by Neuroskeptic
Last year, I blogged about a new and very pretty way of displaying the data about the human ‘connectome’ – the wiring between different parts of the brain.
But there are many beautiful ways of visualizing the brain’s connections, as neuroscientists Daniel Margulies and colleagues of Leipzig discuss in a colourful paper showcasing these techniques.
Here, for example, are two ways of showing the brain’s white matter tracts, as studied with diffusion tensor imaging (DTI):
Another striking image is this one, a representation of the brain’s functional connectivity – the degree to which activation in each part of the brain is correlated with activity in every other part.
The functional connectome is inherently difficult to visualize in 2D (or even 3D), but in this ingenious display, the brain’s surface is shown covered with hundreds of little brains, each one a colour-coded map of the connectivity from that particular point:
The Margulies paper is about more than just pretty pictures, though. The authors also discuss the scientific questions and theoretical tensions that surround the choice of one visualization over another:
Scientific figure and illustrations are – to paraphrase Tufte – where seeing turns into showing. The capacity of these images to influence our interpretation of data and to direct the questions of the scientific community make visualizations worthy of careful consideration during their production…
If we present a figure that clarifies the scientific content, but does so by creating a distortion of brain space, is that bad practice? What if the caption and methods explicitly stated that the contents of the figure were not to be taken literally? To what degree should a visualization be allowed to stand alone?
In my view, the study of connections has been dominated by images, more than any other branch of neuroscience. It’s rarely easy to say where ‘method’ or ‘analysis’ ends and ‘visualization’ begins.
This is not a bad thing – connectivity is spatial, by definition, and to understand space is to visualize it. But it does mean that in the connectome, there is always a danger of valuing aesthetics over accuracy, beauty above brains.
Margulies DS, Böttger J, Watanabe A, & Gorgolewski KJ (2013). Visualizing the Human Connectome. NeuroImage PMID: 23660027
[video]
Neuroscience: Mind-body Genomics -
A new study from investigators at the Benson-Henry Institute for Mind/Body Medicine at Massachusetts General Hospital and Beth Israel Deaconess Medical Center finds that eliciting the relaxation response—a physiologic state of deep rest induced by practices such as meditation, yoga, deep breathing and prayer—produces immediate changes in the expression of genes involved in immune function, energy metabolism and insulin secretion.
“Many studies have shown that mind/body interventions like the relaxation response can reduce stress and enhance wellness in healthy individuals and counteract the adverse clinical effects of stress in conditions like hypertension, anxiety, diabetes and aging,” said Herbert Benson, HMS professor of medicine at Mass General and co-senior author of thereport.
Benson is director emeritus of the Benson-Henry Institute.
“Now for the first time we’ve identified the key physiological hubs through which these benefits might be induced,” he said.
Published in the open-access journal PLOS ONE, the study combined advanced expression profiling and systems biology analysis to both identify genes affected by relaxation response practice and to determine the potential biological relevance of those changes.
“Some of the biological pathways we identify as being regulated by relaxation response practice are already known to play specific roles in stress, inflammation and human disease. For others, the connections are still speculative, but this study is generating new hypotheses for further investigation,” said Towia Libermann, HMS associate professor of medicine at Beth Israel Deaconess and co-senior author of the study.
Benson first described the relaxation response—the physiologic opposite of the fight-or-flight response—almost 40 years ago, and his team has pioneered the application of mind/body techniques to a wide range of health problems. Studies in many peer-reviewed journals have documented how the relaxation response both alleviates symptoms of anxiety and many other disorders and also affects factors such as heart rate, blood pressure, oxygen consumption and brain activity.
In 2008, Benson and Libermann led a study finding that long-term practice of the relaxation response changed the expression of genes involved with the body’s response to stress. The current study examined changes produced during a single session of relaxation response practice, as well as those taking place over longer periods of time.
The study enrolled a group of 26 healthy adults with no experience in relaxation response practice, who then completed an 8-week relaxation-response training course.
Before they started their training, they went through what was essentially a control group session: Blood samples were taken before and immediately after the participants listened to a 20-minute health education CD and again 15 minutes later. After completing the training course, a similar set of blood tests was taken before and after participants listened to a 20-minute CD used to elicit the relaxation response as part of daily practice.
The sets of blood tests taken before the training program were designated “novice,” and those taken after training completion were called “short-term practitioners.” For further comparison, a similar set of blood samples was taken from a group of 25 individuals with 4 to 25 years’ experience regularly eliciting the relaxation response through many different techniques before and after they listened to the same relaxation response CD.
Blood samples from all participants were analyzed to determine the expression of more than 22,000 genes at the different time points.
The results revealed significant changes in the expression of several important groups of genes between the novice samples and those from both the short- and long-term sets. Even more pronounced changes were shown in the long-term practitioners.
A systems biology analysis of known interactions among the proteins produced by the affected genes revealed that pathways involved with energy metabolism, particularly the function of mitochondria, were upregulated during the relaxation response. Pathways controlled by activation of a protein called NF-κB—known to have a prominent role in inflammation, stress, trauma and cancer—were suppressed after relaxation response elicitation. The expression of genes involved in insulin pathways was also significantly altered.
“The combination of genomics and systems biology in this study provided great insight into the key molecules and physiological gene interaction networks that might be involved in relaying beneficial effects of relaxation response in healthy subjects,” said Manoj Bhasin, HMS assistant professor of medicine, co-lead author of the study, and co-director of the Beth Israel Deaconess Genomics, Proteomics, Bioinformatics and Systems Biology Center.
Bhasin noted that these insights should provide a framework for determining, on a genomic basis, whether the relaxation response will help alleviate symptoms of diseases triggered by stress. The work could also lead to developing biomarkers that may suggest how individual patients will respond to interventions.
Benson stressed that the long-term practitioners in this study elicited the relaxation response through many different techniques—various forms of meditation, yoga or prayer—but those differences were not reflected in the gene expression patterns.
“People have been engaging in these practices for thousands of years, and our finding of this unity of function on a basic-science, genomic level gives greater credibility to what some have called ‘new age medicine,’ ” he said.
“While this and our previous studies focused on healthy participants, we currently are studying how the genomic changes induced by mind/body interventions affect pathways involved in hypertension, inflammatory bowel disease and irritable bowel syndrome. We have also started a study—a collaborative undertaking between Dana-Farber Cancer Institute, Mass General and Beth Israel Deaconess—in patients with precursor forms of multiple myeloma, a condition known to involve activation of NF-κB pathways,” said Libermann, who is the director of the Beth Israel Deaconess Medical Center Genomics, Proteomics, Bioinformatics and Systems Biology Center.
(Source: hms.harvard.edu)
Neuroscience: Paralyzed Patient Moves Prosthetic Arm With Her Mind -
It sounds like science fiction, but researchers are gaining ground in developing mind-controlled robotic arms that could give people with paralysis or amputated limbs more independence.
The technology, known as brain-computer (or brain-machine) interface, is in its infancy as far as human…
(Source: health.usnews.com)
Age-defying: Master key of lifespan found in brain
The brain’s mechanism for controlling ageing has been discovered – and manipulated to shorten and extend the lives of mice. Drugs to slow ageing could follow
Tick tock, tick tock… A mechanism that controls ageing, counting down to inevitable death, has been identified in the hypothalamus – a part of the brain that controls most of the basic functions of life.
By manipulating this mechanism, researchers have both shortened and lengthened the lifespan of mice. The discovery reveals several new drug targets that, if not quite an elixir of youth, may at least delay the onset of age-related disease.
The hypothalamus is an almond-sized puppetmaster in the brain. “It has a global effect,” says Dongsheng Cai at the Albert Einstein College of Medicine in New York. Sitting on top of the brain stem, it is the interface between the brain and the rest of the body, and is involved in, among other things, controlling our automatic response to the world around us, our hormone levels, sleep-wake cycles, immunity and reproduction.
While investigating ageing processes in the brain, Cai and his colleagues noticed that ageing mice produce increasing levels of nuclear factor kB (NF-kB) – a protein complex that plays a major role in regulating immune responses. NF-kB is barely active in the hypothalamus of 3 to 4-month-old mice but becomes very active in old mice, aged 22 to 24 months.
To see whether it was possible to affect ageing by manipulating levels of this protein complex, Cai’s team tested three groups of middle-aged mice. One group was given gene therapy that inhibits NF-kB, the second had gene therapy to activate NF-kB, while the third was left to age naturally.
This last group lived, as expected, between 600 and 1000 days. Mice with activated NF-kB all died within 900 days, while the animals with NF-kB inhibition lived for up to 1100 days.
Crucially, the mice that lived the longest not only increased their lifespan but also remained mentally and physically fit for longer. Six months after receiving gene therapy, all the mice were given a series of tests involving cognitive and physical ability.
In all of the tests, the mice that subsequently lived the longest outperformed the controls, while the short-lived mice performed the worst.
Post-mortem examinations of muscle and bone in the longest-living rodents also showed that they had many chemical and physical qualities of younger mice.
Further investigation revealed that NF-kB reduces the level of a chemical produced by the hypothalamus called gonadotropin-releasing hormone (GnRH) – better known for its involvement in the regulation of puberty and fertility, and the production of eggs and sperm.
To see if they could control lifespan using this hormone, the team gave another group of mice – 20 to 24 months old – daily subcutaneous injections of GnRH for five to eight weeks. These mice lived longer too, by a length of time similar to that of mice with inhibited NF-kB.
GnRH injections also resulted in new neurons in the brain. What’s more, when injected directly into the hypothalamus, GnRH influenced other brain regions, reversing widespread age-related decline and further supporting the idea that the hypothalamus could be a master controller for many ageing processes.
GnRH injections even delayed ageing in the mice that had been given gene therapy to activate NF-kB and would otherwise have aged more quickly than usual. None of the mice in the study showed serious side effects.
So could regular doses of GnRH keep death at bay? Cai hopes to find out how different doses affect lifespan, but says the hormone is unlikely to prolong life indefinitely since GnRH is only one of many factors at play. “Ageing is the most complicated biological process,” he says.
“There are dozens of pathways that people will look at thanks to this work,” says Richard Miller at the University of Michigan in Ann Arbor. Miller has previously demonstrated that an immunosuppressant drug called rapamycin can also extend life in mice (see “A guide to defying age”).
Since the hypothalamus – and GnRH in particular – regulate several major biological processes, it may be possible to influence ageing through related mechanisms, says Miller. He wants to look at possible dietary interventions, such as the indirect effect that spikes in glucose may have on the hypothalamus.
Stuart Maudsley at the National Institute on Aging in Baltimore, Maryland, agrees that the hypothalamus could be the route in for age-controlling drugs. “The body is all one big juicy system,” he says. The ideal drug would hit that system at its centre. “Activate that keystone and everything falls into place,” he says.
Though this is the first time that an explicit role has been found for GnRH in the ageing process, previous studies in humans have hinted at a link between longevity and fertility – in which the hormone is known to play a significant role.
As GnRH levels drop, so too does egg production and fertility. In a study presented this month at the annual meeting of the Population Association of America in New Orleans, Graziella Caselli at the University of Rome, Italy, and colleagues found that mothers in Sardinia who’d had their last child over the age of 45 – so were still fertile at a late age – were significantly more likely to reach 100 than those who’d had their last child at a younger age. Since late fertility could be linked to higher levels of GnRH, Cai says those findings are a good match for his own. “There is likely to be some kind of biological correlation between ageing and reproduction,” he says.
“There are maybe 10 steps to controlling ageing,” says Miller. “We’ve taken the first two or three.” The first is simply accepting the idea that ageing can be slowed down, he says. “Many think it can’t. They are wrong.”
Maudsley reckons that we could see drugs that slow ageing in the next 20 years. Initially, though, research is likely to focus on delaying the onset of age-related diseases. “That could solve some real problems,” says Cai.
But since the hypothalamus has an effect on every cell in the body, Maudsley warns that interfering with it could lead to unwanted sequences of events. “You’re playing with fire,” he says.
Journal reference: Nature, 10.1038/nature12143
by Deric Bownds
Soon et al. identified a partial spatial and temporal overlap of choice-predictive signals with activity in the default mode network. The abstract:
Unconscious neural activity has been repeatedly shown to precede and potentially even influence subsequent free decisions. However, to date, such findings have been mostly restricted to simple motor choices, and despite considerable debate, there is no evidence that the outcome of more complex free decisions can be predicted from prior brain signals. Here, we show that the outcome of a free decision to either add or subtract numbers can already be decoded from neural activity in medial prefrontal and parietal cortex 4 s before the participant reports they are consciously making their choice. These choice-predictive signals co-occurred with the so-called default mode brain activity pattern that was still dominant at the time when the choice-predictive signals occurred. Our results suggest that unconscious preparation of free choices is not restricted to motor preparation. Instead, decisions at multiple scales of abstraction evolve from the dynamics of preceding brain activity.
And, a chunk from their discussion:
It is interesting that mental calculation, the more complex task, had less predictive lead time than a simple binary motor choice in our previous study. This could tentatively reflect a general limitation of unconscious processing in the sense that unconscious processes might be restricted in their ability to develop or stabilize complex representations such as abstract intentions. It is also worth noting that both studies showed the same dissociation between cortical regions that were predictive of the content versus the timing of the decision. This implies that the formation of an intention to act depends on interactions between the choice-predictive and time-predictive regions. The temporal profile of this interaction is likely to determine when the earliest choice-predictive information is available and might differ between tasks.
There was a partial spatial overlap between the choice-predictive brain regions and the DMN. Interestingly, the state of the DMN (default mode network) during the early preparatory phase still resembled that during off-task or “resting” periods. This lends further credit to the notion that the preparatory signals were not a result of conscious engagement with the task. Furthermore, the spatial and temporal overlap hints at a potential involvement of the DMN in unconscious choice preparation.
To summarize, we directly investigated the formation of spontaneous abstract intentions and showed that the brain may already start preparing for a voluntary action up to a few seconds before the decision enters into conscious awareness. Importantly, these results cannot be explained by motor preparation or general attentional mechanisms. We found that frontopolar and precuneus/posterior cingulate encoded the content of the upcoming decision, but not the timing. In contrast, the pre-SMA predicted the timing of the decision, but not the content.
Scientists probe the source of a pulsing signal in the sleeping brain
New findings clarify where and how the brain’s “slow waves” originate. These rhythmic signal pulses, which sweep through the brain during deep sleep at the rate of about one cycle per second, are assumed to play a role in processes such as consolidation of memory. For the first time, researchers have shown conclusively that slow waves start in the cerebral cortex, the part of the brain responsible for cognitive functions. They also found that such a wave can be set in motion by a tiny cluster of neurons.
“The brain is a rhythm machine, producing all kinds of rhythms all the time,” says Prof. Arthur Konnerth of the Technische Universitaet Muenchen (TUM). “These are clocks that help to keep many parts of the brain on the same page.” One such timekeeper produces the so-called slow waves of deep sleep, which are thought to be involved in transmuting fragments of a day’s experience and learning into lasting memory. They can be observed in very early stages of development, and they may be disrupted in diseases such as Alzheimer’s.
Previous studies, relying mainly on electrical measurements, have lacked the spatial resolution to map the initiation and propagation of slow waves precisely. But using light, Konnerth’s Munich-based team – in collaboration with researchers at Stanford and the University of Mainz – could both stimulate slow waves and observe them in unprecedented detail. One key result confirmed that the slow waves originate only in the cortex, ruling out other long-standing hypotheses. “The second major finding,” Konnerth says, “was that out of the billions of cells in the brain, it takes not more than a local cluster of fifty to one hundred neurons in a deep layer of the cortex, called layer 5, to make a wave that extends over the entire brain.”
New light on a fundamental neural mechanism
Despite considerable investigation of the brain’s slow waves, definitive answers about the underlying circuit mechanism have remained elusive. Where is the pacemaker for this rhythm? Where do the waves start, and where do they stop? This study – based on optical probing of intact brains of live mice under anesthesia – now provides the basis for a detailed, comprehensive view.
“We implemented an optogenetic approach combined with optical detection of neuronal activity to explore causal features of these slow oscillations, or Up-Down state transitions, that represent the dominating network rhythm in sleep,” explains Prof. Albrecht Stroh of the Johannes Gutenberg University Mainz. Optogenetics is a novel technique that enabled the researchers to insert light-sensitive channels into specific kinds of neurons, to make them responsive to light stimulation. This allowed for selective and spatially defined stimulation of small numbers of cortical and thalamic neurons.
Access to the brain via optical fibers allowed for both microscopic recording and direct stimulation of neurons. Flashes of light near the mouse’s eyes were also used to stimulate neurons in the visual cortex. By recording the flux of calcium ions, a chemical signal that can serve as a more spatially precise readout of the electric activity, the researchers made the slow waves visible. They also correlated optical recordings with more conventional electrical measurements. As a result, it was possible to watch individual wave fronts spread – like ripples from a rock thrown into a quiet lake – first through the cortex and then through other brain structures.
A new picture begins to emerge: Not only is it possible for a tiny local cluster of neurons to initiate a slow wave that will spread far and wide, recruiting multiple regions of the brain into a single event – this appears to be typical. “In spontaneous conditions,” Konnerth says, “as it happens with you and me and everyone else every night in deep sleep, every part of the cortex can be an initiation site.” Furthermore, a surprisingly simple communication protocol can be seen in the slow wave rhythm. During each one-second cycle a single neuron cluster sends its signal and all others are silenced, as if they are taking turns bathing the brain in fragments of experience or learning, building blocks of memory. The researchers view these findings as a step toward a better understanding of learning and memory formation, a topic Konnerth’s group is investigating with funding from the European Research Council. They also are testing how the slow waves behave during disease.
“GB” is a 28 year old man with a curious condition: his optic nerves are in the wrong place.
Most people have an optic chiasm, a crossroads where half of the signals from each eye cross over the midline, in such a way that each half of the brain gets information from one side of space. GB, however, was born with achiasma – the absence of this crossover. It’s an extremely rare disorder in humans, although it’s more common in some breeds of animals, such as Belgian sheepdogs.
Here’s GB and a normal brain for comparison:
Canadian neurologists Davies-Thompson and colleagues describe GB in a new paper using functional neuroimaging to work out how his brain is organized.
In the absence of a left-right crossover, all of the signals from GB’s left eye end up in his left visual cortex, and vice versa. But the question was, how does the brain make sense of it? Normally, remember, each half of the cortex corresponds to half our visual field. But in GB’s brain, each half has to cope with the wholevisual field – twice as much space (even though it’s getting no more signals than normal.)
It turns out that the two halves of space overlap in GB’s visual cortex, as these fMRI results show:
The four colours represent the four quarters of the visual field, and the brain blobs that light up in response to them. Although the bottom and the top of space are separately represented, as they normally are, there’s complete overlap between the areas that respond to bottom-left and bottom-right stimulation, and likewise top-left and top-right. It’s possible that they are separately represented at a smaller scale, however.
Despite this, GB’s vision was remarkably good – he scored around 20/80 vision, one quarter as accurate as a typical person.
This is a fascinating case report, and vision neuroscientists will find much to ponder here. Still, what I’d love to know is how does it feel to have overlapping representations of the two sides of space? Does everything seem to be mirrored vertically? Does GB find it easier to tell objects apart when they’re above and below the other, compared to side-to-side?
Davies-Thompson, J., Scheel, M., Jane Lanyon, L., & Sinclair Barton, J. (2013). Functional organisation of visual pathways in a patient with no optic chiasm Neuropsychologia DOI:10.1016/j.neuropsychologia.2013.03.014
Scientists create phantom sensations in non-amputees
The sensation of having a physical body is not as self-evident as one might think. Almost everyone who has had an arm or leg amputated experiences a phantom limb: a vivid sensation that the missing limb is still present. A new study by neuroscientists at the Karolinska Institutet in Sweden shows that it is possible to evoke the illusion of having a phantom hand in non-amputated individuals.
In an article in the scientific periodical Journal of Cognitive Neuroscience, the researchers describe a perceptual illusion in which healthy volunteers experience having an invisible hand. The experiment involves the participant sitting at a table with their right arm hidden from their view behind a screen. To evoke the illusion, the scientist touches the right hand of the participant with a small paintbrush while imitating the exact movements with another paintbrush in mid-air within full view of the participant.
“We discovered that most participants, within less than a minute, transfer the sensation of touch to the region of empty space where they see the paintbrush move, and experience an invisible hand in that position”, says Arvid Guterstam, lead author of the study. “Previous research has shown that non-bodily objects, such as a block of wood, cannot be experienced as ones own hand, so we were extremely surprised to find that the brain can accept an invisible hand as part of the body.”
The study comprises eleven experiments that explore in detail the illusory experience and include 234 volunteers. To demonstrate that the illusion actually worked, the researchers would make a stabbing motion with a knife towards the empty space ‘occupied’ by the invisible hand and measure the participant’s sweat response to the perceived threat. They found that the participants stress responses were elevated while experiencing the illusion but absent when the illusion was broken.
In another experiment, the volunteers were asked to close their eyes and quickly point with their left hand to their right hand (or to where they perceived it to be). After having experienced the illusion for a while, they would point to the location of the invisible hand rather than to their real hand.
The researchers also measured the brain activity of the participants using functional magnetic resonance imaging (fMRI). Perceiving the invisible hand illusion led to increased activity in the same parts of the brain that are normally active when individuals see their real hand being touched or when participants experience a prosthetic hand as their own.
“Taken together, our results show that the sight of a physical hand is remarkably unimportant to the brain for creating the experience of one’s physical self,” says Arvid Guterstam.
The researchers hope that the results of their study will offer insight into future research on phantom pain in amputees.
“This illusion suggests that the experience of phantom limbs is not unique to amputated individuals, but can easily be created in non-amputees,” says the principal investigator, Dr Henrik Ehrsson, Docent at the Department of Neuroscience. “These results add to our understanding of how phantom sensations are produced by the brain, which can contribute to future research on alleviating phantom pain in amputees.”
Impersonating your younger self makes your body physiologically younger -
by Deric Bownds
An interesting article in the Harvard Magazine describes the life work of Ellen Langer, her demonstrations that our social self image (old versus young, for example) strongly patterns our actual vitality and physiology, her work on Mindfulness, unconscious processing, etc. I recommend that you read the article. Here are some clips from its beginning that hooked me (I actually did my own mini-repeat of the experiment described, a simple self-experiment of pretending that I had been transported back in time to 40 years ago, and convinced myself I was experiencing some of the effects described)…
In 1981, early in her career at Harvard, Ellen Langer and her colleagues piled two groups of men in their seventies and eighties into vans, drove them two hours north to a sprawling old monastery in New Hampshire, and dropped them off 22 years earlier, in 1959. The group who went first stayed for one week and were asked to pretend they were young men, once again living in the 1950s. The second group, who arrived the week afterward, were told to stay in the present and simply reminisce about that era. Both groups were surrounded by mid-century mementos—1950s issues of Life magazine and the Saturday Evening Post, a black-and-white television, a vintage radio—and they discussed the events of the time: the launch of the first U.S. satellite, Castro’s victory ride into Havana, Nikita Khrushchev and the need for bomb shelters.
…Before and after the experiment, both groups of men took a battery of cognitive and physical tests, and after just one week, there were dramatic positive changes across the board. Both groups were stronger and more flexible. Height, weight, gait, posture, hearing, vision—even their performance on intelligence tests had improved. Their joints were more flexible, their shoulders wider, their fingers not only more agile, but longer and less gnarled by arthritis. But the men who had acted as if they were actually back in 1959 showed significantly more improvement. Those who had impersonated younger men seemed to have bodies that actually were younger.
Sound stimulation during sleep can enhance memory
Slow oscillations in brain activity, which occur during so-called slow-wave sleep, are critical for retaining memories. Researchers reporting online April 11 in the Cell Press journal Neuron have found that playing sounds synchronized to the rhythm of the slow brain oscillations of people who are sleeping enhances these oscillations and boosts their memory. This demonstrates an easy and noninvasive way to influence human brain activity to improve sleep and enhance memory.
“The beauty lies in the simplicity to apply auditory stimulation at low intensities—an approach that is both practical and ethical, if compared for example with electrical stimulation—and therefore portrays a straightforward tool for clinical settings to enhance sleep rhythms,” says coauthor Dr. Jan Born, of the University of Tübingen, in Germany.
Dr. Born and his colleagues conducted their tests on 11 individuals on different nights, during which they were exposed to sound stimulations or to sham stimulations. When the volunteers were exposed to stimulating sounds that were in sync with the brain’s slow oscillation rhythm, they were better able to remember word associations they had learned the evening before. Stimulation out of phase with the brain’s slow oscillation rhythm was ineffective.
“Importantly, the sound stimulation is effective only when the sounds occur in synchrony with the ongoing slow oscillation rhythm during deep sleep. We presented the acoustic stimuli whenever a slow oscillation “up state” was upcoming, and in this way we were able to strengthen the slow oscillation, showing higher amplitude and occurring for longer periods,” explains Dr. Born.
The researchers suspect that this approach might also be used more generally to improve sleep. “Moreover, it might be even used to enhance other brain rhythms with obvious functional significance—like rhythms that occur during wakefulness and are involved in the regulation of attention,” says Dr. Born.
Can Meditation Make You a More Compassionate Person?
Scientists have mostly focused on the benefits of meditation for the brain and the body, but a recent study by Northeastern University’s David DeSteno, published in Psychological Science, takes a look at what impacts meditation has on interpersonal harmony and compassion.
Several religious traditions have suggested that mediation does just that, but there has been no scientific proof—until now.
In this study, a team of researchers from Northeastern University and Harvard University examined the effects meditation would have on compassion and virtuous behavior, and the results were fascinating.
THE STUDY
This study—funded by the Mind and Life Institute—invited participants to complete eight-week trainings in two types of meditation. After the sessions, they were put to the test.
Sitting in a staged waiting room with three chairs were two actors. With one empty chair left, the participant sat down and waited to be called. Another actor using crutches and appearing to be in great physical pain, would then enter the room. As she did, the actors in the chair would ignore her by fiddling with their phones or opening a book.
The question DeSteno and Paul Condon – a graduate student in DeSteno’s lab who led the study – and their team wanted to answer was whether the subjects who took part in the meditation classes would be more likely to come to the aid of the person in pain, even in the face of everyone else ignoring her. “We know meditation improves a person’s own physical and psychological wellbeing,” said Condon. “We wanted to know whether it actually increases compassionate behavior.”
MEDITATION WORKS
Among the non-meditating participants, only about 15 percent of people acted to help. But among the participants who were in the meditation sessions “we were able to boost that up to 50 percent,” said DeSteno. This result was true for both meditation groups thereby showing the effect to be consistent across different forms of meditation. “The truly surprising aspect of this finding is that meditation made people willing to act virtuous – to help another who was suffering – even in the face of a norm not to do so,” DeSteno said, “The fact that the other actors were ignoring the pain creates as ‘bystander-effect’ that normally tends to reduce helping. People often wonder ‘Why should I help someone if no one else is?’”
These results appear to prove what the Buddhist theologians have long believed—that meditation is supposed to lead you to experience more compassion and love for all sentient beings. But even for non-Buddhists, the findings offer scientific proof for meditation techniques to alter the calculus of the moral mind.
Decisions – Conscious and Unconscious -
by Janet Kwazniak
Previous experiments have looked at unconscious decision making. A new paper (citation below) confirms those experiments and adds more information.
The authors are looking at the hypothesis that extrastriate and prefrontal neural regions are active during the encoding of decision information and continue to process that information during a subsequent distractor task. “It is possible that reactivation occurring in these extrastriate-hippocampal-dorsolateral prefrontal regions might support continued visual and semantic processing of decision information during an unconscious thought period.” It has been shown by others that a period of unconscious thought can led to better decisions than a period of conscious thought or an immediate decision without a period of thought of either kind, at least with certain types of problem – large, vague, disorganized ones. These researchers confirmed previous results but with fMRI scans to add information on the areas of the brain that were involved.
They used a 2-back memory task as a distractor that made conscious thought on anything but that task impossible. The scans were during: 2-back task alone, 2-back task while making the decision unconsciously, making the decision consciously. The participants first encoded the information need to make the decision and then went on to make the decision consciously or unconsciously. This encoding phase was also scanned.
When the activity associated with the 2-back task was subtracted from the unconscious thought, the remaining activity was in the prefrontal cortex, right thalamus and left frontal operculum. Activity was seen in the left intermediate visual cortex and right dorsolateral prefrontal cortex during encoding and during unconscious thought. The reactivation of the encoding activity predicted the decision-making performance. Neural regions involved in encoding decision information continue to process this information outside of conscious awareness. Conscious thought, on the other hand, had activity in a prefrontal network that did not overlap with any regions active during unconscious thought.
The nature of the unconscious mind has long challenged philosophers and scientists, but the present work offers a new perspective on this topic by way of examining the brain. We find that brain regions that are active during encoding new decision information reactivate while the brain coordinates responses to other unrelated tasks, when participants are prompted to make decisions.
I think it is important to look at the 2-back memory task. This makes very great demands on the working memory and practically no other facility – no arithmetic or logic needed. This is why it works so well at shutting down conscious thought and does not seem to infer with unconscious thought. But this clean division is not likely to be the normal state. Use of working memory, consciousness and unconscious cognition are likely to be active together and in cooperation (except in sleep). What is shown is what unconscious thought is capable of but not how is may be normally used.
Creswell, J., Bursley, J., & Satpute, A. (2013). Neural Reactivation Links Unconscious Thought to Decision Making Performance Social Cognitive and Affective Neuroscience DOI:10.1093/scan/nst004
The Brain Basis of our Superiority Illusion -
by Deric Bownds
One of the most robustly documented findings of psychology is the “optimism” bias, which leads us to put rose-colored glasses on past, future, and our own abilities. (Did you know that a spectacular 94% of college professors rate themselves to have teaching abilities that are above average?.) Equally well documented is the fact the people who have a fully realistic view of their abilities and their importance to groups tend to be depressed. It seems clear that most of us are completely unequipped to function without a vast array of positive delusions about our abilities, our futures, etc.
There is a large literature on this. Dan Dennett and McKay have written a treatise in Brain and Behavioral Science that examines possible evolutionary rationales for mistaken beliefs, bizarre delusions, instances of self-deception, etc., they conclude that only positive illusions meet their criteria for being adaptive. Johnson and his colleagues have produced an evolutionary model suggesting that overconfidence maximizes individual fitness and that populations tend to become overconfident as long as benefits from contested resources are sufficiently large compared with the cost of competition.
Yamada et al. now look at resting state functional connectivity between brain regions whose activity correlates with the superiority illusion. Their abstract, and one figure from their paper:
The majority of individuals evaluate themselves as superior to average. This is a cognitive bias known as the “superiority illusion.” This illusion helps us to have hope for the future and is deep-rooted in the process of human evolution. In this study, we examined the default states of neural and molecular systems that generate this illusion, using resting-state functional MRI and PET. Resting-state functional connectivity between the frontal cortex and striatum regulated by inhibitory dopaminergic neurotransmission determines individual levels of the superiority illusion. Our findings help elucidate how this key aspect of the human mind is biologically determined, and identify potential molecular and neural targets for treatment for depressive realism.
Influence of striatal D2 availability on superiority illusion is mediated through dorsal anterior cingulate - striatal functional connectivity. Assuming an inverse relationship between D2 receptor availability and presynaptic dopamine release, dopamine likely acts on striatal D2 receptors to suppress functional connectivity between the dorsal striatum and dACC (2). This connectivity predicts individual differences in the superiority illusion The indirect effect of striatal D2 receptor availability on the superiority illusion is significantly mediated through dACC-striatal functional connectivity . “+” indicates a positive relationship; “–,” a negative relationship.
Human Astrocytes are Different -
by Janet Kwazniak
Comparing human brains (and to a lesser extent all primate brains) to other animals like the mouse, we have many more, much bigger and much more complex astrocytes. Astrocytes have contributed to our larger brain by an order of magnitude more than neurons have. Astrocytes make contact and ‘surround’ synapses; one human astrocyte can encompasses 2 million synapses. They seem to look over the communication between neurons and are involved in long-term potentiation, the first stage of memory and learning. They release TNFalpha which increases the strength of synaptic transmissions. One human astrocyte makes contact with more synapses because of their bigger size and longer thin fibrils reaching to more distant synapses.
Astrocytes communicate with neighbouring astrocytes through movement of calcium ions. Waves of calcium pass through groups of astrocytes. These waves are faster and more extensive in human astrocytes. So as a communicating group, astrocytes affect the electrical and chemical environment of neuron synapses. And human astrocytes appear to do it better.
So… clever idea – put human astrocytes in mice and see what happens. Xiaoning Han et al (citation below) injected new born mice with human cells destined to become astrocytes. The human cells florished at the expense of the mouse ones, migrated to the right places and intergrated with each other and the mouse astrocytes. But they were the size and complexity that they would have been in a human brain. So the mice ended up with the more numerous, bigger and more connected human astrocytes amongst their own mouse ones. Like in humans the calcium waves were faster and the TNFalpha more potent. That this procedure worked as well as it did is a bit of a surprise.
When the mice were adult they were tested against control mice that had transplants of mouse rather than human astrocytes. The human astrocytes gave significantly better memories and learning. When the TNFalpha was disrupted, the human astrocyte advantage was much reduced.
What can be done with this development?
First, we could think of the brain differently. Last year, I posted what if? One of the imagined shifts of viewpoint was:
“There is a trickle of new results about the function of glial cells (those ignored cells that outnumber the neurons by factors like 10). What if: more of less all the work in the brain was actually done by very local groups of glial cells and neurons functioned like a kind of telephone system between groups of glia.”
Second, we can stop taking the simpler computer metaphors, ones containing only neurons and weighted connections, as a reasonably detailed model of the brain. “We are our connectome” also becomes less believable. The Neuron Theory has taken a little knock – there is more to brain processing then neurons firing.
Thirdly, these mice can be used to study astrocytes using procedures that are possible in animals but not humans.
Fourthly, they would be good systems to study diseases of the astrocytes and even to show whether a disease involves astrocytes or not.
Here is the paper’s summary:
Human astrocytes are larger and more complex than those of infraprimate mammals, suggesting that their role in neural processing has expanded with evolution. To assess the cell-autonomous and species-selective properties of human glia, we engrafted human glial progenitor cells (GPCs) into neonatal immunodeficient mice. Upon maturation, the recipient brains exhibited large numbers and high proportions of both human glial progenitors and astrocytes. The engrafted human glia were gap-junction-coupled to host astroglia, yet retained the size and pleomorphism of hominid astroglia, and propagated Ca 2+ signals 3-fold faster than their hosts. Long-term potentiation (LTP) was sharply enhanced in the human glial chimeric mice, as was their learning, as assessed by Barnes maze navigation, object-location memory, and both contextual and tone fear conditioning. Mice allografted with murine GPCs showed no enhancement of either LTP or learning. These findings indicate that human glia differentially enhance both activity-dependent plasticity and learning in mice.
Han, X., Chen, M., Wang, F., Windrem, M., Wang, S., Shanz, S., Xu, Q., Oberheim, N., Bekar, L., Betstadt, S., Silva, A., Takano, T., Goldman, S., & Nedergaard, M. (2013). Forebrain Engraftment by Human Glial Progenitor Cells Enhances Synaptic Plasticity and Learning in Adult Mice Cell Stem Cell, 12 (3), 342-353 DOI: 10.1016/j.stem.2012.12.015
