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  • richardmitnick 4:36 pm on August 24, 2016 Permalink | Reply
    Tags: , , Neuroscience, In unstable times the brain reduces cell production to help cope   

    From Princeton: “In unstable times, the brain reduces cell production to help cope” 

    Princeton University
    Princeton University

    August 24, 2016
    Morgan Kelly

    People who experience job loss, divorce, death of a loved one or any number of life’s upheavals often adopt coping mechanisms to make the situation less traumatic.

    While these strategies manifest as behaviors, a Princeton University and National Institutes of Health study suggests that our response to stressful situations originates from structural changes in our brain that allow us to adapt to turmoil.

    A study conducted with adult rats showed that the brains of animals faced with disruptions in their social hierarchy produced far fewer new neurons in the hippocampus, the part of the brain responsible for certain types of memory and stress regulation. Rats exhibiting this lack of brain-cell growth, or neurogenesis, reacted to the surrounding upheaval by favoring the company of familiar rats over that of unknown rats, according to a paper published in The Journal of Neuroscience.

    1
    A Princeton University and National Institutes of Health study suggests that our response to stressful situations originates from structural changes in our brain that allows us to adapt to turmoil. Adult rats with disruptions in their social hierarchy produced far fewer new neurons in the hippocampus, the part of the brain responsible for certain types of memory and stress regulation. They also reacted to the disruption by favoring the company of familiar rats. Their behavior manifested six weeks after social disruption, during which time brain-cell growth, or neurogenesis, had decreased by 50 percent. The photo shows adult hippocampal neurons that are less than two weeks old. (Image courtesy of Maya Opendak, New York University)

    The research is among the first to show that adult neurogenesis — or the lack thereof — has an active role in shaping social behavior and adaptation, said first author Maya Opendak, who received her Ph.D. in neuroscience from Princeton in 2015 and conducted the research as a graduate student. The preference for familiar rats may be an adaptive behavior triggered by the reduction in neuron production, she said.

    “Adult-born neurons are thought to have a role in responding to novelty, and the hippocampus participates in resolving conflicts between different goals for use in decision-making,” said Opendak, who is now a postdoctoral research fellow of child and adolescent psychology at the New York University School of Medicine.

    “Data from this study suggest that the reward of social novelty may be altered,” she said. “Indeed, sticking with a known partner rather than approaching a stranger may be beneficial in some circumstances.”

    The findings also show that behavioral responses to instability may be more measured than scientists have come to expect, explained senior author Elizabeth Gould, Princeton’s Dorman T. Warren Professor of Psychology and department chair. Gould and her co-authors were surprised that the disrupted rats did not display any of the stereotypical signs of mental distress such as anxiety or memory loss, she said.

    “Even in the face of what appears to be a very disruptive situation, there was not a negative pathological response but a change that could be viewed as adaptive and beneficial,” said Gould, who also is a professor of neuroscience in the Princeton Neuroscience Institute (PNI).

    “We thought the animals would be more anxious, but we were making our prediction based on all the bias in the field that social disruption is always negative,” she said. “This research highlights the fact that organisms, including humans, are typically resilient in response to disruption and social instability.”

    Co-authors on the paper include: Lily Offit, who received her bachelor’s degree in psychology and neuroscience from Princeton in 2015 and is now a research assistant at Columbia University Medical Center; Patrick Monari, a research specialist in PNI; Timothy Schoenfeld, a postdoctoral researcher at the National Institutes of Health (NIH) who received his Ph.D. in psychology and neuroscience from Princeton in 2012; Anup Sonti, an NIH researcher; and Heather Cameron, an NIH principal investigator of neuroplasticity.

    The study is unusual for mimicking the true social structure of rats, Gould said. Rats live in structured societies that contain a single dominant male. The researchers placed rats into several groups consisting of four males and two females in to a large enclosure known as a visible burrow system. They then monitored the groups until the dominant rat in each one emerged and was identified. After a few days, the alpha rats of two communities were swapped, which reignited the contest for dominance in each group.

    The rats from disrupted hierarchies displayed their preference for familiar fellows six weeks after those turbulent times, during which time neurogenesis had decreased by 50 percent, Opendak said. (Any neurons generated during the time of instability would take four to six weeks to be incorporated into the hippocampus’ circuitry, she said.)

    When the researchers chemically restored adult neurogenesis in these rats, however, the animals’ interest in unknown rats returned to pre-disruption levels. At the same time, the researchers inhibited neuron growth in “naïve” transgenic rats that had not experienced social disruption. They found that the mere cessation of neurogenesis produced the same results as social disruption, particularly a preference for spending time with familiar rats.

    “These results show that the reduction in new neurons is directly responsible for social behavior, something that hasn’t been shown before,” Gould said. The exact mechanism behind how lower neuron growth led to the behavior change is not yet clear, she said.

    Bruce McEwen, professor of neuroendocrinology at The Rockefeller University, said that the research is a “major step forward” in efforts to explore the role of the dentate gyrus — a part of the hippocampus — in social behavior and antidepressant efficacy.

    “The ventral dentate gyrus, where they found these effects, is now implicated in mood-related behaviors and the response to antidepressants,” said McEwen, who is familiar with the research but had no role in it.

    “The connection to social behavior shown here is an important addition because social withdrawal is a key aspect of depression in humans, and the anterior hippocampus in humans is the homolog of the ventral hippocampus in rodents,” McEwen said. “Although there is no ‘animal model’ of human depression, the individual behaviors such as social avoidance, and brain changes such as neurogenesis, have been very useful in elucidating brain mechanisms in human depression.”

    At this point, the extent to which the exact mechanism and behavioral changes the researchers observed in the rats would apply to humans is unknown, Gould and Opendak said. The study’s overall conclusion, however, that social disruption and instability lead to neurological changes that help us to better cope is likely universal, they said.

    “Most people do experience some disruption in their lives, and resilience is the most typical response,” Gould said. “After all, if organisms always responded to stress with depression and anxiety, it’s unlikely early humans would have made it because life in the wild is very stressful.”

    “For people who are exposed to social disruption frequently, our animal model suggests that these life events may be accompanied by long-term changes in brain function and social behavior,” Opendak said. “Although we hope that our findings may guide research on the mechanisms of resilience in humans, it is important as always to exercise caution when extrapolating these data across species.”

    The paper, Lasting Adaptations In Social Behavior Produced By Social Disruption And Inhibition of Adult Neurogenesis, was published June 29 in The Journal of Neuroscience. This work was supported by the National Institute for Mental Health (NIMH).

    See the full article here .

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    About Princeton: Overview

    Princeton University is a vibrant community of scholarship and learning that stands in the nation’s service and in the service of all nations. Chartered in 1746, Princeton is the fourth-oldest college in the United States. Princeton is an independent, coeducational, nondenominational institution that provides undergraduate and graduate instruction in the humanities, social sciences, natural sciences and engineering.

    As a world-renowned research university, Princeton seeks to achieve the highest levels of distinction in the discovery and transmission of knowledge and understanding. At the same time, Princeton is distinctive among research universities in its commitment to undergraduate teaching.

    Today, more than 1,100 faculty members instruct approximately 5,200 undergraduate students and 2,600 graduate students. The University’s generous financial aid program ensures that talented students from all economic backgrounds can afford a Princeton education.

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  • richardmitnick 11:03 am on August 23, 2016 Permalink | Reply
    Tags: , , Neuroscience,   

    From Scripps: “A Look Deep Inside the Human Brain Reveals a Surprise” 

    Scripps
    Scripps Research Institute

    8.23.16
    No writer credit

    In the field of neuroscience, researchers often make the assumption that information they obtain from a tiny brain sample is true for the entire brain.

    Now, a team of scientists at The Scripps Research Institute (TSRI), University of California, San Diego (UC San Diego) and Illumina, Inc., has completed the first large-scale assessment of the way thousands of single neuronal nuclei produce proteins from genetic information (“transcription”) – revealing a surprising diversity in the process. The findings could improve both our understanding of the brain’s normal functioning and how it’s damaged by diseases such as Alzheimer’s, Parkinson’s, ALS and depression.

    [The study is published in Science.]

    The researchers accomplished this feat by isolating and analyzing 3,200 single human neurons, more than 10-fold greater than prior publications, from six Brodmann Areas (larger regions having functional roles) of the human brain.

    “Through a wonderful scientific collaboration, we found an enormous amount of transcriptomic diversity from cell to cell that will be relevant to understanding the normal brain and its diseases such as Alzheimer’s, Parkinson’s, ALS and depression,” said TSRI Professor and neuroscientist Jerold Chun, who co-led the study with bioengineers Kun Zhang and Wei Wang of UC San Diego and Jian-Bing Fan of Illumina.

    While parts of the cerebral cortex look different under a microscope – with different cell shapes and densities that form cortical layers and larger regions having functional roles called “Brodmann Areas” – most researchers treat neurons as a fairly uniform group in their studies. “From a tiny brain sample, researchers often make assumptions that obtained information is true for the entire brain,” said Dr. Chun.

    But the brain isn’t like other organs, Dr. Chun explained. There’s a growing understanding that individual brain cells are unique, and a possibility has been that the microscopic differences among cerebral cortical areas may also reflect unique transcriptomic differences – i.e., differences in the expressed genes, or messenger RNAs (mRNAs), which carry copies of the DNA code outside the nucleus and determine which proteins the cell makes.

    With the help of newly developed tools to isolate and sequence individual cell nuclei (where genetic material is housed in a cell), the researchers deciphered the minute quantities of mRNA within each nucleus, revealing that various combinations of the 16 subtypes tended to cluster in cortical layers and Brodmann Areas, helping explain why these regions look and function differently.

    Neurons exhibited anticipated similarities, yet also many differences in their transcriptomic profiles, revealing single neurons with shared, as well as unique, characteristics that likely lead to differences in cellular function.

    “Now we can actually point to an enormous amount of molecular heterogeneity in single neurons of the brain,” said Gwendolyn E. Kaeser, a UC San Diego Biomedical Sciences Graduate Program student studying in Dr. Chun’s lab at TSRI and co-first author of the study.

    Interestingly, some of these differences in gene expression have roots in very early brain development taking place before birth. The researchers found markers on some neurons showing that they originated from a specific region of fetal brain called the ganglionic eminence, which generates inhibitory neurons destined for the cerebral cortex. These neurons may have particular relevance to developmental brain disorders.

    In future studies, the researchers hope to investigate how single-neuron DNA and mRNA differ in single neurons, groups and between human brains – and how these may be influenced by factors such as stress, medications or disease.

    See the full article here .

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    The Scripps Research Institute (TSRI), one of the world’s largest, private, non-profit research organizations, stands at the forefront of basic biomedical science, a vital segment of medical research that seeks to comprehend the most fundamental processes of life. Over the last decades, the institute has established a lengthy track record of major contributions to the betterment of health and the human condition.

    The institute — which is located on campuses in La Jolla, California, and Jupiter, Florida — has become internationally recognized for its research into immunology, molecular and cellular biology, chemistry, neurosciences, autoimmune diseases, cardiovascular diseases, virology, and synthetic vaccine development. Particularly significant is the institute’s study of the basic structure and design of biological molecules; in this arena TSRI is among a handful of the world’s leading centers.

    The institute’s educational programs are also first rate. TSRI’s Graduate Program is consistently ranked among the best in the nation in its fields of biology and chemistry.

     
  • richardmitnick 6:54 am on July 28, 2016 Permalink | Reply
    Tags: , , Neuroscience,   

    From Science: “Neurons get fresh ‘batteries’ after stroke” 

    AAAS

    AAAS

    Jul. 27, 2016
    Emily Underwood

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    When neurons are damaged, cells called astrocytes (above) may assist by donating cellular power plants called mitochondria, a new study suggests. GerryShaw/Wikimedia Commons

    If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say.

    “This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study.

    To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell.

    In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury.

    To find out whether this kind of donation was taking place in the brain, Lo and Hayakawa teamed up with researchers in Bejing to test whether astrocytes could be coaxed into expelling healthy, working mitochondria. Previous studies hinted that astrocytes may pick up on neurons’ “help me” signals using an enzyme called CD38, Lo says. The enzyme, produced throughout the body in response to injury or damage, is also made by astrocytes. When Lo and colleagues genetically engineered mice to produce excess CD38, astrocytes from the rodents—extracted and deposited into fluid-filled dishes—expelled large numbers of still-functional mitochondrial particles. Researchers then dumped the mitochondria-rich fluid into another dish containing dying mouse neurons, and found that the cells did, in fact, absorb the mitochondria within 24 hours. The recharged neurons also grew new branches, lived longer, and had higher levels of ATP than cells not receiving the replacement batteries, suggesting that the astrocytes’ mitochondria were beneficial.

    Next, the team needed to determine whether the same phenomenon happens in living animals. So they subjected live, anesthetized mice to a strokelike injury and then injected damaged brain regions with astrocyte-derived mitochondria. After 24 hours, scientists killed the mice, cut into their brains, and examined the tissue microscopically. They saw that the mice neurons had not only absorbed the mitochondria, but also had significantly higher levels of molecules known to promote survival in distressed cells than did mice that had not received the mitochondrial cocktail.

    Finally, the team tested whether CD38 was necessary for the transfer. They injected mice with short segments of RNA designed to interfere with the enzyme’s function. Mice who received the treatment after their simulated “strokes” had far fewer astrocytic mitochondria in their neurons. The rodents also fared twice as badly on neurological tests compared with ones in which CD38 was unblocked , the team reports today in Nature. Lo emphasizes that the work is merely a “proof-of-concept study,” but adds that the outcomes of the neurological tests “tells you [the enzyme] is clinically relevant.”

    Given that CD38 plays many important roles throughout the body, including the immune system, the data are “way too preliminary” to start pursuing drugs that would increase or alter its activity, cautions Frances Lund, a microbiologist at the University of Birmingham in Alabama. It’s not clear, for example, whether the transfer of mitochondria was caused by, or merely correlated with, CD38 levels, she says.

    Still, Jun Chen, a neurobiologist at the University of Pittsburgh in Pennsylvania, is hopeful that the finding could lead to new treatments for diseases attributed to mitochondrial dysfunction. Parkinson’s disease, for example, is a neurodegenerative disorder strongly associated with mitochondrial dysfunction, in which dopamine-producing neurons in certain brain regions die en masse. If the new research pans out, he says, clinicians may one day be able to deliver healthy mitochondria into sick, but still viable, neurons.

    See the full article here .

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  • richardmitnick 10:10 am on June 29, 2016 Permalink | Reply
    Tags: , , NeuroFab, Neuroscience, New Stanford engineering tools record electrical activity of cells, , Stanford Neurosciences Institute   

    From Stanford: “New Stanford engineering tools record electrical activity of cells” 

    Stanford University Name
    Stanford University

    June 28, 2016
    Amy Adams

    When asked for the biggest idea that would transform neuroscience, Stanford mechanical engineer Nicholas Melosh came up with this: using engineering tools he and his colleagues were developing to record the electrical activity of cells.

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    Stanford researchers Greg Pitner and Matt Abramian finalize sample preparation in the Neurofab, mounting the cell culture vessel to the suspended wafer. (Image credit: L.A. Cicero)

    If it works, Melosh’s big idea could help neuroscientists improve on devices that interface with the brain – such as those currently used to relieve symptoms of Parkinson’s disease – screen drugs for electrophysiology side effects, and understand with greater precision the electrical currents that underlie our thoughts, behaviors and memories.

    To make this idea a reality, Melosh, an associate professor of materials science, engineering and photon science, founded the NeuroFab as an initiative of the Stanford Neurosciences Institute. It was one of seven interdisciplinary “Big Ideas” initiatives intended to tackle fundamental problems in neuroscience.

    “Eventually we’d like to create a toolset that would impact many neuroscience labs,” he said.

    Building a bridge

    The NeuroFab serves as both a physical space where engineers and neuroscientists can collaborate on new tools and an intellectual space with regular meetings to discuss ideas.

    Melosh said neuroscience and engineering have a lot in common.

    “Neural activity is electrical in nature and is a natural fit for engineers,” he said. But the language, cultures and skills of the two groups have been hard to bridge.

    John Huguenard is one of the neuroscientists on the other side of that bridge.

    “There is a cultural difference between engineers and biologists,” said Huguenard, a Stanford professor of neurology and neurological sciences.

    “When they start talking about device characteristics, it is lost on us. Similarly, when we say there are different types of neurons with very different properties, it’s lost on them.”

    Huguenard studies widespread neural activity in the brain, such as what occurs in sleep patterns or epilepsy.

    “This work requires us to record from many parts of the brain simultaneously,” he said, something that has been challenging with existing technology.

    Currently, neuroscientists have two primary methods to record cellular electrical activity. One is highly accurate, but can only record from one cell at a time, inevitably killing the cell within about two hours. The other can record long-term from an array of cells, but is not very sensitive.

    So far, teams within the NeuroFab are experimenting with a variety of approaches for reading electrical signals. Two of the more well-developed ones involve conductive nanomaterials, either in the form of nanopillars, which poke up into cells from below, or arrays of linear nanotubes that pass through cells like a bead on a string.

    Other approaches involve the optical recording of electrical fields, massively parallel interfaces based on computer chips, and membrane-fusing electrodes.

    Nanotubes

    Early in the NeuroFab’s existence, Melosh started talking with Philip Wong, a Stanford professor of electrical engineering, whose lab is developing ways of using highly conductive carbon nanotubes for next-generation computer chips. Wong brought in graduate student Gregory Pitner, who had experience with techniques for making those carbon nanotubes in a variety of configurations.

    “We grow them aligned, we grow them dense, we grow them consistently and reproducibly,” Pitner said, who believes that the dense, aligned nanotubes could provide a conductive surface for cells to grow on.

    That initial design changed when Pitner got a lesson in cell biology from Matthew Abramian, a postdoctoral fellow in Huguenard’s lab.

    Cells, Abramian explained, are surrounded by a halo of sugars and proteins and it’s these molecules that are in contact with a lab dish, not the cell itself. To get access to electrical changes within the cell, Pitner learned that his nanotubes needed to be suspended in a way that would allow the cell to encompass and incorporate the tube.

    “There are all sorts of practical details to understand about cell behavior that go way beyond high school biology,” Pitner said.

    The new design has small troughs for the cells to grow in, containing a single nanotube leading out to a recording station. With that new design, the pair needed to find that right cell type to test whether the idea works.

    If it succeeds, they envision being able to record from any kind of conductive cell including different types of neurons or heart muscle.

    “This would be a device where you can get data on hundreds of neurons at one time,” Abramian said.

    Cultural surprises

    Abramian said the pace of biology came as a surprise to engineers.

    “Engineers just think we’ll grow some cells and the next day we’re going to record,” he said. “That’s not how it works at all.”

    Cells can take up to weeks to grow, and then they don’t always have the anticipated properties, he added.

    By contrast, Abramian said he was amazed by the amount of control engineers have over their designs.

    “They have methods for building really intricate devices, and they can test them right way,” he said.

    By including faculty and students from many disciplines, Pitner said. the NeuroFab helps bridge these gaps in knowledge and expertise.

    “These kinds of relationships are almost impossible to create in a vacuum,” he said.

    Melosh said he hopes tools developed in the NeuroFab will enable bidirectional communication with neurons in a dish, and eventually the brain, which may start to unlock secrets of the brain by measuring from many places at once.

    See the full article here .

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  • richardmitnick 1:13 pm on January 22, 2016 Permalink | Reply
    Tags: , , Montreal Neurological Institute goes "Open science", Neuroscience   

    From AAAS: “Montreal institute going ‘open’ to accelerate science” 

    AAAS

    AAAS

    Jan. 21, 2016
    Brian Owens

    Temp 1
    The Montreal Neurological Institute plans to free up its findings, including data that point to connections between brain regions communicating at different neural rhythms. SÉBASTIEN DERY, MCCONNELL BRAIN IMAGING CENTRE, MONTREAL NEUROLOGICAL INSTITUTE

    Guy Rouleau, the director of McGill University’s Montreal Neurological Institute (MNI) and Hospital in Canada, is frustrated with how slowly neuroscience research translates into treatments. “We’re doing a really shitty job,” he says. “It’s not because we’re not trying; it has to do with the complexity of the problem.”

    So he and his colleagues at the renowned institute decided to try a radical solution. Starting this year, any work done there will conform to the principles of the “open-
science” movement—all results and data will be made freely available at the time of publication, for example, and the institute will not pursue patents on any of its discoveries. Although some large-scale initiatives like the government-funded Human Genome Project have made all data completely open, MNI will be the first scientific institute to follow that path, Rouleau says.

    “It’s an experiment; no one has ever done this before,” he says. The intent is that neuroscience research will become more efficient if duplication is reduced and data are shared more widely and earlier. Opening access to the tissue samples in MNI’s biobank and to its extensive databank of brain scans and other data will have a major impact, Rouleau hopes. “We think that it is a way to accelerate discovery and the application of neuroscience.”

    After a year of consultations among the institute’s staff, pretty much everyone—about 70 principal investigators and 600 other scientific faculty and staff—has agreed to take part, Rouleau says. Over the next 6 months, individual units will hash out the details of how each will ensure that its work lives up to guiding principles for openness that the institute has developed. They include freely providing all results, data, software, and algorithms; and requiring collaborators from other institutions to also follow the open principles.

    Staff at the institute were generally in favor of the plan, according to Lesley Fellows, a neurologist at MNI, though there were concerns about how to implement some aspects of it—such as how to protect patient confidentiality, and whether there would be sufficient financial support. Yet there is a “moral imperative,” according to Fellows, for research to be shared as openly as possible.

    “While the scale of ‘open’ that can be pursued right now may vary across research areas and will certainly depend on the resources that can be brought to bear, the practical challenges seem worth contending with,” she says. Participation is voluntary, and researchers can pursue patents on their own, but MNI will not pay the fees or help with the paperwork.

    Advocates of open science have welcomed MNI’s move. Brian Nosek, a psychologist and director of the Center for Open Science at the University of Virginia in Charlottesville, says he is “very impressed” with the institute’s plans. “It’s clear they are looking to move the organization towards the ideals of science,” he says.

    Nosek says the decision to eschew patents is especially intriguing. “I haven’t seen others do that before,” he says. But it’s not something that will necessarily work in other scientific fields, like engineering, Nosek predicts. “There is lots of debate in the life sciences now about what should and should not be patented, but that may not translate across disciplines smoothly.”

    Rouleau concedes that the patent ban might mean MNI has to forgo some future licensing income. But he says the kind of early-stage science that the institute does is not really worth protecting. “There is a fair amount of patenting by people at the institute, but the outcomes have not been very useful,” he says, adding that the institute would rather provide data that others could use to develop patentable medicines. “It comes down to what is the reason for our existence? It’s to accelerate science, not to make money.”

    The insistence that any organization or institute that collaborates with MNI will also have to follow open-science principles for that project could help to spread the approach, says Dan Gezelter, a chemist and open-science advocate at the University of Notre Dame in South Bend, Indiana. “It’s a little bit viral. I’ve never seen that before,” he says. Nosek agrees. “There is little that is more powerful in changing behavior than peer pressure,” he says.

    MNI is developing metrics to monitor its open-science experiment and determine whether it has the hoped-for impact. Officials will look at participation by the institute’s own staff, how much their open resources are being used by other researchers, and whether new products or therapies are being developed more quickly. “In 5 years,” 
Rouleau says, “we’ll be able to say ‘these things worked, and these things didn’t.’”

    See the full article here .

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  • richardmitnick 6:02 pm on December 11, 2015 Permalink | Reply
    Tags: , Neuroscience,   

    From NOVA: “Newly Discovered ‘Stop Neurons’ Could Save Your Life” 

    PBS NOVA

    NOVA

    11 Dec 2015
    Margaux Phares

    Neuroscientists have known since the 1960s what nerves tell a person’s legs to step off the curb to cross the street. But until now, they had no idea which hold the person back to avoid getting hit by a car.

    By stimulating nerve cells with light, a group of neuroscientists at the Karolinska Institut in Stockholm both defined the aptly named “stop neurons” and saw how they work in walking mice. The team used a “bottom-up approach” to explore how the spinal cord, lower in the chain of neural command, communicates with the brain stem, which is higher in the chain.

    1
    “Stop neurons” tell our bodies to stop moving.Photo credits: O. Bendorf/Flickr (CC BY-NC-ND), Julien Bouvier.

    Nerve cells that give rise to other functions we do not consciously think about, like breathing and keeping balance, are located in same area—effectively, as coauthor Ole Kiehn puts it, “one big mess of integrated networks.”

    To find the stop neurons, Kiehn and Julien Bouvier first modified a mouse’s brain stem to be sensitive to light stimulation, then sliced it into smaller and smaller segments. They removed parts until light no longer stimulated the segment. From this, the researchers pinpointed a cluster of “stop neurons” that extend down part of the spinal cord that, when stimulated tell the spinal cord to halt locomotion.

    What particularly surprised Bouvier was that “those stop cells are excitatory.” In order to stop motion, the cells need to be stimulated. It’s not enough to simply interrupt the locomotion signal.

    Bouvier compares it to driving a car. As long as you press the gas pedal, your car will move forward. Going into the study, scientists thought that releasing the pedal would eventually stop the car, or gradually mute the instructions to keep walking. ”But what we found was a brake pedal used only to stop,” Bouvier said.

    Watching the pathway unfold in mice supported their earlier findings. When the researchers pulsed light on stop neurons, the mice came to a stop. Light did not have an effect on mice that had blocked stop neurons—instead of stopping, they kept walking.

    2
    A mouse rigged for an optogenetics experiment is given a blue activation signal.

    Interestingly, the mice that could stop did so smoothly. They finished the step they were about to do. This behavior is very different from freezing, an all-over muscle contraction in response to fear. Bouvier said the smooth stopping allows animals to “keep posture,” making them less likely to fall or lose balance.

    The study, published in the November issue of Cell, is a step toward understanding how the body controls marching orders at the neural level and beyond the muscular level. Thomas Knopfel, a professor of neuroscience at Imperial College London, thinks Bouvier’s study “might be a step forward with medical problems associated with the brain and spinal cord.”

    Leg paralysis from a damaged nerve can disrupt communication between the brain and spinal cord. Knopfel speculated that an implantable device could be connected to this injured nerve, which could help patch this faulty circuit and help a patient learn to move his or her leg again. The same technology the researchers at Karolinska used—called optogenetics—could be used to make this device.

    Kiehn speculated that stop neuron activity might contribute to motor symptoms of Parkinson’s disease. One common symptom of late stage Parkinson’s is an involuntary “freezing gait.” Kiehn thinks this could be a sign that the locomotion “start signal” does not work properly, or that stop neurons may be less active than normal. Future tests will involve trying to identify these neurons in diseased mice.

    Bouvier has further questions in further exploring stop neurons and understanding how the spinal cord is controlled by brain stem. Among them: Are these neurons a “general brake for all behaviors?”

    We may not consciously think about every time we start and stop to walk, but locomotion is the output of many brain activities. Stop neurons are a critical link in this chain of command; they are the neural brake pedal that saves us from cars having to slam theirs’ in the crosswalk. “Even though movement may sound like a boring, noncognitive behavior, it is really one of the most important behaviors,” Kiehn said.

    See the full article here .

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    NOVA is the highest rated science series on television and the most watched documentary series on public television. It is also one of television’s most acclaimed series, having won every major television award, most of them many times over.

     
  • richardmitnick 1:20 pm on August 13, 2015 Permalink | Reply
    Tags: , , , Neuroscience   

    From Nautilus: “The Neuron’s Secret Partner” 

    Nautilus

    Nautilus

    August 13, 2015
    Ferris Jabr
    Illustrations by Jackie Ferrentino

    When we speak of brain cells we usually mean neurons: those gregarious, energetic darlings of cell biology that intertwine their many branches in complex webs and constantly crackle with their own electric chatter. But neurons make up only half the cells in the brain. The rest, known as neuroglia or simply glia, have long lived in the neuron’s shadow.

    French physiologist Henri Dutrochet first documented glia in 1824, though he had no idea what they were—he simply noted globules between the nerves of mollusks. In 1856, German biologist Rudolf Virchow gave those blobs the name “neuroglia,” describing them as “a sort of putty in which the nervous elements are embedded.” In the following decades, scientists learned that this putty was in fact made of individual cells—at least six major types, we now know—that formed intricate structural networks with both neurons and blood vessels. Yet they still regarded glia (which is Greek for “glue”) as mere fluff ‘n stuff, the brain’s packing peanuts, an inert plasma holding everything else in place.

    By the early 1900s, that notion had begun to erode. Many leading neuroscientists proposed that glia were in fact much more active than previously realized: Perhaps they were feeding neurons, or helping them communicate, or repairing them after injury. From the 1960s onward, thanks in large part to a suite of sophisticated laboratory tools, neuroscientists confirmed that glia are the brain’s architects, doctors, police, janitors, and gardeners. In the last five years, researchers have finally brought glia into the limelight as the highly dynamic, incomparably versatile, and indispensable partners of the neuron. Here are five recently discovered roles glia play in the brain:

    1

    Wiring

    Neurons are not always born where they are meant to reside. In the developing brain, so-called radial glial cells form a widespread lattice of cables along which neurons crawl like inchworms to their permanent homes. When this scaffolding is no longer required, radial glia transform into other kinds of glia, such as starburst-shaped astrocytes and octopus-like oligodentrocytes, or even into neurons. Scientists recently discovered that a specific subset of radial glial cells are fated to become neurons in the upper-most region of the cerebral cortex, the brain’s wrinkly outer layer responsible for our most sophisticated mental talents.

    Because the cerebral cortex of the human brain is so large and dense for a mammal our size, these glial cells likely played a key role in our evolution. A series of studies in the last three years have also confirmed that some glial cells excrete molecules that promote the formation of new connections between neurons, while others engulf and digest weak and underused synapses, changing the brain’s micro-circuitry throughout life.

    Clearing Clutter

    2

    Every organ in the body needs a
clean-up crew: a means of clearing away
 superfluous fluid, dead cells, and lingering cellular debris that could impede business as usual. The brain is no exception. Scientists have known for years that finely branched glial cells called microglia play a major role on the brain’s waste management team. Microglia roam about scavenging harmful tangles of proteins, the remains of dead cells, and bits of unneeded DNA. But a study published just last year indicated that microglia are essential for eliminating clumps of amyloid beta and other protein clusters associated with Alzheimer’s and related neurodegenerative disorders.

    Microglia are not the only members of the glia tribe that help take out the trash, though. Three years ago, Jeffrey Iliff, then of the University of Rochester Medical Center, and his colleagues injected fluorescent molecules into the fluid surrounding the brains of live mice. The molecules traveled through a previously unrecognized network of channels formed by glia known as astrocytes, which flank arteries and veins. Perhaps these glial ducts, Iliff and his team surmised, act as a drainage system for the brain. When they introduced amyloid beta into the rodents’ brains it was indeed cleansed away via the astrocyte aqueduct.

    Helping Neurons Talk

    3

    The oligodendrocyte precursor cell (OPC) is one of the most unique and active types of glia. OPCs eventually mature into adult oligodendrocytes that wrap their many tentacles around neuronal branches, sheathing them like rubber insulating electrical wire. Scientists discovered more than a decade ago that OPCs form synapses with neurons and change their own behavior based on the electrical signals they receive from those neurons. They are the only glial cells to do this. Now, emerging evidence indicates that the communication between OPCs and neurons goes both ways.

    The surfaces of OPCs are studded with a distinct protein known as NG2, and in a study published last fall, Dominik Sakry and Angela Neitz of Johannes Gutenberg University Mainz showed that the electrical impulses OPCs receive from neurons sometimes trigger enzymes to cleave NG2 from the cell membrane, allowing the protein to drift away and contact nearby neurons. When the cleaved fragments of NG2 bind to neurons, they make the cells more responsive to neurotransmitters such as glutamate, which are essential players in neuronal communication. When Sakry and Neitz eliminated either NG2 or its associated enzymes from mice, the animals’ ability to pick up sensory information was impaired: They were slower than typical mice to realize that a repeated startling sound was innocuous, and they showed less interest in new smells. That suggests the cross-talk between neurons and OPCs is not mere idle chatter, but rather an essential dialogue that underlies behavior.

    Helping You Breathe

    4

    The glia known as astrocytes wrap
 tightly around blood vessels feeding neurons, which puts them in
 an excellent position to monitor 
blood contents and adjust circulation as needed. Alexander 
Gourine of University College 
London and his colleagues studied how astrocytes in a rat brain might respond to fluctuating blood levels of
 oxygen and carbon dioxide. First, they genetically engineered the astrocytes of living rats to glow when the cells revved up their internal calcium signals, which help orchestrate activities within the cell. Then they exposed the astrocytes to differing pH levels.

    Only astrocytes in the medulla oblongata, a part of the brain stem that controls breathing and heart rate, responded. When those astrocytes detected a drop in blood pH, which would correspond to elevated levels of carbon dioxide, they increased their internal calcium signaling and began to secrete adenosine triphosphate (ATP)—a molecule used to store energy and perform a wide range of cellular tasks. The ATP stimulated surrounding neurons to fire, which increased the breathing rate in live rats, eventually bringing more oxygen to the brain. Raising the pH, which would correlate with oxygenated blood, had the opposite effect. This suggests that glia are crucial for every breath you take.

    Making You Smart

    5

    In Daniel Keyes’s 1958 short story Flowers for Algernon, scientists perform experimental brain surgery on a man named Charlie Gordon to dramatically increase his intelligence. First, though, as so often happens in medical research, they test out the procedure on a mouse—the eponymous Algernon. A few years ago, scientists did something spookily similar (to a mouse, that is, not a human). Steven Goldman and Maiken Nedergaard of the University of Rochester Medical Center and their colleagues injected immature human brain cells into the heads of infant mice.

    A few months later, those part-human mice performed much better on tests of memory and intelligence than mice with typical brains. They were quicker to find the escape route out of a maze and to learn that a certain sound signaled an imminent electric shock. Here’s the thing: The scientists did not infuse the mice with neurons, but rather melded the mice brains with human glial cells. There are likely several reasons for this glial-fueled boost in brain power. Several months after the surgery, many immature glial cells had matured into human astrocytes and essentially taken over the mice’s forebrains. Human astrocytes are larger and more powerful than their rodent counterparts: They have about 10 times more branching tendrils and their internal waves of calcium ions travel three times faster. By absorbing and releasing neurotransmitters, and thereby modifying the availability of these molecules, astrocytes change how frequently and forcefully neurons fire. In mice with human astrocytes, neurons sent stronger signals and were more likely to fire in the first place, leaving them with super-charged forebrains. One can only imagine what our glia can do with a forebrain full of human neurons, or how different we’d be without them.

    See the full article here.

    Please help promote STEM in your local schools.

    STEM Icon

    Stem Education Coalition

    Welcome to Nautilus. We are delighted you joined us. We are here to tell you about science and its endless connections to our lives. Each month we choose a single topic. And each Thursday we publish a new chapter on that topic online. Each issue combines the sciences, culture and philosophy into a single story told by the world’s leading thinkers and writers. We follow the story wherever it leads us. Read our essays, investigative reports, and blogs. Fiction, too. Take in our games, videos, and graphic stories. Stop in for a minute, or an hour. Nautilus lets science spill over its usual borders. We are science, connected.

     
  • richardmitnick 8:12 am on August 19, 2014 Permalink | Reply
    Tags: , Neuroscience, The Brain   

    From Sandia Lab: “Watching neurons fire from a front-row seat” 


    Sandia Lab

    July 28, 2014
    Sue Holmes, sholmes@sandia.gov, (505) 844-6362

    They are with us every moment of every day, controlling every action we make, from the breath we breathe to the words we speak, and yet there is still a lot we don’t know about the cells that make up our nervous systems. When things go awry and nerve cells don’t communicate as they should, the consequences can be devastating. Speech can be slurred, muscles stop working on command and memories can be lost forever.

    Better understanding of how neurons and brains work could lead to new prevention, diagnostic and treatment techniques, but the brain is complex and difficult to study. If you were to hold your brain, you would likely marvel at how much it feels and moves like Jell-O. This tissue is composed of neurons and other supporting cells with tiny cell bodies, which generate electrical signals that determine how the brain and the nervous system function.

    Those signals can be recorded and measured if a suitably small electrode is in the vicinity, but that presents challenges. Brain tissue is always moving in response to the body’s movement and breathing patterns. In addition, the nerve tissue is incredibly sensitive. If disrupted by a foreign body, the cells trigger an immune response to encapsulate the intruder and barricade it from the electrical signal it’s trying to capture and understand.

    Working to develop intelligent neural interfaces

    man
    Sandia National Laboratories researcher Murat Okandan holds one of the microscale actuators that could lead to better understanding of brain function, which could help with prevention, diagnostic and treatment techniques for brain disorders. (Photo by Randy Montoya)

    That challenge led Jit Muthuswamy, an associate professor of biomedical engineering at Arizona State University, Tempe (ASU), to pursue a robotic electrode system that would seek and maintain contact with neurons of interest autonomously in a subject going through normal behavioral routines. That led him to Sandia National Laboratories.

    “We are working to develop chronic, reliable, intelligent neural interfaces that will communicate with single neurons in a variety of applications, some of which are emerging and others that are closer to market,” Muthuswamy said. “Applications like brain prostheses are critically dependent on us being able to interface and communicate with single neurons reliably over the course of a patient’s life. Such reliable neural interfaces are also critical to help us understand the dynamic changes in the wiring diagram of the brain.”

    Key to the success of that robotic approach are the microscale actuators needed to reposition the electrodes. This led Muthuswamy in 2000 to seek out Sandia engineer Murat Okandan and the unique microsystems engineering capabilities available at Sandia’s Microsystems and Engineering Sciences Applications facility.

    “The process flow we use to make these isn’t available anywhere else in the world, so the level of complexity and mechanical design space we had to design and fabricate these was immensely larger than what other researchers might have,” Okandan said. He has been working with Muthuswamy’s research team since that initial contact to find a suitable method to track individual neurons as they fire.

    Earlier probes were made of a sharpened metal wire inserted in the tissue. The closer the probe is to the neuron, the stronger the signal, so experimenters ideally try to get as close as possible without disrupting surrounding tissue. The problem is that even a thin wire is too big; such a probe can take measurements around the neuron, but is far too cumbersome to be reliable over time.

    Equally important is capturing the signals from an awake animal. Given their size and rigidity, current probes aren’t suited to gather recordings as the animal responds to its environment. Those units aren’t self-contained, so they keep the animals from moving around freely.

    Microscale key to capturing signals from awake, moving animals

    Microscale actuators and microelectrodes are critical to addressing both of those issues so probes can interact with individual nerve cells while doing minimal damage to surrounding tissue. The microscale actuators and associated packaging system developed at ASU and Sandia let a probe move autonomously in and out of the areas surrounding the cell, collecting measurements while compensating for any movement in the neuron or brain tissue.

    About the size of a thumbnail, the self-contained unit has three microelectrodes and associated micro actuators. When a current runs through the thermal actuator, it expands and pushes the microelectrodes outward over the edge of the unit, which is flat to fit against the tissue. Because the actuator is so small, it can be heated to several hundred degrees Celsius and cooled again 1,000 times per second. It takes 540 cycles to fully extend the probe, but that can be done quickly – in a second or less.

    The probes were implanted in the somatosensory cortex of rodents and rigorously tested in numerous experiments, both in acute and long-term conditions, Muthuswamy said. Animal procedures were carried out with the approval of ASU’s Institute of Animal Care and Use Committee, and experiments were done in accordance with National Institute of Health guidelines.

    Muthuswamy said the neural probes demonstrated significant improvement in the quality and reliability of the signals when the probes were moved with precision using the Sandia microactuators in response to loss of neural signals. Further, he said, adding autonomous closed-loop controls to compensate for microscale perturbations in brain tissue significantly improved the stability of neural recordings from the brain.

    Scale of this system is unique

    Thermal actuators have been used for years at Sandia and elsewhere, but the scale of this system is unique. “The idea that we could build this system to achieve multiple millimeters of total displacement out of a micron-scaled device was a significant milestone,” said Sandia engineer Michael Baker, who designed the actuator. “We used electrostatic actuators in the past, but the thermal actuator provides much higher force, which is needed to move the probe in tissue.”

    The microelectrodes are made of highly conductive polysilicon, which the team discovered has a number of advantages. It is almost metal-like in its conductivity, but durable enough for millions of cycles. It provides a signal-to-noise ratio much greater than previous wire probes and provides high-quality measurement signals.

    Muthuswamy and Okandan currently are seeking to produce richer data with resolution in the submicron range to be able to go inside cells and take measurements there. They also are working on stacking the existing neural probe chips and decreasing the spaces between probes. Muthuswamy’s Neural Microsystems lab at ASU has developed a unique stacking approach for creating three-dimensional arrays of actuated microelectrodes.

    “By building a three-dimensional array, we would have access to significantly more information, rather than just a slice,” Okandan said. “We’re very encouraged by the progress we have made, and are looking forward to building on that progress.”

    See the full article here.

    Sandia National Laboratories is a multiprogram laboratory operated by Sandia Corporation, a wholly owned subsidiary of Lockheed Martin Corporation, for the U.S. Department of Energy’s National Nuclear Security Administration. With main facilities in Albuquerque, N.M., and Livermore, Calif., Sandia has major R&D responsibilities in national security, energy and environmental technologies, and economic competitiveness.
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  • richardmitnick 3:13 pm on July 28, 2014 Permalink | Reply
    Tags: , Neuroscience   

    From Sandia Lab: “Watching neurons fire from a front-row seat” 


    Sandia Lab

    July 28, 2014
    Sue Holmes, sholmes@sandia.gov, (505) 844-6362

    They are with us every moment of every day, controlling every action we make, from the breath we breathe to the words we speak, and yet there is still a lot we don’t know about the cells that make up our nervous systems. When things go awry and nerve cells don’t communicate as they should, the consequences can be devastating. Speech can be slurred, muscles stop working on command and memories can be lost forever.

    Better understanding of how neurons and brains work could lead to new prevention, diagnostic and treatment techniques, but the brain is complex and difficult to study. If you were to hold your brain, you would likely marvel at how much it feels and moves like Jell-O. This tissue is composed of neurons and other supporting cells with tiny cell bodies, which generate electrical signals that determine how the brain and the nervous system function.

    Those signals can be recorded and measured if a suitably small electrode is in the vicinity, but that presents challenges. Brain tissue is always moving in response to the body’s movement and breathing patterns. In addition, the nerve tissue is incredibly sensitive. If disrupted by a foreign body, the cells trigger an immune response to encapsulate the intruder and barricade it from the electrical signal it’s trying to capture and understand.

    Working to develop intelligent neural interfaces

    man
    Sandia National Laboratories researcher Murat Okandan holds one of the microscale actuators that could lead to better understanding of brain function, which could help with prevention, diagnostic and treatment techniques for brain disorders. (Photo by Randy Montoya) Click on the thumbnail for a high-resolution image

    That challenge led Jit Muthuswamy, an associate professor of biomedical engineering at Arizona State University, Tempe (ASU), to pursue a robotic electrode system that would seek and maintain contact with neurons of interest autonomously in a subject going through normal behavioral routines. That led him to Sandia National Laboratories.

    “We are working to develop chronic, reliable, intelligent neural interfaces that will communicate with single neurons in a variety of applications, some of which are emerging and others that are closer to market,” Muthuswamy said. “Applications like brain prostheses are critically dependent on us being able to interface and communicate with single neurons reliably over the course of a patient’s life. Such reliable neural interfaces are also critical to help us understand the dynamic changes in the wiring diagram of the brain.”

    Key to the success of that robotic approach are the microscale actuators needed to reposition the electrodes. This led Muthuswamy in 2000 to seek out Sandia engineer Murat Okandan and the unique microsystems engineering capabilities available at Sandia’s Microsystems and Engineering Sciences Applications facility.

    “The process flow we use to make these isn’t available anywhere else in the world, so the level of complexity and mechanical design space we had to design and fabricate these was immensely larger than what other researchers might have,” Okandan said. He has been working with Muthuswamy’s research team since that initial contact to find a suitable method to track individual neurons as they fire.

    Earlier probes were made of a sharpened metal wire inserted in the tissue. The closer the probe is to the neuron, the stronger the signal, so experimenters ideally try to get as close as possible without disrupting surrounding tissue. The problem is that even a thin wire is too big; such a probe can take measurements around the neuron, but is far too cumbersome to be reliable over time.

    Equally important is capturing the signals from an awake animal. Given their size and rigidity, current probes aren’t suited to gather recordings as the animal responds to its environment. Those units aren’t self-contained, so they keep the animals from moving around freely.

    Microscale key to capturing signals from awake, moving animals

    Microscale actuators and microelectrodes are critical to addressing both of those issues so probes can interact with individual nerve cells while doing minimal damage to surrounding tissue. The microscale actuators and associated packaging system developed at ASU and Sandia let a probe move autonomously in and out of the areas surrounding the cell, collecting measurements while compensating for any movement in the neuron or brain tissue.

    About the size of a thumbnail, the self-contained unit has three microelectrodes and associated micro actuators. When a current runs through the thermal actuator, it expands and pushes the microelectrodes outward over the edge of the unit, which is flat to fit against the tissue. Because the actuator is so small, it can be heated to several hundred degrees Celsius and cooled again 1,000 times per second. It takes 540 cycles to fully extend the probe, but that can be done quickly – in a second or less.

    The probes were implanted in the somatosensory cortex of rodents and rigorously tested in numerous experiments, both in acute and long-term conditions, Muthuswamy said. Animal procedures were carried out with the approval of ASU’s Institute of Animal Care and Use Committee, and experiments were done in accordance with National Institute of Health guidelines.

    Muthuswamy said the neural probes demonstrated significant improvement in the quality and reliability of the signals when the probes were moved with precision using the Sandia microactuators in response to loss of neural signals. Further, he said, adding autonomous closed-loop controls to compensate for microscale perturbations in brain tissue significantly improved the stability of neural recordings from the brain.

    Scale of this system is unique

    Thermal actuators have been used for years at Sandia and elsewhere, but the scale of this system is unique. “The idea that we could build this system to achieve multiple millimeters of total displacement out of a micron-scaled device was a significant milestone,” said Sandia engineer Michael Baker, who designed the actuator. “We used electrostatic actuators in the past, but the thermal actuator provides much higher force, which is needed to move the probe in tissue.”

    The microelectrodes are made of highly conductive polysilicon, which the team discovered has a number of advantages. It is almost metal-like in its conductivity, but durable enough for millions of cycles. It provides a signal-to-noise ratio much greater than previous wire probes and provides high-quality measurement signals.

    Muthuswamy and Okandan currently are seeking to produce richer data with resolution in the submicron range to be able to go inside cells and take measurements there. They also are working on stacking the existing neural probe chips and decreasing the spaces between probes. Muthuswamy’s Neural Microsystems lab at ASU has developed a unique stacking approach for creating three-dimensional arrays of actuated microelectrodes.

    “By building a three-dimensional array, we would have access to significantly more information, rather than just a slice,” Okandan said. “We’re very encouraged by the progress we have made, and are looking forward to building on that progress.”

    See the full article here.

    Sandia National Laboratories is a multiprogram laboratory operated by Sandia Corporation, a wholly owned subsidiary of Lockheed Martin Corporation, for the U.S. Department of Energy’s National Nuclear Security Administration. With main facilities in Albuquerque, N.M., and Livermore, Calif., Sandia has major R&D responsibilities in national security, energy and environmental technologies, and economic competitiveness.
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  • richardmitnick 8:45 am on July 9, 2014 Permalink | Reply
    Tags: , Human brain, , Neuroscience   

    From Livermore Lab: “DARPA selects Lawrence Livermore to develop world’s first neural device to restore memory” 


    Lawrence Livermore National Laboratory

    07/08/2014
    Kenneth K Ma, LLNL, (925) 423-7602, ma28@llnl.gov

    The Department of Defense’s Defense Advanced Research Projects Agency (DARPA) awarded Lawrence Livermore National Laboratory (LLNL) up to $2.5 million to develop an implantable neural device with the ability to record and stimulate neurons within the brain to help restore memory, DARPA officials announced this week.

    one
    Lawrence Livermore engineer Vanessa Tolosa holds up a silicon wafer containing micromachined implantable neural devices.

    brain
    Lawrence Livermore National Laboratory (LLNL) will develop an implantable neural device with the ability to record and stimulate neurons within the brain to help restore memory.

    The research builds on the understanding that memory is a process in which neurons in certain regions of the brain encode information, store it and retrieve it. Certain types of illnesses and injuries, including Traumatic Brain Injury (TBI), Alzheimer’s disease and epilepsy, disrupt this process and cause memory loss. TBI, in particular, has affected 270,000 military service members since 2000.

    two
    Lawrence Livermore engineers Angela Tooker and Vanessa Tolosa load silicon wafers into a metal deposition chamber during the development of neural devices.

    The goal of LLNL’s work — driven by LLNL’s Neural Technology group and undertaken in collaboration with the University of California, Los Angeles (UCLA) and Medtronic — is to develop a device that uses real-time recording and closed-loop stimulation of neural tissues to bridge gaps in the injured brain and restore individuals’ ability to form new memories and access previously formed ones.

    The research is funded by DARPA’s Restoring Active Memory (RAM) program.

    Specifically, the Neural Technology group will seek to develop a neuromodulation system — a sophisticated electronics system to modulate neurons — that will investigate areas of the brain associated with memory to understand how new memories are formed. The device will be developed at LLNL’s Center for Bioengineering.

    “Currently, there is no effective treatment for memory loss resulting from conditions like TBI,” said LLNL’s project leader Satinderpall Pannu, director of the LLNL’s Center for Bioengineering, a unique facility dedicated to fabricating biocompatible neural interfaces. “This is a tremendous opportunity from DARPA to leverage Lawrence Livermore’s advanced capabilities to develop cutting-edge medical devices that will change the health care landscape.”

    LLNL will develop a miniature, wireless and chronically implantable neural device that will incorporate both single neuron and local field potential recordings into a closed-loop system to implant into TBI patients’ brains. The device — implanted into the entorhinal cortex and hippocampus — will allow for stimulation and recording from 64 channels located on a pair of high-density electrode arrays. The entorhinal cortex and hippocampus are regions of the brain associated with memory.

    The arrays will connect to an implantable electronics package capable of wireless data and power telemetry. An external electronic system worn around the ear will store digital information associated with memory storage and retrieval and provide power telemetry to the implantable package using a custom RF-coil system.

    Designed to last throughout the duration of treatment, the device’s electrodes will be integrated with electronics using advanced LLNL integration and 3D packaging technologies. The microelectrodes that are the heart of this device are embedded in a biocompatible, flexible polymer.

    Using the Center for Bioengineering’s capabilities, Pannu and his team of engineers have achieved 25 patents and many publications during the last decade. The team’s goal is to build the new prototype device for clinical testing by 2017.

    Lawrence Livermore’s collaborators, UCLA and Medtronic, will focus on conducting clinical trials and fabricating parts and components, respectively.

    “The RAM program poses a formidable challenge reaching across multiple disciplines from basic brain research to medicine, computing and engineering,” said Itzhak Fried, lead investigator for the UCLA on this project and professor of neurosurgery and psychiatry and biobehavioral sciences at the David Geffen School of Medicine at UCLA and the Semel Institute for Neuroscience and Human Behavior. “But at the end of the day, it is the suffering individual, whether an injured member of the armed forces or a patient with Alzheimer’s disease, who is at the center of our thoughts and efforts.”

    LLNL’s work on the Restoring Active Memory program supports President Obama’s Brain Research through Advancing Innovative Neurotechnologies (BRAIN) initiative.

    “Our years of experience developing implantable microdevices, through projects funded by the Department of Energy (DOE), prepared us to respond to DARPA’s challenge,” said Lawrence Livermore Engineer Kedar Shah, a project leader in the Neural Technology group.

    See the full article here.

    Operated by Lawrence Livermore National Security, LLC, for the Department of Energy’s National Nuclear Security
    Administration
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