.
The rostral ventrolateral medulla commands the body’s sympathetic nervous system, which among other things controls blood pressure on a minute-by-minute basis by altering blood-vessel constriction. Although most of the science related to the rostral ventrolateral medulla has been completed using animals, imaging studies in people suggest that we have the same brain region and it functions similarly.
A well-regulated sympathetic nervous system correctly directs blood vessels to widen or contract as needed and blood to flow, so that you can, say, scurry away from a predator or rise from your office chair without fainting. But an overly responsive sympathetic nervous system is problematic, said Patrick Mueller, an associate professor of physiology at Wayne State University who oversaw the new study. Recent science shows that “overactivity of the sympathetic nervous system contributes to cardiovascular disease,” he said, by stimulating blood vessels to constrict too much, too little or too often, leading to high blood pressure and cardiovascular damage.
The sympathetic nervous system will respond erratically and dangerously, scientists theorize, if it is receiving too many and possibly garbled messages from neurons in the rostral ventrolateral medulla.
And, as it turned out, when the scientists looked inside the brains of their rats after the animals had been active or sedentary for about 12 weeks, they found noticeable differences between the two groups in the shape of some of the neurons in that region of the brain.
Using a computerized digitizing program to recreate the inside of the animals’ brains, the scientists established that the neurons in the brains of the running rats were still shaped much as they had been at the start of the study and were functioning normally.
But many of the neurons in the brains of the sedentary rats had sprouted far more new tentacle-like arms known as branches. Branches connect healthy neurons into the nervous system. But these neurons now had more branches than normal neurons would have, making them more sensitive to stimuli and apt to zap scattershot messages into the nervous system.
In effect, these neurons had changed in ways that made them likely to overstimulate the sympathetic nervous system, potentially increasing blood pressure and contributing to the development of heart disease.
This finding is important because it adds to our understanding of how, at a cellular level, inactivity increases the risk of heart disease, Dr. Mueller said. But even more intriguing, the results underscore that inactivity can change the structure and functioning of the brain, just as activity does.
Of course, rats are not people, and this is a small, short-term study. But already one takeaway is that not moving has wide-ranging physiological effects. In upcoming presentations, Dr. Mueller said, he plans to show slides of the different rat neurons and, echoing the old anti-drug message, point out that “‘this is your brain.’ And this is your brain on the couch.”

neuromorphogenesis:

How Inactivity Changes the Brain

A number of studies have shown that exercise can remodel the brain by prompting the creation of new brain cells and inducing other changes. Now it appears that inactivity, too, can remodel the brain, according to a notable new report.

The study, which was conducted in rats but likely has implications for people too, the researchers say, found that being sedentary changes the shape of certain neurons in ways that significantly affect not just the brain but the heart as well. The findings may help to explain, in part, why a sedentary lifestyle is so bad for us.

Until about 20 years ago, most scientists believed that the brain’s structure was fixed by adulthood, that you couldn’t create new brain cells, alter the shape of those that existed or in any other way change your mind physically after adolescence.

But in the years since, neurological studies have established that the brain retains plasticity, or the capacity to be reshaped, throughout our lifetimes. Exercise appears to be particularly adept at remodeling the brain, studies showed.

But little has been known about whether inactivity likewise alters the structure of the brain and, if so, what the consequences might be.

So for a study recently published in The Journal of Comparative Neurology, scientists at Wayne State University School of Medicine and other institutions gathered a dozen rats. They settled half of them in cages with running wheels and let the animals run at will. Rats like running, and these animals were soon covering about three miles a day on their wheels.

The other rats were housed in cages without wheels and remained sedentary.

After almost three months of resting or running, the animals were injected with a special dye that colors certain neurons in the brain. In this case, the scientists wanted to mark neurons in the animals’ rostral ventrolateral medulla, an obscure portion of the brain that controls breathing and other unconscious activities central to our existence.

The rostral ventrolateral medulla commands the body’s sympathetic nervous system, which among other things controls blood pressure on a minute-by-minute basis by altering blood-vessel constriction. Although most of the science related to the rostral ventrolateral medulla has been completed using animals, imaging studies in people suggest that we have the same brain region and it functions similarly.

A well-regulated sympathetic nervous system correctly directs blood vessels to widen or contract as needed and blood to flow, so that you can, say, scurry away from a predator or rise from your office chair without fainting. But an overly responsive sympathetic nervous system is problematic, said Patrick Mueller, an associate professor of physiology at Wayne State University who oversaw the new study. Recent science shows that “overactivity of the sympathetic nervous system contributes to cardiovascular disease,” he said, by stimulating blood vessels to constrict too much, too little or too often, leading to high blood pressure and cardiovascular damage.

The sympathetic nervous system will respond erratically and dangerously, scientists theorize, if it is receiving too many and possibly garbled messages from neurons in the rostral ventrolateral medulla.

And, as it turned out, when the scientists looked inside the brains of their rats after the animals had been active or sedentary for about 12 weeks, they found noticeable differences between the two groups in the shape of some of the neurons in that region of the brain.

Using a computerized digitizing program to recreate the inside of the animals’ brains, the scientists established that the neurons in the brains of the running rats were still shaped much as they had been at the start of the study and were functioning normally.

But many of the neurons in the brains of the sedentary rats had sprouted far more new tentacle-like arms known as branches. Branches connect healthy neurons into the nervous system. But these neurons now had more branches than normal neurons would have, making them more sensitive to stimuli and apt to zap scattershot messages into the nervous system.

In effect, these neurons had changed in ways that made them likely to overstimulate the sympathetic nervous system, potentially increasing blood pressure and contributing to the development of heart disease.

This finding is important because it adds to our understanding of how, at a cellular level, inactivity increases the risk of heart disease, Dr. Mueller said. But even more intriguing, the results underscore that inactivity can change the structure and functioning of the brain, just as activity does.

Of course, rats are not people, and this is a small, short-term study. But already one takeaway is that not moving has wide-ranging physiological effects. In upcoming presentations, Dr. Mueller said, he plans to show slides of the different rat neurons and, echoing the old anti-drug message, point out that “‘this is your brain.’ And this is your brain on the couch.”

neuromorphogenesis:

Thinking hard weighs heavy on the brain

When the mind is at work, the brain literally gets heavier.

That fact may be surprising, but it isn’t new: In the late 1880s, Italian scientist Angelo Mosso built an intricate full-body balance and reported that mental activity tips the scales. Now, a modern-day version of Mosso’s “human circulation balance” backs him up. Compared with a brain at rest, a brain listening to music and watching a video is indeed heavier, David Field and Laura Inman of the University of Reading in England report January 9 inBrain.

While teaching a course about brain-imaging techniques, Field grew curious whether Mosso’s general approach would work. So he and some students decided to find out. “It was a bit of a mad idea, to be honest,” Field says.

At the heart of both balances lies a simple seesaw lever. As weight shifts in a body, presumably from blood moving, the lever tilts the head or the feet downward, Mosso observed. Field and Inman’s contraption doesn’t actually tip. The researchers put a sensitive scale under the head end, which would register changes in force.

After lots of troubleshooting, which involved eliminating signals created by bodily processes that move blood such as breathing and heart beats, Field and Ingram were able to test mental tasks. Fourteen participants were asked to lie still on the lever, and listen to music or listen to music and simultaneously watch a video of colorful geometric shapes. The part of the brain that detects sound is relatively small, Field says, so the audio plus video test was used to activate a wider swath of the brain and increase the chances of a measurable blood shift.

Right after a two-second blip of either audio or audio and video, blood leaves the brain, as measured by a drop in force, Field and Inman found. This quick dip in blood volume, a phenomenon that’s also seen in functional MRI, may represent the brain preparing for work by shunting waste-ridden blood out via the jugular vein. Seconds after that, a surge of new blood enters the brain, increasing the force measured by the scale.

These changes in force were very small — about 0.005 newtons — and most prominent in the people who both listened to music and watched a video, Field says. It’s hard to calculate how much blood rushes into the brain with each mental task. To know that value, scientists would need to know the distance of the head from the lever’s fulcrum, which could be easily measured, and exactly where the blood came from, which is nearly impossible to know.  

In his original experiments, Mosso found that tasks that required more mental energy made the brain heavier. Reading a page from a mathematics manual seemed to tip the balance more than reading a page from a newspaper. Strong emotions also tipped the scales: When a subject read a letter from an angry creditor, Mosso wrote, “the balance fell at once.”

Until recently, Mosso’s scientific manuscripts had not been described in detail. But Stefano Sandrone of King’s College London unearthed Mosso’s papers in archives and published a description in Brain in 2013.

“We have been neglecting Mosso and his work for so many years. It’s good that someone has begun to find interest in the papers that he wrote,” Sandrone says of the modern-day experiment. He and his colleagues are working on an exhibition of Mosso’s original balance.

Many neuroscientists use functional MRI to detect changes in blood flow in the brain. Usually, fMRI spots regional differences, as when a little blood moves from one part of the brain to another. In contrast, the balance describes overall changes in brain workload, Field says.

The balance is not going to replace modern neuroimaging as a way to see what happens inside the brain. But with refinements, it might ultimately prove to be useful, Sandrone says. “The more measures we have, the more we can approximate the complexity of the brain.” 

Image2: BALANCING ACT  In the 1880s, Angelo Mosso used the human circulation balance illustrated here to measure the movement of blood to the brain during taxing mental tasks. 

neuromorphogenesis:

Breathing In vs. Spacing Out

neuromorphogenesis:

SHY hypothesis explains that sleep is the price we pay for learning

Why do animals ranging from fruit flies to humans all need to sleep? After all, sleep disconnects them from their environment, puts them at risk and keeps them from seeking food or mates for large parts of the day.

Two leading sleep scientists from the University of Wisconsin School of Medicine and Public Health say that their synaptic homeostasis hypothesis of sleep or “SHY” challenges the theory that sleep strengthens brain connections.

The SHY hypothesis, which takes into account years of evidence from human and animal studies, says that sleep is important because it weakens the connections among brain cells to save energy, avoid cellular stress, and maintain the ability of neurons to respond selectively to stimuli.

“Sleep is the price the brain must pay for learning and memory,” says Dr. Giulio Tononi, of the UW Center for Sleep and Consciousness. “During wake, learning strengthens the synaptic connections throughout the brain, increasing the need for energy and saturating the brain with new information. Sleep allows the brain to reset, helping integrate newly learned material with consolidated memories, so the brain can begin anew the next day.”

Tononi and his co-author Dr. Chiara Cirelli, both professors of psychiatry, explain their hypothesis in a review article in today’s issue of the journal Neuron. Their laboratory studies sleep and consciousness in animals ranging from fruit flies to humans; SHY takes into account evidence from molecular, electrophysiological and behavioral studies, as well as from computer simulations.”Synaptic homeostasis” refers to the brain’s ability to maintain a balance in the strength of connections within its nerve cells.

Why would the brain need to reset? Suppose someone spent the waking hours learning a new skill, such as riding a bike. The circuits involved in learning would be greatly strengthened, but the next day the brain will need to pay attention to learning a new task. Thus, those bike- riding circuits would need to be damped down so they don’t interfere with the new day’s learning.

“Sleep helps the brain renormalize synaptic strength based on a comprehensive sampling of its overall knowledge of the environment,” Tononi says, “rather than being biased by the particular inputs of a particular waking day.”  

The reason we don’t also forget how to ride a bike after a night’s sleep is because those active circuits are damped down less than those that weren’t actively involved in learning. Indeed, there is evidence that sleep enhances important features of memory, including acquisition, consolidation, gist extraction, integration and “smart forgetting,” which allows the brain to rid itself of the inevitable accumulation of unimportant details.

However, one common belief is that sleep helps memory by further strengthening the neural circuits during learning while awake. But Tononi and Cirelli believe that consolidation and integration of memories, as well as the restoration of the ability to learn, all come from the ability of sleep to decrease synaptic strength and enhance signal-to-noise ratios.

While the review finds testable evidence for the SHY hypothesis, it also points to open issues. One question is whether the brain could achieve synaptic homeostasis during wake, by having only some circuits engaged, and the rest off-line and thus resetting themselves.

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