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Neuroscience Roi-Girard
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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 - https://store.kobobooks.com/fr-fr/ebook/la-theorie-sensorielle  
AMAZON.fr - http://www.amazon.fr/theorie-Sensorielle-arch%C3%A9ologie-perception-sensorielle/product-reviews/1622874854/ref=dpx_acr_txt?showViewpoints=1
Analogy - http://www.theoriesensorielle.com/analogy-between-the-urukean-harp-and-the-auditory-system/                    
#Neuroscience #ScienceCognitive #Archaeology #Mesopotamia #Uruk #Inventions #Discovery #Research #Senses #SensorialAnalogies #SensoryOrgans #brain #neurons #knowledge #Uruk  
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Neanderthal genes still influencing health and the brain activity today
(Traduction française en bas de page)
New Scientist reports that a recent genetic study shows that Neanderthal DNA that survives in people of non-African descent is still controlling how some genes work. University of Washington geneticist Joshua Akey led a team that did a comprehensive DNA analysis of 214 Americans of European ancestry, and was able to isolate Neanderthal genes that were active in 52 kinds of tissue. In some cases, individuals had both a human and Neanderthal copy of a gene, and the team could compare the copies and find which variant controlled gene expression. They found that in the case of one gene that is a known risk factor for schizophrenia, the Neanderthal DNA controls the gene in such a way that it reduces the risk of developing the disease. “Strikingly, we find that Neanderthal sequences present in living individuals are not silent remnants of hybridization that occurred over 50,000 years ago, but have ongoing, widespread, and measurable impacts on gene activity,” says Akey. In other genes, such as ones that regulate brain activity, the influence of Neanderthal DNA is much less pronounced.
http://www.archaeology.org/news/5332-170224-neanderthal-genes-still-control-expression
Les gênes de neandertal influencent toujours la santé aujourd'hui
New Scientist rapporte qu'une récente étude génétique montre que l'ADN néandertalien qui survit chez les personnes de descendance non africaine contrôle encore la façon dont certains gènes fonctionnent. Le généticien de l'Université de Washington Joshua Akey a dirigé une équipe qui a effectué une analyse complète de l'ADN de 214 Américains d'ascendance européenne et a été en mesure d'isoler les gènes de Neandertal qui étaient actifs dans 52 types de tissus. Dans certains cas, les individus avaient à la fois une copie d'un gène Homo Sapiens- Sapiens et une copie d'un gène Néandertalien. Ainsi l'équipe a pu comparer les copies et trouver quelques variantes qui contrôlaient l'expression des gènes. Ils ont constaté que dans le cas d'un gène qui est un facteur de risque connu pour la schizophrénie, l'ADN de Neandertal le contrôlait de telle manière qu'il réduisait le risque de développer cette maladie. "Il est frappant de constater que les séquences néandertaliennes présentes chez les individus vivants ne sont pas des vestiges silencieux d'hybridation qui se sont produits il y a plus de 50 000 ans, mais qu'elles ont des impacts continus, étendus et mesurables sur l'activité génétique", explique Akey. Dans d'autres gènes, tels que ceux qui régulent l'activité cérébrale, l'influence de l'ADN néandertalien est beaucoup moins prononcée.
#CognitiveArchaeology #Archaeology #Neanderthal #DNA #Human #HomoSapiensSapiens #HumanBody #biology #Study #genetic #schizophrenia #archéologie #ADN #humain #gènes #génétique

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ARTIFICIAL SYNAPSE BRIDGES THE GAP TO BRAINIER COMPUTERS
The human brain is nature's most powerful processor, so it's not surprising that developing computers that mimic it has been a long-term goal. Neural networks, the artificial intelligence systems that learn in a very human-like way, are the closest models we have, and now Stanford scientists have developed an organic artificial synapse, inching us closer to making computers more efficient learners.
In an organic brain, neuronal cells send electrical signals to each other to process and store information. Neurons are separated by small gaps called synapses, which allow the cells to pass the signals to each other, and every time that crossing is made, that connection gets stronger, requiring less energy each time after. That strengthening of a connection is how the brain learns, and the fact that processing the information also stores it is what makes the brain such a lean, mean, learning machine.
Neural networks model this on a software level. These AI systems are great for handling huge amounts of data, and like the human brain that inspired them, the more information they're fed, the better they become at their job. Recognizing and sorting images and sounds are their main area of expertise at the moment, and these systems are driving autonomous cars, beating humanity's best Go players, creating trippy works of art and even teaching each other. The problem is, these intelligent software systems are still running on traditional computer hardware, meaning they aren't as energy efficient as they could be.
"Deep learning algorithms are very powerful but they rely on processors to calculate and simulate the electrical states and store them somewhere else, which is inefficient in terms of energy and time," says Yoeri van de Burgt, lead author of the study. "Instead of simulating a neural network, our work is trying to make a neural network."
So the team set about building a physical, artificial synapse that mimics the real thing by processing and storing information simultaneously. Based on a battery and working like a transistor, the device is made up of two thin films and three terminals, with salty water acting as an electrolyte between them. Electrical signals jump between two of the three terminals at a time, controlled by the third.
_First, the researchers trained the synapse by sending various electric signals through it, to figure out what voltage they need to apply to get it to switch into a certain electrical state. Digital transistors have two states – zero and one – but with its three terminal layout, the artificial synapse is capable of having up to 500 different states programmed in, exponentially expanding the computational power it could be capable of.
Better still, switching between states takes a fraction of the energy of other systems. That's still not in the ballpark of a brain – the artificial synapse uses 10,000 times the energy of a biological one – but it's a step in the right direction, and with further testing in smaller devices, the researchers hope to eventually improve that efficiency.
"More and more, the kinds of tasks that we expect our computing devices to do require computing that mimics the brain because using traditional computing to perform these tasks is becoming really power hungry," says A. Alec Talin, senior author of the study. "We've demonstrated a device that's ideal for running these type of algorithms and that consumes a lot less power."
While only one artificial synapse has been built so far, the team ran extensive experiments on it, and extrapolated the data gathered to simulate how an array of artificial synapses could process information. Making use of the visual recognition skills of a neural network, the researchers tested its ability to identify handwritten numbers – 0 to 9 – in three different styles, and found that the system could recognize the digits up to 97 percent of the time.
Earlier examples of artificial synapses, like that from USC in 2011, were not only less powerful, but weren't made completely from organic materials. Composed mostly of hydrogen and carbon and running on the same voltages as human neurons, the Stanford synapse could eventually integrate with biological brains, opening up the possibility of devices that can be more directly controlled by thought, like prosthetics and brain-machine interfaces.
The next step for the researchers is to test the simulated results by producing a physical array of the artificial synapses.
The research was published in the journal Nature Materials.
Source: Stanford University
http://newatlas.com/artificial-synapse-mimic-human-brain/48088/
#Brain #ArtificialIntelligence #learning #StanfordUniversity #IA #neuroscience #SynapticTransmission #neurology #cells #medicine #neurons #synapses #BrainCells #cortex #research #discovery #learning #behavior #memories #ManipulatingBrain #MedicalResearch #BrainActivity #neurotransmitters #studies #NatureNeuroscience
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Researchers uncover brain circuitry central to reward-seeking behavior
The prefrontal cortex, a large and recently evolved structure that wraps the front of the brain, has powerful "executive" control over behavior, particularly in humans. The details of how it exerts that control have been elusive, but UNC School of Medicine scientists, publishing today in Nature, have now uncovered some of those details, using sophisticated techniques for recording and controlling the activity of neurons in live mice.
The UNC scientists, led by Garret Stuber, PhD, associate professor in UNC's departments of psychiatry and cell biology & physiology, examined two distinct populations of prefrontal neurons, each of which project to a different brain region outside the cortex. The researchers found that as mice learn to associate a particular sound with a rewarding sugary drink, one set of prefrontal neurons becomes more active and promotes what researchers call reward-seeking behavior - a sign of greater motivation. By contrast, other prefrontal neurons are silenced in response to the tone, and those neurons act like a brake on reward-seeking.
"We've known that there are a lot of differences in how prefrontal neurons respond to stimuli, but nobody has really been able to map these differences onto the intrinsic wiring of the brain," said Stuber, senior author of the study and member of the UNC Neuroscience Center.
Stuber and colleagues obtained their findings with the use of three sophisticated and relatively new neuroscience tools: deep-brain two-photon imaging, optogenetics, and genetic techniques for labeling neurons by their projection targets in the brain. The successful combination of these tools heralds their future common use in defining the pathways and functions of many other brain networks to help uncover the roots of both normal and abnormal behavior.
The study, conducted by first authors and UNC postdoctoral fellows James Otis, PhD, and Vijay Namboodiri, PhD, focused on the dorsomedial (upper-middle) prefrontal cortex, or dmPFC.
"This region is critical for reward processing, decision making, and cognitive flexibility among other things, but how distinct populations of neurons within dmPFC orchestrate such phenomena were unclear," Stuber said.
Stuber and colleagues examined how the activity of dmPFC neurons changes during a Pavlovian reward-conditioning process. In this process, mice learn to associate an auditory tone with a taste of sugary liquid until the tone itself is enough to make the animals start licking around their mouths in anticipation.
"This simple experiment models a learning phenomenon that occurs in lots of different brain regions," Stuber said. "It is critical for motivation and decision making, and of course it can go awry in drug and food addiction, depression, and other neuropsychiatric disorders."
As the mice in the experiment learned to associate the tone with the sweet drink, the researchers found that a subset of the mouse dmPFC neurons became increasingly excited when the tone sounded, whereas another subset went increasingly silent. The researchers were able to observe this phenomenon by using a deep-brain version of two-photon imaging, a technique in which a microscope visualizes hundreds of brain cells simultaneously in mice that are awake and able to perform some ordinary behaviors.
The dmPFC is known to output many of its chemical signals to two other brain regions, the nucleus accumbens (NAc) and the paraventricular nucleus of the thalamus (PVT), both of which are considered important for reward-directed behavior. Stuber's team found that the NAc-projecting neurons in the dmPFC were the ones that became increasingly excited by the tone, and the PVT-projecting neurons were the ones that became increasingly suppressed. The two sets of neurons turned out to be physically separate within the dmPFC only by a few hundred micrometers.
The team then used optogenetic techniques to artificially drive the activities of these neurons. Optogenetics allows researchers to use beams of light to activate specific populations of neurons. Driving the NAc-projecting neurons caused the mice to anticipate their sweet reward more intensely, with more licks after the tone. By contrast, driving the PVT-projecting neurons muted that anticipatory, reward-seeking behavior.
The findings represent a basic demonstration of how the dmPFC has evolved anatomically distinct neuronal populations that have functionally distinct control over behavior, Stuber said. And the discovery points to the existence of similar combinations of control mechanisms elsewhere in the brain.
https://medicalxpress.com/news/2017-02-uncover-brain-circuitry-central-reward-seeking.html
Image - Green: NAc-projecting prefrontal cortex neurons become active during the presentation of a reward-predictive cue, and this activity drives reward-seeking behavior. Purple: PVT-projecting prefrontal cortex neurons inhibited during reward-predictive cue. Credit: The Stuber Lab (UNC School of Medicine)
#neuroscience #brain #cells #heart #neuron #HumanBrain #plasticity #SynapticTransmission #neurology #cells #medicine #neurons #synapses #BrainCells #cortex #research #discovery #learning #behavior #memories #ManipulatingBrain #MedicalResearch #BrainActivity #neurotransmitters #studies #NatureNeuroscience

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Discovery : A new brain mechanism hiding in plain sight.
Researchers have discovered a brand new mechanism that controls the way nerve cells in our brain communicate with each other to regulate learning and long-term memory.
The fact that a new brain mechanism has been hiding in plain sight is a reminder of how much we have yet to learn about how the human brain works, and what goes wrong in neurodegenerative disorders such as Alzheimer's and epilepsy.
"These discoveries represent a significant advance and will have far-reaching implications for the understanding of memory, cognition, developmental plasticity, and neuronal network formation and stabilisation," said lead researcher Jeremy Henley from the University of Bristol in the UK.
"We believe that this is a groundbreaking study that opens new lines of inquiry which will increase understanding of the molecular details of synaptic function in health and disease."
The human brain contains around 100 billion nerve cells, and each of those makes about 10,000 connections - known as synapses - with other cells.
That's a whole lot of connections, and each of them is strengthened or weakened depending on different brain mechanisms that scientists have spent decades trying to understand.
Until now, one of the best known mechanisms to increase the strength of information flow across synapses was known as LTP, or long-term potentiation.
LTP intensifies the connection between cells to make information transfer more efficient, and it plays a role in a wide range of neurodegenerative conditions - too much LTP, and you risk disorders such as epilepsy, too little, and it could cause dementia or Alzheimer's disease.
As far as researchers were aware, LTP is usually controlled by the activation of special proteins called NMDA receptors.
But now the UK team has discovered a brand new type of LTP that's regulated in an entirely different way.
After investigating the formation of synapses in the lab, the team showed that this new LTP mechanism is controlled by molecules known as kainate receptors, instead of NMDA receptors.
"These data reveal a new and, to our knowledge, previously unsuspected role for postsynaptic kainate receptors in the induction of functional and structural plasticity in the hippocampus," the researchers write in Nature Neuroscience.
This means we've now uncovered a previously unexplored mechanism that could control learning and memory.
"Untangling the interactions between the signal receptors in the brain not only tells us more about the inner workings of a healthy brain, but also provides a practical insight into what happens when we form new memories," said one of the researchers, Milos Petrovic from the University of Central Lancashire.
"If we can preserve these signals it may help protect against brain diseases."
Not only does this open up a new research pathway that could lead to a better understanding of how our brains work, but if researchers can find a way to target these new pathways, it could lead to more effective treatments for a range of neurodegenerative disorders.
It's still early days, and the discovery will now need to be verified by independent researchers, but it's a promising new field of research.
"This is certainly an extremely exciting discovery and something that could potentially impact the global population," said Petrovic.
The research has been published in Nature Neuroscience.
http://www.sciencealert.com/we-just-found-evidence-neurons-can-communicate-in-a-way-we-never-anticipated
#neuroscience #brain #cells #heart #neuron #HumanBrain #plasticity #SynapticTransmission #neurology #cells #medicine #neurons #synapses #BrainCells #cortex #research #discovery #learning #behavior #memories #ManipulatingBrain #MedicalResearch #BrainActivity #neurotransmitters #studies #NatureNeuroscience
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Neuroscience: desperately seeking sensation: fear, reward, and the human need for novelty.
Why are some people drawn to intense, even fear-inducing thrills while others shun the mere thought? How is it that the same horror movie can be entertainment to one person and tension-filled torture to another? Is something different going on in the brains of these people?
Sensation-seeking, the tendency to seek out novel experiences, is a general personality trait that has been extensively studied in psychological research, but neuroscience is just beginning to take aim at it. Beyond understanding why one person relishes the fright factor while the next studiously avoids it, scientists are asking how sensation-seeking relates to substance abuse, addiction, and anxiety disorders like Post-Traumatic Stress Disorder, areas where the clinical and public-health implications are most clear.
Some studies suggest that people who seek out high-sensation experiences even at great personal risk—so-called high-sensation seekers—are more vulnerable to drug and alcohol abuse and more likely to engage in other risky behaviors, such as sex with multiple partners. The hope is that by understanding the neural mechanisms underlying such behaviors, both at the molecular level and at the systems level, it might be possible to develop pharmacological or behavioral therapies to prevent or treat addiction or help people channel their taste for adventure toward safer pursuits.
Neuroscience is beginning to tease apart how the brain of a high-sensation seeker might be different from that of someone who generally avoids risk. Recent brain imaging studies have offered some intriguing clues, finding a direct link between the size of the hippocampus and experience-seeking behaviori and shedding light on how the brain responds differently to intense or arousing stimuli in highs vs. lows.
In a study using functional MRI,ii Jane Joseph, Ph.D., and colleagues at the University of Kentucky found that different brain areas are activated in high- vs. low-sensation seekers in response to strongly arousing stimuli. The subjects viewed emotionally arousing pictures—some intensely arousing, others more neutral—while researchers recorded their brain activity. Regardless of whether the pictures were pleasant (e.g., mild erotica) or unpleasant (e.g., a snake poised to strike), the high-sensation seekers showed early and strong activation in the insula. (See Figure 1a.) This brain structure acts in part as a gateway where visceral signals from the body are first received and interpreted by the brain, Joseph says, so it made sense to her team that it was active in high-arousal states.
In contrast, in the low-sensation seekers, insula activity barely rose above baseline levels. (See Figure 1b.) Instead, there was pronounced early activity in the anterior cingulate, a part of the cortex strongly linked to the regulation of emotions (and many other things). In high-sensation seekers, anterior cingulate activation was delayed in relation to the lows, though it eventually reached a similar peak.
These patterns are consistent, the researchers said, with an overactive “approach” system in high-sensation seekers and a stronger emotional-inhibitory response in low-sensation seekers.
As with any brain imaging study, the findings are correlational, and Joseph was careful not to draw conclusions at this point. One hypothesis her team will explore further is that, in lows, the anterior cingulate may be, in effect, putting the brakes on any “arousal” response in the insula. “If you look at the data, you can see that the insula response in the lows starts to rise, just as in the highs, but then the anterior cingulate kicks in and almost seems to deflect the insula response in the low-sensation seekers,” Joseph said.
Sensation-seeking also intersects with the fear system. Individual differences in how the brain responds to fear, balanced with how it is wired for reward, may help explain differences in sensation-seeking.
“There is clearly a component of excitement and novelty involved in thrill-seeking, but there is also likely to be a component of worry and fear,” says Kerry Ressler, M.D., Ph.D., a neurobiologist and psychiatrist at Emory University and a member of the Dana Alliance for Brain Initiatives. He points out that the amygdala, the brain region most associated with fear processing, is the same region involved in addictive and appetitive behaviors.
"Each of us, based on our genetic make-up and environmental influences, has different propensities for being drawn toward something that is attractive and appetitive, and on the opposite side, being averse to things that are dangerous or fearful,” Ressler says. “My guess is that the difference between a thrill-seeking person and someone who is not is probably a combination of the level of reward they get from novelty, thrill, or adventure and how much they’re afraid of it."_
It’s possible, for example, that high-sensation seekers may have a lower set-point for fear extinction—meaning they can more easily turn off, or at least tamp down, the physiological response to a fearful event. They may be able to more effectively engage cognitive brain regions to put a fearsome stimulus into proper context, which is pertinent to some activities.
“Thrill-seekers may be able to use cognitive parts of the brains to recognize that the scary movie or ride isn’t really going to hurt them,” Ressler says. “They can put the brakes on the flight and avoidance response and experience the emotional salience of the fear.”
This may be one reason frightening films are so popular, Zuckerman notes. “People who would never engage in high-risk activities themselves get vicarious excitement from movies,” he says. “They know that the [monsters] aren’t going to jump out of the screen and get them, so they get a little kick of fear in a safe environment.”
In an interview included on the DVD release of the horror flick The Grudge, Joseph Ledoux, Ph.D., a member of the Dana Alliance and a neurobiologist at Columbia University who studies the fear response, said: “I guess the real reason that we love to be scared so much when we go to the movies is because we get that adrenaline rush in a completely safe context. We don’t have the worry and anxiety that this will actually affect us in a personal and deep way.”
Text : Brenda Patoine
#SensationSeeking #neuroscience #sensations #brain #neuron #plasticity #neurology #medicine #cortex #research #discovery #learning #behavior #fMRI #neurotransmitters #MedicalResearch #BrainActivity #stess #BrainScanner #scientists #SynapticSignals #protein #PsychiatricDisorders #HealthSciences
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Neural probes 100 times smaller than that of a human hair
For over two decades, electrodes implanted in the brain have made it possible to electrically measure the activity of individual neurons. While the technology has continued to progress over the years, the implanted probes have continued to suffer from poor recording ability brought on by biocompatibility issues, limiting their efficacy over the long term.
It turns out that size matters: In this case, the smaller the better. Researchers at the University of Texas at Austin have developed neural probes made from a flexible nanoelectronic thread (NET). These probes are so thin and tiny that when they are implanted, they don’t trigger the human body to create scar tissue, which limits their recording efficacy. Without that hindrance, the threadlike probes can work effectively for months, making it possible to follow the long-term progression of such neurovascular and neurodegenerative diagnoses as strokes and Parkinson’s and Alzheimer’s diseases.
In research described in the journal Science Advances, UT researchers fabricated the multilayered nanoprobes out of five to seven nanometer-scale functional layers with a total thickness of around 1 micrometer.
“The thickness of all the functional layers, including recording electrodes, interconnects, two to three layers of insulation are all on the nanoscale,” explained Chong Xie, an assistant professor and one of the paper’s co-authors, in an e-mail interview with IEEE Spectrum. “This ultra-small thickness is crucial for the ultra-flexibility that is necessary to completely suppress tissue reactions to the implanted probes and leads to reliable long-term neural recording.”
Xie adds that the device’s flexibility is not the result of choosing the softest materials, but instead by engineering the dimensions and geometry of the device in particular the ultra-thin thickness.
The probe functions just like currently used neural electrodes. The recording sites (electrodes) are evenly spaced along the probe, which are individually addressed by micro-fabricated interconnects that connect to bonding pads for external inputs/outputs.
In the demonstration of the device, the electrodes were implanted into a living mouse cortex. The voltage signal is recorded at a high sampling rate (greater than 20 kiloHertz) detected on the electrodes, which represents the electrical activities from nearby neurons, including action potentials and local field potentials.
Xie and his colleagues faced some difficult technical challenges to make the neural probes extremely thin and to keep them implanted in a living brain with continued function for months. The researchers already knew from other work that larger neural probes made from thicker and stronger materials experienced structural damage that reduced their function after being implanted for just a few weeks. The key, according to Xie, was engineering the structure, materials, and fabrication details so that the interlayer adhesion is greatly enhanced. They also were surprised with how well some of the materials behaved.
“It is quite amazing that insulation layers with just hundreds of nanometers in thickness are sufficient to protect all the electrical components including millimeter-long interconnects in a living mouse brain for months,” explained Xie. “From our previous experience we knew that the photoresists we were using make good insulation with low defect rates, which was the reason for our material choice, but we were still surprised about its supreme performance.”
While the initial results of the probe were positive, there remain some pretty significant challenges ahead. The implementation strategy for the probes was tricky business.
These probes have a cross section area greater than 100 times smaller than that of a human hair and cannot free stand in air. As a result, the researchers had to come up with a way to precisely manipulate them to targeted positions and engage with microscale shuttle devices with micrometer accuracy. If this technology is to ever reach beyond the lab, this part of the process will need to be optimized.
“The surgical procedure for implanting these probes in a clinical environment needs to be further optimized,” said Xie. “We need to design new devices and an implantation strategy for clinical application. We have already started collaboration with neurosurgeons to develop the next generation of NETs for human patients.”
The next steps in the research will look to test the neural probes in primates. In the meantime, Xie and his colleagues are looking to improve the underlying technology.
Xie added: “I am continuing to enrich the technologies for novel neural interfaces in rodent models, including high-density recording and chronic recording over years and longer.”
http://spectrum.ieee.org/nanoclast/biomedical/diagnostics/flexibility-gives-nanothread-brain-probes-longterm-durability
#technologies #invention #electrodes #nanothread #NeuralProbes #stroke #neuroscience #cells #memory #neurobiology #neurons #dendrites #DendriticSpines #brain #neuron #HumanBrain #plasticity #neurology #medicine #synapses #SynapticTransmission #cortex #neurons #BrainCells #research #discovery #learning #behavior 
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Aberrant synapse protein can lead to neurological and psychiatric disorders.
'Timing is everything' in the transmission of signals between neurons in the brain. Most of the complex functions that humans are capable of performing would be severely impaired if their neurons were not capable of communicating accurately with one another to a thousandth of a second. Interpersonal communication, learning processes, focusing attention, the rapid processing of sensory stimuli, even the correct execution of movements would no longer be possible. The Israeli scientist Noa Lipstein-Thoms at the Max Planck Institute for Experimental Medicine in Göttingen has now discovered a new genetic disease mechanism that affects the strength and precise timing of neuronal signals and leads to movement disorders (dyskinesia), attention deficit hyperactivity disorder (ADHD) and autism.
Lipstein-Thoms studies the fundamental mechanisms of signal transmission between neurons. This process takes place at the synapses as they are known. A transmitting neuron triggers the release of a chemical messenger in response to an electrical stimulus. This chemical messenger is recognised by the recipient neuron and converted into an electric signal. A series of regulatory proteins guarantees that this signal transmission process, which is biologically extremely complex, operates with the necessary millisecond precision. The proteins control the release of the messenger at synapses. One of these proteins is known by the cryptic name of Munc13-1.
"Our genetic research on mice has shown that Munc13-1 is vital for the transmission of signals at synapses," explains Lipstein-Thoms. "When it is missing, the brain does not function because the messenger is blocked and cannot be released at synapses. The affected mouse dies." Even minor changes to the Munc13-1 protein often has catastrophic consequences because the precise timing of the synaptic signals is lost.
Because of this fundamental importance, Munc13-1 has up until now only been of interest to the basic researchers among the neuroscientists. "Disorders that could only be caused by a malfunction of Munc13-1 were not known," says Lipstein-Thoms. "My colleagues and I did not expect that the protein could play a role in a disorder as even small disruptions in the functioning of Munc13-1 have grave consequences. We suspected for a long time that a defect in Munc13-1 inevitably led to the death of an organism."
This view has changed dramatically as a result of a new study conducted by Lipstein-Thoms. Together with Göttingen-based neurobiologist Nils Brose and psychiatrists, neurologists and geneticists at the University of Utrecht in the Netherlands, Lipstein-Thoms describes a patient with a Munc13-1 protein that has been changed by mutation. The patient, who is currently seven years old and is being examined and treated in Utrecht, suffers from an unusual combination of dysfunctional movement patterns, ADHD and autism.
Lipstein-Thoms' Dutch colleagues discovered the Munc13-1 mutation during an in-depth genetic examination of the patient. They assume that this mutation is in all probability responsible for the specific symptoms. "This is the first case of a Munc13-1 mutation that is a factor in a disorder. But my colleagues could not explain why this mutation caused the disorder. However, that is the basis on which they can develop a treatment."
"This is where we came in," says Nils Brose, who supervised Lipstein-Thoms when she was a doctoral student and has worked with her for the last ten years. "Here at the Max Planck Institute for Experimental Medicine we have developed a huge repertoire of methods, reagents and animal models to analyse very precisely Munc13 proteins and the synapse functions associated with them. And we know a lot about these proteins." Using the tools and knowledge at her disposal, Lipstein-Thoms demonstrated that the Munc13-1 mutation discovered in the patient initially leads to an unexpected boosting of the synaptic signal transmission but the affected synapses weaken much faster than normal synapses in the case of persistent activity and especially when the activity is intense and very frequent.
"While the changed transmission characteristics of the synapses are rather small, they can explain the complex symptoms in the affected patient," says Lipstein-Thoms, describing the state of her findings. Many neurological and psychiatric medications already target synapses. "We know which process in the patient's synapses is damaged and could even try to correct the hyperactivity of synapses that we have described using medications that are already licensed," explains Lipstein-Thoms. "That would be a wonderful example of how basic research is essential to medical application."
https://medicalxpress.com/news/2017-02-aberrant-synapse-protein-neurological-psychiatric.html#jCp
#MaxPlanckInstitute #neuroscience #autism #brain #neuron #plasticity #neurology #medicine #cortex #research #discovery #learning #behavior #fMRI #neurotransmitters #MedicalResearch #BrainActivity #memories #BrainScanner #scientists #SynapticSignals #Munc13-1 #protein #PsychiatricDisorders #HealthSciences


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How cancer tumors exploit neuronal signals
A growing body of work indicates that cancer cells not only grow near nerves but also respond to the chemical signals that neurons secrete. Now, a new paper by Stanford University neuroscientists reviews how tumors exploit neuronal signals.
Cancer cells rely on the healthy cells that surround them for sustenance. Tumors reroute blood vessels to nourish themselves, secrete chemicals that scramble immune responses, and, according to recent studies, even recruit and manipulate neurons for their own gain. This pattern holds true not just for brain cancers, but also for prostate cancer, skin cancer, pancreatic cancer, and stomach cancer.
Michelle Monje of the Stanford University School of Medicine, who co-authored the article with PhD candidate Humsa Venkatesh, explains: “There is no part of the body that isn’t well innervated. The nervous system is an extremely arborized tree that reaches every aspect of every tissue and contributes importantly to tissue development. Those growth signals are already there, so why shouldn’t cancer cells co-opt them?”
Cancer treatments often target tumors by cutting off blood vessels and other nutrient supply routes, so Monje and others are interested to learn whether it may be possible to target nerves via analogous therapies or by simply blocking secreted neural growth factors.
The challenge is that growth-promoting signals vary by neuron and cancer type. Furthermore, blocking neural activity can be dangerous.
“In the brain, modulating neuronal activity isn’t a great option because we don’t want to silence the brain. Brains need to be active and functioning,” says Monje. “But we can interrupt the specific molecular pathways that are being co-opted by the tumor.”
Monje first became interested in neurons’ role supporting tumors while working on childhood glioma, a cancer that strikes in the precursors to glial cells in the developing brain. In 2015, her lab published a paper in Cell that found that both adult and pediatric glioma cells grew faster when adjacent to highly active neurons.
Timothy Wang at Columbia recently published work that showed that recruitment of nerves into the tumor micro-environment is necessary and sufficient for stomach cancer progression, and that blocking a neurotransmitter in the nerves that line the stomach could represent a novel therapy. It’s only a first step, but it raises the possibility of treating cancers by targeting nearby nerves says Monje.
“Seeds don’t tend to grow in the air. They have to be in the right soil,” Monje says. “Cancers are very much like that. They have to be in the right microenvironment.”
Nerve cells and the chemicals they secrete can go a long way toward making cancer cells feel at home.
The connection between tumor cells and nerves opens many new questions but also sheds light on some longstanding cancer pathology observations. Brain cancer cells often cluster around neurons, a phenomenon called perineuronal satellitosis, and the extent of innervation in tumors has long been recognized as predictive of patient outcome. Migrating cancer cells also use nerves as shortcuts into new tissues.
However, so far researchers have only investigated neurons’ role in a handful of cancers, and the full molecular details of cancer-nerve partnerships are still being worked out.
http://reliawire.com/cancer-tumors-neuronal-signals/
#StanfordUniversity #neuroscience #cancer #brain #HealthSciences #neuron #plasticity #neurology #medicine #cortex #research #discovery #learning #behavior #fMRI #neurotransmitters #MedicalResearch #BrainActivity #memories #BrainScanner #scientists #MigratingCancer #CancerTherapy #therapy #tumor

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Protecting children from pollutants that can damage their brains : EPA staff fear cuts to health programs under Trump
The Environmental Protection Agency’s (EPA) advisory panel on children’s health gathered last week to consider a few items that had long been on its agenda: getting lead out of water, cutting pollution-related asthma, and educating doctors about toxins in toys. The panel also took up an issue that few members could have foreseen several months ago: keeping the program off the chopping block.
Caroline Cox, a member of the Children’s Health Protection Advisory Committee, suggested a letter to the incoming EPA chief, touting the economic benefits of protecting children from pollutants that can damage their brains or cause illness later in life. (“That might resonate,” she said.) Tom Neltner, an Environmental Defense Fund lawyer and a member of the advisory group since 2011, said the message must be more urgent.
“With any administration change there are people who don’t have any idea about this issue,” Neltner said. “We should emphasize that kids don’t get a second chance to develop a brain. They don’t get a second chance on a reproductive system.”
For scientists, the issue of environmental health is not typically seen as politically fraught as climate change. But interviews with staffers throughout the EPA underline widespread concern — and some panic — about the fate of environmental health regulation under President Trump and Scott Pruitt, his nominee to lead the agency.
Both EPA and the National Institutes of Environmental Health Sciences oversee hundreds of studies annually. Some evaluate the cognitive impacts of metals such as lead, arsenic, and mercury on children living near Superfund sites, including those in impoverished areas. Others test the impact of pesticides on the behavior of children of farmworkers or the relationship between pesticide exposure and depression.
Many researchers fear that their funding from the EPA will be cut in the Trump administration; and even if it’s not, many suspect, the agency will no longer issue protective rules based on their scientific evidence.
“The tragedy is that no one who voted for President Trump voted for dirty water, dirty air, or more dangerous pesticides in their food,” said Scott Faber, vice president of governmental affairs for the Environmental Working Group, a nonprofit research organization based in Washington. “But every indication is that Scott Pruitt will methodically weaken the basic environmental health protections.’’
To date under Trump, the EPA has blocked about 30 pending regulations, not unusual for a new administration. But a review of those rules shows many of them were designed to protect the public from environmental hazards, including air pollution, contaminated water, and hazardous chemicals.
Read more - https://www.statnews.com/2017/02/08/environmental-health-trump-epa/
#neuroscience #EPA #children #Trump #WhiteHouse #ScottPruitt #Pruitt #brain #HealthSciences #VirtualBrain #VirtualReality #technologies #neuron #plasticity #neurology #medicine #cortex #research #discovery #learning #behavior #ManipulatingBrain #neurotransmitters #MedicalResearch #BrainActivity #memories #BrainScanner #scientists #baby #child #infant #babe #contamination #pollution #pollutants

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