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Neuroscience Roi-Girard
Researchers in Cognitive Science. Authors of "La Théorie Sensorielle"
Researchers in Cognitive Science. Authors of "La Théorie Sensorielle"


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When neuroscience meets archaeology.
In the fourth millennium B.C., in the south of Mesopotamia, the Urukeans invented seven remarkable tools: the ard, the normalized brick mould, writing, accounting, the harp, the vertical weaving loom and cone images. These inventions have been found to mirror biological mechanisms which allow sensory organs to perceive the world in which we live and to codify it so as to transmit a representation to the brain. How did man devise such instruments at a time when the functioning of sensory organs was inaccessible to his comprehension and perception? To answer this question, since 1996 Philippe Roi and Tristan Girard have dedicated themselves to writing « La Théorie Sensorielle ». Their research enabled them to discover the existence of ‘Sensorial Analogies’ which establish a logical link between the Urukean inventions and the sensory organs. Through this approach, they have connected knowledge together that had previously been fragmented and compartmentalised in diverse disciplines.
KOBO - -
Analogy -
#Neuroscience #ScienceCognitive #Archaeology #Mesopotamia #Uruk #Inventions #Discovery #Research #Senses #SensorialAnalogies #SensoryOrgans #brain #neurons #knowledge #Uruk #TheorieSensorielle
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5 Ways Technology is Altering our Brains
Technology is changing our brains as well as our lives. If you’re reading this, it’s likely that you’re staring into a screen. Our inability to look away from our tablets, smartphones and social networking platforms is changing the way we process information and perceive the world, according to Adam Alter, author of the new book “Irresistible: The Rise of Addictive Technology and the Business of Keeping Us Hooked.”
In one Gallup Panel survey, 52 percent of smartphone owners reported checking their mobile devices a few times an hour or more. Data confirms that young people are even more wired: More than seven in 10 young smartphone users check their device a few times an hour or more often, and 22 percent admit to looking at it every few minutes.
The digital age is transforming our behavior when we limit our communication to 140 characters and use emojis to express our emotions. When we’re bored, we simply reach for our gadgets.
To mark Brain Awareness Week, here are five ways that modern technology is impacting our brains and our lives.
We have decreased attention spans:
It takes a much shorter time for us to grow bored and move onto the next thing. "Ten years ago, before the iPad and iPhone were mainstream, the average person had an attention span of about 12 seconds," Alter said in an NPR interview this week. Now, he says, "research suggests that there's been a drop from 12 to eight seconds ... shorter than the attention of the average goldfish, which is nine seconds."
We are more easily distracted:
A Microsoft Corp. study surveyed 2,000 participants and studied the brain activity of 112 others using electroencephalograms (EEGs) while they performed several activities across devices. It found that “heavy multi-screeners find it difficult to filter out irrelevant stimuli — they’re more easily distracted by multiple streams of media.” In other words, it’s hard to complete a necessary task when our phone signals in incoming message.
In “The Distracted Mind: Ancient Brains in a High-Tech World,” the authors argue that distraction impacts our productivity, relationships, and ability to learn. They say our brains have not changed much since we were cavemen, yet our ancestors did not have to deal with the vast amounts of digital data inundating our lives.
We can more easily multitask:
The Microsoft report says our ability to multitask has drastically improved in the mobile age. While that may sound like good news, Psychology Today reminds us that, “multitasking, as most people understand it, is a myth that has been promulgated by the ‘technological-industrial complex’ to make overly scheduled and stressed-out people feel productive and efficient.” That’s because performing various activities involving the same type of brain processing isn’t possible; you can’t talk on the phone, read e-mail, send an instant message, and watch YouTube videos all at the same time and still retain information.
We have grown addicted to digital technology:
Admit it; you’ve been tempted to stop working and check your Facebook feed to see how many “likes” you’ve received on your latest post. Similar to chemical dependence, technology and its built-in gratification are hard to resist. We simply can’t stop ourselves from compulsively checking our texts and scrolling down our social media feeds.
“The technology is designed to hook us that way. Email is bottomless. Social media platforms are endless. Twitter? The feed never really ends. You could sit there 24 hours a day and you’ll never get to the end. And so you come back for more and more,” Alter told the New York Times. “We are engineered in such a way that as long as an experience hits the right buttons, our brains will release the neurotransmitter dopamine. We’ll get a flood of dopamine that makes us feel wonderful in the short term, though in the long term you build a tolerance and want more.”
Our ability to socially interact in person is impaired:
It’s a common sight to see two people eating together at a restaurant, but instead of talking to each other they are staring down at their cellphones. The consequences may be worse for children growing up in the digital age. In his book, Alter spells out research that shows kids who spend a lot of time staring at screens rather than engaging with others suffer from an inability to empathize and read social cues.
“When kids are asked to detect people's emotions — happy, sad, angry, surprised — based on nonverbal cues, those who spend a lot of time on tech struggle to decipher one emotion from another at a much higher rate than kids who spend more time interacting in the real world,” Alter said in an interview. "One of the things that happens with our brains is we get used to whatever is the most rapid thing we're experiencing.”
The good news is that there are ways to rely on technology and still have balanced lives. The authors of “The Distracted Mind” and others say we can recalibrate our brains and lead healthier lives with meditation and physical exercise as well as putting down our phones during meals and offline social interactions.
#brain #neuron #neuroscience #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #DNA #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research #BrainCells #pioneer #technology
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Secrets of Secretion
New research explains the inner workings of protein-lipid machinery involved in cell communication
Accurate and timely cell-to-cell communication ensures the integrity and normal function of virtually all organisms. Cells communicate with each other by sending chemical “messages,” a process known as secretion, controlled through a symphony of proteins and lipids working together.
While scientists have gained a relatively good understanding of the roles many proteins play in this process, whether and how they interact with key lipids to control cell secretion has remained largely unknown.
A new study, published April 18 in Neuron, by a team led by Harvard Medical School scientists unravels the inner workings of the relationship between one protein-lipid pair in nerve cells, or neurons.
The findings help solve the long-standing mystery of how secretion happens efficiently and at just the right place to ensure optimal cellular communication and could eventually help elucidate what might go wrong in neurologic and other diseases intimately tied to neuronal secretion, including schizophrenia and autism.
“Cell-to-cell communication—be it between neurons or between other types of cells—is critical to ensuring the integrity of multiple physiological functions, such as cognition, muscle movement and many more,” explained study senior author Pascal Kaeser, assistant professor of neurobiology at Harvard Medical School. “We believe our findings shed much-needed new light on how this process occurs and can help explain what goes awry in a range of diseases.”
Neuronal secretion begins when nerve cells receive a “fire away” signal, a phenomenon known as action potential. When this occurs, lipid-packed bags called vesicles fuse internally with the cell membrane at specialized docking sites known as active zones, located at neuronal synapses, the junctions that connect one neuron to another.
When a neuron gets this “fire away” signal it secretes chemicals within a thousandth of a second, enabling neurons to send messages that induce various sensations or actions, such as pain or muscle movement.
For this to occur, scientists have long known that three things need to occur in perfect synchrony: First, vesicles need to undergo maturation steps, known as docking and priming, that prepare them for rapid fusion. Second, the channels that ferry calcium ions need to be anchored at the docking site. Third, a lipid known as PIP2 must also be present there.
A protein called RIM ensures the first two. However, because PIP2 is present in just a tiny section of the cell membrane, it’s been unclear how it manages to be near the docking site just when it’s needed, especially given the short time scale of vesicle fusion after an action potential.
Suspecting that RIM may also be important for connecting the active zone to PIP2, Kaeser, along with Arthur de Jong, a former postdoctoral fellow in Kaeser’s lab, and their colleagues, investigated whether the pair, in fact, interacts. The researchers examined the sequence of amino acids that make up RIM to see which area might bind to this lipid. Their search landed on a stretch known as the C2B domain.
To test whether this domain is important for secretion, the scientists recorded signal transmission from mouse neurons showing that, indeed, cell-to-cell communication was predicated on a proper connection between RIM C2B and PIP2. This binding didn’t need the influx of calcium from an action potential to take place, suggesting that this protein-lipid pair could be “preassembled” in the cell membrane—a step that might enhance dramatically vesicle fusion after an action potential.
When they removed the C2B domain from RIM in neurons growing in lab dishes, these cells were still capable of releasing some vesicles after the “fire” signal, or action potential. However, the process was extremely inefficient compared to cells with unmodified RIM.
Additional experiments in neurons missing the C2B domain revealed that modified RIM was still present in the active zone and still able to perform its functions for vesicle maturation and anchoring calcium channels, even if it
couldn’t bind PIP2 and trigger vesicles to fuse. However, adding just the C2B domain back into cells didn’t rescue this function—a finding that shows that in order for C2B to work, it must be attached to RIM.
Taken together, Kaeser says, these findings closely tie the function of RIM and its C2B domain with that of PIP2. Given that C2 and RIP2 are present in all known cells that have a secretory function, including those that exude hormones, digestive enzymes, insulin and more. Their interaction, the researchers said, likely represents part of a universal underlying mechanism that allows cells to efficiently release signaling chemicals.
“We think this could be a fundamental principle through which cells connect the protein machinery for fusion with the lipid machinery for fusion,” Kaeser says.
“The more we learn about this process, the better we’ll be able to identify the role it plays in a range of disorders.” #brain #neuron #neuroscience #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #DNA #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research #BrainCells #pioneer
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Your brain gets smaller as you sleep (and you forget things)
Every day, as we learn new things and make new memories, our brains physically swell. And at night, as we sleep, those memories are pruned and our brains shrink a little.
“Maybe you had a girlfriend or boyfriend 20 years ago that you rarely think about. Every night, the memory of that distant partner gets a little bit weaker, a little bit fainter, until it fades away to nothing,” says Dr John Lesku, one of the world’s leading experts on sleep evolution.
Welcome to the new science of sleep – the science of forgetting.
To you, sleep seems utterly essential.
But evolutionary biologists don’t see it that way. To them, sleep is ostensibly pretty dumb.
When an animal sleeps, it is at its most vulnerable – defenceless and unaware. Plus sleep is essentially wasted time when a creature could be eating or mating. “It’s a really bad idea,” says Dr Lesku, who leads a sleep research group at La Trobe University.
Sleep is extraordinarily inefficient, and natural selection has a particular mean streak for inefficiency.
But every animal sleeps. In fact, many of the simplest animals, with neural systems we would not recognise as brains, sleep more than humans.
Roundworms have about 300 neurons and no brain to speak of, and they sleep. Jellyfish have a ‘nerve net’, a ring-shaped set of neurons, and they sleep.
At the Queensland Brain Institute, Associate Professor Bruno van Swinderen is keeping fruit flies up all night.
“We have a mechanical device that just jolts them – we keep them awake all night,” he says.
Flies have about 100,000 neurons in their brain. Humans have something like 100 billion.
“So you’d think humans need more sleep, but a fly needs just as much – if not more,” he says.
If simple, ancient animals like worms, flies and jellyfish need their shut-eye, it suggests sleep evolved very early on in life. And brains are not required (at least, not for all sleep's functions).
“These are brainless animals, sleeping,” says Dr Lesku. “It means the biological target of sleep function is not the brain, as we once thought, but is probably something like a neuron or synapse.”
The military has been trying to find a way to let soldiers go sleepless for days. “But they have never been able to,” says Professor van Swinderen.
Sleep performs something so vital to life neither natural selection nor the military-industrial complex have been able to get rid of it.
The theory scientists have come up with in the last decade to explain this is remarkable.
Humans, like flies, sleep in stages. There is rapid-eye-movement sleep. There is dream sleep. And there is deep sleep.
In 2003, sitting around the lunch table in a break room at the University of Wisconsin, Giulio Tononi and Chiara Cirelli were kicking around a new discovery: if you subject networks of neurons in lab dishes to electrical pulses at 1 hertz, the connections between them seem to weaken.
Wasn’t it remarkable, someone pointed out, that 1 Hz was the exact same speed brain waves slowed to during deep sleep? The two scientists looked at each other. Wasn’t it, indeed?
Their theory, ‘sleep homeostasis’, caused a huge stir when it was published in 2003, in part because it was so weird. A decade later it is now a mainstream theory. Here's how it works.
Every day as the brain is exposed to new stimuli, the connections between the most-used neurons grow physically thicker. As you practice guitar, the connections involved get stronger - and you get better.
We have about one trillion neuron-connections (known as synapses) in our brain. If each were to grow by just 1 per cent a day, “that would be unsustainable – the brain would explode after a couple of days,” says Professor van Swinderen.
Every night during deep sleep, the theory posits, every connection in the brain grows weaker. The brain grows physically smaller. Every night, the memory of your ex-partner grows a little weaker, until one day it is gone.
Every day the most-used connections grow strong, and every night every connection grows weaker. Over time only the most-used connections remain strong. This is why you can learn the guitar – because your brain is freeing up space by forgetting your ex-girlfriends.
Professor van Swinderen studies flies, and Dr Lesku studies, among other beasts, the elegant crested tinamou, a fast-running bird with a head plumage that curls like the eyebrow of an extremely-unimpressed high school teacher.Ethical guidelines prevent researchers from peeling off the skull of sleeping humans to get at the neurons, meaning nearly all such research is done in animals.
So synaptic homeostasis, in humans at least, remains a theory, and a controversial one at that.
And even if it proves true, it only explains one part of sleep’s function. Animals have rapid-eye-movement sleep too. Reptiles even have something that looks a lot like dream-sleep.
Do lizards dream? “It’s impossible to know,” says Professor van Swinderen. “But it sure looks like it.”
#brain #neuron #neuroscience #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #dream #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research #BrainCells #sleep
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UCLA scientists pioneer new method for watching brain cells interact in real time
An advance by UCLA neuroscientists could lead to a better understanding of astrocytes, star-shaped brain cells that are believed to play a key role in neurological disorders like Lou Gehrig’s, Alzheimer’s and Huntington’s diseases.
Reported in Neuron, the new method enables researchers to peer deep inside a mouse’s brain and watch astrocytes’ influence over the communication between nerve cells in real time. The test relies on fluorescence resonance energy-transfer microscopy, or FRET microscopy, a technique that uses light to measure the tiniest of distances between molecules.
The UCLA team focused on astrocytes’ relationship with synapses, the junctions between neurons that enable them to signal each other and convey messages. Neuroscientists have tried for years to measure how astrocytes’ tentacles interact with synapses to perform important brain functions. Until now, however, no one had developed a test suitable for viewing adult brain tissue in living mice.
“We’re now able to see how astrocytes and synapses make physical contact, and determine how these connections change in disorders like Alzheimer’s and Huntington’s diseases,” said Baljit Khakh, the study’s lead author and a professor of physiology and neurobiology at the David Geffen School of Medicine at UCLA. “What we learn could open up new strategies for treating those diseases, for example, by identifying cellular interactions that support normal brain function.”
Khakh’s team sent different colors of light through a lens to magnify objects that are invisible to the naked eye. Using FRET microscopy allowed them to see objects about 100 times smaller than would be viewable using conventional light microscopy. As a result, the researchers could observe how interactions between synapses and astrocytes change over time, as well as during various diseases, in mice.
“We know that astrocytes play a major role in how the brain works and also influence disease,” said Chris Octeau, the study’s first author and a UCLA postdoctoral fellow in physiology. “But exactly how the cells accomplish these tasks has remained murky.”
It had been unclear to scientists how often astrocytes make contact with synapses and how these interactions change during disease or as a result of different types of cellular activity. The UCLA advance should enable scientists to address those questions.
“This new tool makes possible experiments that we have been wanting to perform for many years,” said Khakh, who also is a member of the UCLA Brain Research Institute. “For example, we can now observe how brain damage alters the way that astrocytes interact with neurons and develop strategies to address these changes.”
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Image : A new method enables scientists to see an astrocyte (green) physically interacting with a synapse (red) in real time, and producing an optical signal (yellow) ©Khakh Lab/UCLA Health.
#brain #neuron #neuroscience #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #DNA #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research #BrainCells #pioneer
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Adult human brains don’t grow new neurons in hippocampus, contrary to prevailing view.
When our recent study met significant skepticism, we weren’t surprised. After all, we ourselves remained skeptical of what we were seeing throughout our investigation. But repeated and varied experiments convinced us our conclusions were correct: New brain cells don’t grow (or are extremely rare) in the adult human hippocampus, a region important for learning and memory. The birth of new neurons in human memory circuits, in other words, declines during childhood to undetectable levels in the adult.
Our research findings sparked healthy debate because for about 20 years, brain scientists have thought that neurons continue to be born in the adult human hippocampus. The question of whether and how new neurons are born in adults is important for understanding how our brains adapt to changing life circumstances and how we might be able to repair brain injury. Science advances with the collection of more evidence that helps refine and revise theories. As neuroscientists, we too are adjusting our ideas of how adult human learning must work in light of our recent study.
Adult neurogenesis: Animal models to humans
One of us, Arturo, has been studying how new neurons are born and integrated into brain circuits since the 1980s. He was a member of Fernando Nottebohm’s lab at Rockefeller University, which was at the time producing a groundbreaking series of papers showing that the brains of songbirds produce new neurons each season as they get ready to learn new songs. Earlier research from the 1960s had found evidence that rodent brains produce new neurons during adulthood, but this idea remained highly controversial until Nottebohm’s songbird studies convinced most neuroscientists that adult brains could make new neurons.
Since then, several studies have found signs of new neurons in the adult human hippocampus, leading many researchers to accept that this part of the brain could renew itself throughout life in people too. The idea stimulated interest in figuring out how to increase this regenerative capacity and perhaps stave off age-related declines in brain function.
In fact, we began our own search for newborn neurons in the adult human hippocampus because previous human studies had estimated 700 new cells are born in the adult hippocampus per day. We wanted to contrast this with another region of the brain where we had recently reported finding far fewer new neurons than seen in other animals.
Compiling evidence to prove a negative
The first sign that something different might be occurring came when Arturo visited the lab of our collaborator Zhengang Yang at Fudan University in China to study several well-preserved human brain specimens. They were not able to detect any new neurons in the adult hippocampus at all.
When Arturo returned from China to our lab and shared with Mercedes and Shawn the observation that new neurons were missing from the adult human hippocampus, we were faced with a challenge: How do you prove a negative? How could we be sure that we weren’t just missing the new neurons that other studies had seen?
As some critics have pointed out, identifying new neurons in human brain tissue is complicated. Typically, researchers look for the presence of certain proteins that we know are produced by young neurons. But we were looking at donated brain samples from dead people; maybe these “identifier” proteins degrade after death. They may also have other roles and be produced by other kinds of cells.
So we needed to use multiple approaches to look for new neurons. First we examined several different proteins that are present in young neurons. We next studied the cells closely with high-resolution light and electron microscopes. We wanted to be sure that any cell we would report would have the distinctive appearance of young neurons; they tend to have a simpler shape that differentiates them from mature neurons, which are usually bigger with long, elaborate branches. We also looked at overall patterns of gene expression in this region and observed a similar decline in genes associated with young neurons. In addition, we looked for evidence of the stem cells that make young neurons, which have their own protein markers and can be detected when they divide. None of the adult hippocampal tissue we examined with these techniques showed evidence of young neurons or their dividing stem cell parents.
To make sure that our techniques were even capable of detecting young neurons or dividing neural stem cells, we looked at the same region of the hippocampus before birth, when we knew they should be present. In these fetal brain samples, we clearly saw plentiful new neurons. Using the same techniques, we then looked for these cells in brain tissue from people who died in infancy, childhood or early adolescence. We saw the number of new neurons sharply declined until few remained by the age of 13; by 18 and 19 years, we could not find any. If neurogenesis continues in the adult human hippocampus, it is a very rare phenomenon.
Could our inability to see these cells be due to unknown differences between young and old brain tissue? We knew that there are very rare young neurons in other parts of the adult human brain, so we looked in those regions. When we readily found those rare young neurons, we became more confident that what we were seeing, or not seeing, in the hippocampus was not simply an artifact of aging brain tissue.
Could something about the patients’ history prior to death, or the way the samples had been collected have obscured evidence of new neurons that had been present when the brains had been alive? To convince ourselves that the tissue was as representative of adult brains as possible, we studied brains collected by many different collaborators around the world and saw the same results.
Could the time between death and preservation of the brains lead to our inability to detect young neurons? To test this, we collected more than a dozen tissue samples from patients who were having brain tissue removed as part of surgical treatment for severe epilepsy. These are samples we collected and preserved quickly to maximize their quality. In addition, we looked at two samples where the brains had been collected and preserved almost immediately at the time of death and saw the same results.
In total we examined 59 brains, a collection comparable to previous studies. In all these cases, we saw the same results: no signs of new neurons in the adult hippocampus. We concluded that if new neurons are being born in the adult human hippocampus, they are extremely rare.
So what have other researchers seen that made them believe that new neurons are born in the adult human hippocampus? Previous studies frequently used only a single protein to identify new neurons. Unfortunately, we found that the most common protein used to do this, one called doublecortin, can also be seen in non-neuronal brain cells (called glia) that are known to regenerate throughout life.
One other research group tried a different technique more commonly used by archaeologists and geologists: carbon-14 dating. This is a very creative way to determine the age of cells, especially in a field where we need new ways to study the human brain. However, it’s not clear how precisely this method can identify neurons or if there are other reasons the radioactive carbon levels might change beyond the cell division that would lead to new neurons.
Left with plenty more to investigate
Our research left us with the lingering question – why does this decline in neurogenesis happen? Why does the hippocampus continue to create new neurons into adulthood in other animals, but not in the human?
To wrap our heads around this question, we examined the hippocampus of macaque monkeys, which are known to continue producing new neurons into adulthood. Using labeling techniques that are not typically possible in humans for ethical reasons, we tracked the generation of new neurons in living animals. We discovered that the neural stem cells that generate new neurons coalesce into a ribbon-like layer in the monkey hippocampus before birth. This layer was present and contained dividing cells even in juvenile monkeys. When we looked back at our data from the newborn human hippocampus we saw that the stem cells did not organize themselves in this fashion – a clear developmental difference between human brains and those of other primates.
Our study only pertains to the hippocampus; many other brain regions in the human brain – which is very big – have not been investigated and remain to be explored for the possible presence of new neurons. The development of better methods to directly study the human brain will help researchers understand more about how plasticity occurs in the human hippocampus. And future research can work to determine if there are ways to reignite the birth of new neurons in this region.
But what does our finding mean? Should we lament the lack of new neurons in the adult human hippocampus? We think not.
First, the process of making a new neuron is fascinating and is already teaching us many new things. Adult neurogenesis should continue to be an area of study in birds, mice, rats and other species where it occurs. One day this work might teach us how to induce it in the human brain.
Second, our brains operate for decades – much longer than the mouse brain, despite the rodent’s plentiful new neurons. Indeed, the long lives of humans may be linked to the decline in hippocampal neurogenesis; we might run out of progenitors in childhood.
Our work also raises new questions – clearly a rich and healthy lifestyle does improve our brain function and hold back the decline of age, even without new neurons. Developing a deeper understanding of human brain development may yet provide new treatments and therapies for brain diseases of aging.
Image : The hippocampus is the red structure in the interior of the brain (source Wikipedia)
#memory #learning #neuroscience #brain #hippocampus #neurogenesis #BrainDevelopment #Neurons #Neuron #neurobiology #cells #HumanBrain #plasticity #neurology #interaction #memories #discovery #BrainCells #research #TheorieSensorielle

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What magic has taught us about how the brain works
Magicians don’t have supernatural powers after all, but they are experts at exploiting powerful and surprising limitations in human cognition. They’re now sharing their secrets with scientists to study how the brain works.
Jay Olson, a former professional magician, now studies psychiatry at Montreal’s McGill University and is featured in the documentary, The Science of Magic : “We’re trying to find these pieces of knowledge that magicians have, that as psychologists, we don’t understand. We bring them into the lab and try to figure out how they work.”
Magician’s force is powerful
Using ‘‘magician’s force”, these tricksters influence our decision-making process to steer the choices we make — like when we select a card from a deck. Olson took to the streets and found that 98% of people chose the card he influenced them to choose and 91% of them say they felt like they made a free choice. He and others who are working in this new field are providing fresh insights into how the brain works.
Here are some concepts that magicians reveal to us in The Science of Magic.
Often we can’t see obvious things that are right in front of us. Most magic involves a lot of appearing and disappearing and scientific research has shown us how easily magicians are able to trick us.
Our eyes can only see clearly in the centre area of our visual field. This means we can only really see one thing at a time. To see more objects in our environment, we actually have to move our eyes around a couple of times a second. But each time we move them, our brain needs to attend to something new creating a lag of about 1/10 of a second. Our brain fills in those gaps based on what it expects will happen.
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#brain #magic #neuron #neuroscience #magician #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #DNA #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research #conjuror #enchanter #magus #HarryPotter #fantastic #magie #magicien

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New neurons in the adult brain are involved in sensory learning
Although we have known for several years that the adult brain can produce new neurons, many questions about the properties conferred by these adult-born neurons were left unanswered. What advantages could they offer that could not be offered by the neurons generated shortly after birth?
Scientists from the Institut Pasteur and the CNRS have demonstrated that the new neurons produced in adults react preferentially to reward-related sensory stimuli and help speed up the association between sensory information and reward. Adult-born neurons therefore play an important role in both the identification of a sensory stimulus and the positive value associated with that sensory experience. The neurons generated shortly after birth are unable to perform this function.
These findings are published in the Proceedings of the National Academy of Sciences (PNAS) on February 19, 2018.
Although most neurons are generated during embryogenesis, some brain regions in mammals are capable of constantly regenerating their neurons in adulthood. The existence of these adult-born neurons has been proven, but many questions about their function and the way in which they integrate into their target areas remain unanswered.
Research carried out by the Perception and Memory team (Institut Pasteur/CNRS), directed by Pierre-Marie Lledo, a CNRS Director of Research, has recently revealed the specific role of these neurons produced in the adult brain. This study demonstrates that assigning positive values to sensory experiences is closely based on the activity of adult-born neurons, and not the neurons formed shortly after birth. It is these new neurons that may enable individuals to anticipate the delivery of a reward.
The scientists focused on the production of new neurons in adult mice, in particular those neurons that integrate into the olfactory bulb, the brain region responsible for analyzing odors. These new neurons are thought to play a major role in providing flexibility for learning and memorizing olfactory sensory experiences.
The scientists from the Institut Pasteur and the CNRS observed that the new neurons were able to react differently to an odor depending on the consequences associated with that sensory experience, such as whether or not there would be a reward. They also demonstrated that olfactory learning, in which the mice had to associate an odor with positive reinforcement, became easier once the new neurons had been activated. Finally, simply activating these adult-born neurons could be assimilated with a reward-predicting odor.
In short, this research shows that adult-born neurons are involved in the value associated with sensory stimuli rather than just the identification of the nature of a given sensory stimulus. It demonstrates that reward-motivated learning depends largely on adult neurogenesis.
Transferred to humans, these findings could improve our understanding of the role played by new neurons in the adult hippocampus in associative learning processes.
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Story Source : Materials provided by Institut Pasteur. Note : Content may be edited for style and length.
#brain #neuron #neuroscience #neurobiology #dendrites #cells #DendriticSpines #HumanBrain #plasticity #neurology #DNA #interaction #learning #memory #memories #discovery #synapses #SynapticTransmission #BrainCells #research
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Researchers invent tiny, light-powered wires to modulate brain's electrical signals
The human brain largely remains a black box: How the network of fast-moving electrical signals turns into thought, movement and disease remains poorly understood. But it is electrical, so it can be hacked—the question is finding a precise, easy way to manipulate electrical signaling between neurons.
A new University of Chicago study shows how tiny, light-powered wires could be fashioned out of silicon to provide these electrical signals. Published Feb. 19 in Nature Nanotechnology, the study offers a new avenue to shed light on—and perhaps someday treat—brain disorders.
Ten years ago, the science world was alive with speculation about a recently discovered technique called optogenetics, which would manipulate neural activity with light. The problem is that it has to be done with genetics: inserting a gene into a target cell that would make it respond to light. Other ways of modulating neurons have since been suggested, but a perfect alternative remains elusive.
A team led by Asst. Prof. Bozhi Tian built minuscule wires previously designed for solar cells. These nanowires are so small that hundreds of them could sit side by side on the edge of a sheet of paper—putting them on the same scale as the parts of cells they’re trying to communicate with.
These nanowires combine two types of silicon to create a small electrical current when struck by light. Gold, diffused by a special process onto the surface of the wire, acts as a catalyst to promote electrochemical reactions.
“When the wire is in place and illuminated, the voltage difference between the inside and outside of the cell is slightly reduced. This lowers the barrier for the neuron to fire an electrical signal to its neighboring cells,” Tian said.
The team tested the approach with rat neurons grown in a lab, and saw they could indeed trigger neurons to fire these electrical signals.
“The nice thing about it is that both gold and silicon are biologically compatible materials,” said graduate student Ramya Parameswaran, the first author on the study. “Also, after they’re injected into the body, structures of this size would degrade naturally within a couple of months.”
“It’s a fundamental but very promising approach,” Tian said. They plan next to test the system in animals, which could both help researchers further understand how these electrical signals work in the brain as well as suggest ways to address problems like Parkinson’s disease or psychiatric disorders.
The other co-authors were Francisco Bezanilla, the Lillian Eichelberger Cannon Professor of Biochemistry and Molecular Biology; Erin Adams, the Joseph Regenstein Professor of Biochemistry and Molecular Biology; graduate students John Zimmerman (now at Harvard), Kelliann Koehler, Yuanwen Jiang and Andrew Phillips; postdoctoral researchers Jaeseok Yi and João Carvalho-de-Souza; and undergraduate student Michael Burke.
Source : “Photoelectrochemical modulation of neuronal activity with free-standing coaxial silicon nanowires.” Nature Nanotechnology, Parameswaran et al, Feb. 19, 2018. DOI 10.1038/s41565-017-0041-7.
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