Links for Keyword: Glia

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 82

Katarina Zimmer Long believed to be simple, pathogen-eating immune cells, macrophages have a far more extensive list of job duties. They appear to have specialized functions across body tissues, help repair damaged tissue, play a key role in regulating inflammation and pain, and participate in other roles scientists are just beginning to reveal. Now, a group of researchers in the Netherlands has identified a mechanism by which macrophages may help resolve inflammatory pain in mice. In a study recently posted as a preprint to bioRxiv, they report that the immune cells shuttle mitochondria to sensory neurons that innervate inflamed tissue, and that this helps resolve pain. The researchers speculate that the mechanism could replenish functional mitochondria in neurons during chronic inflammatory conditions, which is associated with dysfunctional mitochondria. “I think the transfer of mitochondria is quite convincing,” Jan Van den Bossche, an immunologist at Amsterdam University Medical Center who wasn’t involved in the research, writes to The Scientist in an email. If the findings can be replicated, “this could have [implications for] many diseases with chronic inflammation and pain,” he adds. The research is the result of a five-year project that began when Niels Eijkelkamp, a neuroimmunologist at the University Medical Center Utrecht, and his colleagues started investigating how inflammatory pain resolves, “so we could understand what causes chronic pain,” he says. © 1986–2020 The Scientist

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27097 - Posted: 03.06.2020

Elena Renken The sting of a paper cut or the throb of a dog bite is perceived through the skin, where cells react to mechanical forces and send an electrical message to the brain. These signals were believed to originate in the naked endings of neurons that extend into the skin. But a few months ago, scientists came to the surprising realization that some of the cells essential for sensing this type of pain aren’t neurons at all. It’s a previously overlooked type of specialized glial cell that intertwines with nerve endings to form a mesh in the outer layers of the skin. The information the glial cells send to neurons is what initiates the “ouch”: When researchers stimulated only the glial cells, mice pulled back their paws or guarded them while licking or shaking — responses specific to pain. This discovery is only one of many recent findings showing that glia, the motley collection of cells in the nervous system that aren’t neurons, are far more important than researchers expected. Glia were long presumed to be housekeepers that only nourished, protected and swept up after the neurons, whose more obvious role of channeling electric signals through the brain and body kept them in the spotlight for centuries. But over the last couple of decades, research into glia has increased dramatically. “In the human brain, glial cells are as abundant as neurons are. Yet we know orders of magnitude less about what they do than we know about the neurons,” said Shai Shaham, a professor of cell biology at the Rockefeller University who focuses on glia. As more scientists turn their attention to glia, findings have been piling up to reveal a family of diverse cells that are unexpectedly crucial to vital processes. All Rights Reserved © 2020

Related chapters from BN8e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27002 - Posted: 01.28.2020

By Donna Jackson Nakazawa More than a decade ago, I was diagnosed with a string of autoimmune diseases, one after another, including a bone marrow disorder, thyroiditis, and then Guillain-Barré syndrome, which left me paralyzed while raising two young children. I recovered from Guillain-Barré only to relapse, becoming paralyzed again. My immune system was repeatedly and mistakenly attacking my body, causing the nerves in my arms, legs, and those I needed to swallow to stop communicating with my brain, leaving me confined to — and raising my children from — bed. As I slowly began to recover and learn to walk again, I noticed that along with residual physical losses I had experienced shifts in my mood and clarity of mind. Although I’d always been an optimistic person, I felt a bleak unshakable dread, which didn’t feel like the “old me.” I also noticed cognitive glitches. Names, words, and facts were hard to bring to mind. I can still recall cutting up slices of watermelon, putting them in a bowl, and staring down at them thinking, “What is this again?” I knew the word but couldn’t remember it. I covered my lapse by bringing the bowl to the table and waiting for my children to call out, “Yay! Watermelon!” And I thought, “Yes. Of course. Watermelon.” As a science journalist whose niche spans neuroscience, immunology, and human emotion, I knew at the time that it didn’t make scientific sense that inflammation in the body could be connected to — much less cause — illness in the brain. At that time, scientific dogma held that the brain was the only organ in the body not ruled by the immune system. The brain was considered to be “immune privileged.” © 2020 STAT

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26971 - Posted: 01.20.2020

Heidi Ledford Tumour cells can plug into — and feed off — the brain’s complex network of neurons, according to a trio of studies. This nefarious ability could explain the mysterious behaviour of certain tumours, and point to new ways of treating cancer. The studies1,2,3, published on 18 September in Nature, describe this startling capability in brain cancers called gliomas, as well as in some breast cancers that spread to the brain. The findings bolster a growing realization among doctors and scientists that the nervous system plays an important role in the growth of cancers, says Michelle Monje, a paediatric neuro-oncologist at Stanford University in California and lead author of one of the studies1. Even so, finding cancer cells that behave like neurons was a surprise. “It’s unsettling,” Monje says. “We don’t think of cancer as forming an electrically active tissue like the brain.” Feeding off the brain Frank Winkler, a neurologist at Heidelberg University in Germany and a lead author on another of the Nature studies2, stumbled on the phenomenon in 2014 while studying communication networks established by cells in some brain tumours. He and his team discovered synapses, structures that neurons use to communicate with one another, in the tumours. It was “crazy stuff”, Winkler says. “Our first reaction was, ‘This is just difficult to believe.’” The researchers assumed that the tumour synapses would be a random occurrence. But as Winkler and his colleagues report in their latest study, they found synapses in glioma samples taken from cancer cells grown in culture, human glioma tumours transplanted into mice and glioma samples taken from ten people.

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26625 - Posted: 09.19.2019

By Kenneth Miller A model of Ben Barres’ brain sits on the windowsill behind his desk at Stanford University School of Medicine. To a casual observer, there’s nothing remarkable about the plastic lump, 3-D-printed from an MRI scan. Almost lost in the jumble of papers, coffee mugs, plaques and trophies that fill the neurobiologist’s office, it offers no hint about what Barres’ actual gray matter has helped to accomplish: a transformation of our understanding of brains in general, and how they can go wrong. Barres is a pioneer in the study of glia. This class of cells makes up 90 percent of the human brain, but gets far less attention than neurons, the nerve cells that transmit our thoughts and sensations at lightning speed. Glia were long regarded mainly as a maintenance crew, performing such unglamorous tasks as ferrying nutrients and mopping up waste, and occasionally mounting a defense when the brain faced injury or infection. Over the past two decades, however, Barres’ research has revealed that they actually play central roles in sculpting the developing brain, and in guiding neurons’ behavior at every stage of life. “He has made one shocking, revolutionary discovery after another,” says biologist Martin Raff, emeritus professor at University College London, whose own work helped pave the way for those advances. Recently, Barres and his collaborators have made some discoveries that may revolutionize the treatment of neurodegenerative ailments, from glaucoma and multiple sclerosis to Alzheimer’s disease and stroke. What drives such disorders, their findings suggest, is a process in which glia turn from nurturing neurons to destroying them. Human trials of a drug designed to block that change are just beginning.

Related chapters from BN8e: Chapter 17: Learning and Memory; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26258 - Posted: 05.22.2019

By Ashley Yeager At first glance, neurons and muscle cells are the stars of gross motor function. Muscle movement results from coordination between nerve and muscle cells: when an action potential arrives at the presynaptic neuron terminal, calcium ions flow, causing proteins to fuse with the cell membrane and release some of the neuron’s contents, including acetylcholine, into the cleft between the neuron and muscle cell. Acetylcholine binds to receptors on the muscle cell, sending calcium ions into it and causing it to contract. But there’s also a third kind of cell at neuromuscular junctions, a terminal/perisynaptic Schwann cell (TPSC). These cells are known to aid in synapse formation and in the repair of injured peripheral motor axons, but their possible role in synaptic communications has been largely ignored. Problems with synaptic communication can underlie muscle fatigue, notes neuroscientist Thomas Gould of the University of Nevada, Reno, in an email to The Scientist. “Because these cells are activated by synaptic activity, we wondered what the role of this activation was.” To investigate, he and his colleagues stimulated motor neurons from neonatal mouse diaphragm tissue producing a calcium indicator, and found that TPSCs released calcium ions from the endoplasmic reticulum into the cytosol and could take in potassium ions from the synaptic cleft between neurons and muscle cells. However, TPSCs lacking the protein purinergic 2Y1 receptor (P2Y1R) didn’t release calcium or appear to take in potassium ions. © 1986-2018 The Scientist

Related chapters from BN8e: Chapter 11: Motor Control and Plasticity; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24964 - Posted: 05.12.2018

By NEIL GENZLINGER Ben Barres, a neuroscientist who did groundbreaking work on brain cells known as glia and their possible relation to diseases like Parkinson’s, and who was an outspoken advocate of equal opportunity for women in the sciences, died on Wednesday at his home in Palo Alto, Calif. He was 63. In announcing the death, Stanford University, where Dr. Barres was a professor, said he had had pancreatic cancer. Dr. Barres was transgender, having transitioned from female to male in 1997, when he was in his 40s and well into his career. That gave him a distinctive outlook on the difficulties that women and members of minorities face in academia. and especially in the sciences. An article he wrote for the journal Nature in 2006 titled “Does Gender Matter?” took on some prominent scholars who had argued that women were not advancing in the sciences because of innate differences in their aptitude. “I am suspicious when those who are at an advantage proclaim that a disadvantaged group of people is innately less able,” he wrote. “Historically, claims that disadvantaged groups are innately inferior have been based on junk science and intolerance.” The article cited studies documenting obstacles facing women, but it also drew on Dr. Barres’s personal experiences. He recounted dismissive treatment he had received when he was a woman and how that had changed when he became a man. “By far,” he wrote, “the main difference that I have noticed is that people who don’t know I am transgendered treat me with much more respect: I can even complete a whole sentence without being interrupted by a man.” Dr. Barres (pronounced BARE-ess) was born on Sept. 13, 1954, in West Orange, N.J., with the given name Barbara. “I knew from a very young age — 5 or 6 — that I wanted to be a scientist, that there was something fun about it and I would enjoy doing it,” he told The New York Times in 2006. “I decided I would go to M.I.T. when I was 12 or 13.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 8: Hormones and Sex
Link ID: 24472 - Posted: 12.30.2017

Acclaimed Stanford neuroscientist Ben Barres, MD, PhD, died on Dec. 27, 20 months after being diagnosed with pancreatic cancer. He was 63. Barres’ path-breaking discoveries of the crucial roles played by glial cells — the unsung majority of brain cells, which aren’t nerve cells — revolutionized the field of neuroscience. Barres was incontestably visionary yet, ironically, face-blind — he suffered from prosopagnosia, an inability to distinguish faces, and relied on voices or visual cues such as hats and hairstyles to identify even people he knew well. And there were many of them. A professor of neurobiology, of developmental biology and of neurology, Barres was widely praised as a stellar and passionate scientist whose methodologic rigor was matched only by his energy and enthusiasm. He was devoted to his scholarly pursuits and to his trainees, advocating unrelentingly on their behalf. He especially championed the cause of women in academia, with whom he empathized; he was transgender. “Ben was a remarkable person. He will be remembered as a brilliant scientist who transformed our understanding of glial cells and as a tireless advocate who promoted equity and diversity at every turn,” said Marc Tessier-Lavigne, PhD, president of Stanford University. “He was also a beloved mentor to students and trainees, a dear friend to many in our community and a champion for the fundamental dignity of us all.”

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 24461 - Posted: 12.28.2017

By Shawna Williams THE PAPER P. Réu et al., “The lifespan and turnover of microglia in the human brain,” Cell Rep, 20:779-84, 2017. A RENEWABLE RESOURCE? Evidence has emerged that some of the brain’s cells can be renewed in adulthood, but it is difficult to study the turnover of cells in the human brain. When it comes to microglia, immune cells that ward off infection in the central nervous system, it’s been unclear how “the maintenance of their numbers is controlled and to what extent they are exchanged,” says stem cell researcher Jonas Frisén of the Karolinska Institute in Sweden. NUCLEAR SIGNATURE Frisén and colleagues used brain tissue from autopsies, together with the known changes in concentrations of carbon-14 in the atmosphere over time, to estimate how frequently microglia are renewed. They also analyzed microglia from the donated brains of two patients who had received a labeled nucleoside as part of a cancer treatment trial in the 1990s. SLOW CHURN Microglia, which populate the brain as blood cell progenitors during fetal development, were replaced at a median rate of 28 percent per year; on average, the cells were 4.2 years old. For Marie-Ève Tremblay, a neuroscientist at the Université Laval in Québec City who was not involved in the study, what stands out is the range of microglia ages found—from brand-new to more than 20 years old. “That’s quite striking!” she writes in an email to The Scientist. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 13: Memory, Learning, and Development
Link ID: 24159 - Posted: 10.07.2017

Laurel Hamers Zika’s damaging neurological effects might someday be enlisted for good — to treat brain cancer. In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone. Jeremy Rich, a regenerative medicine scientist at the University of California, San Diego, and colleagues report the findings online September 5 in the Journal of Experimental Medicine. Previous studies had shown that Zika kills stem cells that generate nerve cells in developing brains (SN: 4/2/16, p. 26). Because of similarities between those neural precursor cells and stem cells that turn into glioblastomas, Rich’s team suspected the virus might also target the cells that cause the notoriously deadly type of cancer. In the United States, about 12,000 people are expected to be diagnosed with glioblastoma in 2017. (It’s the type of cancer U.S. Senator John McCain was found to have in July.) Even with treatment, most patients live only about a year after diagnosis, and tumors frequently recur. In cultures of human cells, Zika infected glioblastoma stem cells and halted their growth, Rich and colleagues report. The virus also infected full-blown glioblastoma cells but at a lower rate, and didn’t infect normal brain tissues. Zika-infected mice with glioblastoma either saw their tumors shrink or their tumor growth slow compared with uninfected mice. The virus-infected mice lived longer, too. In one trial, almost half of the mice survived more than six weeks after being infected with Zika, while all of the uninfected mice died within two weeks of receiving a placebo. |© Society for Science & the Public 2000 - 2017. A

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 13: Memory, Learning, and Development
Link ID: 24039 - Posted: 09.06.2017

Jon Hamilton Doctors use words like "aggressive" and "highly malignant" to describe the type of brain cancer discovered in Arizona Sen. John McCain. The cancer is a glioblastoma, the Mayo Clinic said in a statement Wednesday. It was diagnosed after doctors surgically removed a blood clot from above McCain's left eye. Doctors who were not involved in his care say the procedure likely removed much of the tumor as well. Glioblastomas, which are the most common malignant brain tumor, tend to be deadly. Each year in the U.S., about 12,000 people are diagnosed with the tumor. Most die within two years, though some survive more than a decade. "It's frustrating," says Nader Sanai, director of neurosurgical oncology at the Barrow Neurological Institute in Phoenix. Only "a very small number" of patients beat the disease, he says. And the odds are especially poor for older patients like McCain, who is 80. "The older you are, the worse your prognosis is," Sanai says, in part because older patients often aren't strong enough to tolerate aggressive radiation and chemotherapy. Arizona Sen. John McCain on Capitol Hill in April 2017, three months before he was diagnosed with brain cancer. © 2017 npr

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23857 - Posted: 07.21.2017

By Teal Burrell In neuroscience, neurons get all the glory. Or rather, they used to. Researchers are beginning to discover the importance of something outside the neurons—a structure called the perineuronal net. This net might reveal how memories are stored and how various diseases ravage the brain. The realization of important roles for structures outside neurons serves as a reminder that the brain is a lot more complicated than we thought. Or, it’s exactly as complicated as neuroscientists thought it was 130 years ago. In 1882, Italian physician and scientist Camillo Golgi described a structure that enveloped cells in the brain in a thin layer. He later named it the pericellular net. His word choice was deliberate; he carefully avoided the word “neuron” since he was engaged in a battle with another neuroscience luminary, Santiago Ramón y Cajal, over whether the nervous system was a continuous meshwork of cells that were fused together—Golgi’s take—or a collection of discrete cells, called neurons—Ramón y Cajal’s view. Ramón y Cajal wasn’t having it. He argued Golgi was wrong about the existence of such a net, blaming the findings on Golgi’s eponymous staining technique, which, incidentally, is still used today. Ramón y Cajal’s influence was enough to shut down the debate. While some Golgi supporters labored in vain to prove the nets existed, their findings never took hold. Instead, over the next century, neuroscientists focused exclusively on neurons, the discrete cells of the nervous system that relay information between one another, giving rise to movements, perceptions, and emotions. (The two adversaries would begrudgingly share a Nobel Prize in 1906 for their work describing the nervous system.) © 1996-2016 WGBH Educational Foundation

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22252 - Posted: 05.26.2016

By Amina Zafar, Tragically Hip frontman ​Gord Downie's resilience and openness about his terminal glioblastoma and his plans to tour could help to reduce stigma and improve awareness, some cancer experts say. Tuesday's news revealed that the singer has an aggressive form of cancer that originated in his brain. An MRI scan last week showed the tumour has responded well to surgery, radiation and chemotherapy, doctors said. "I was quickly impressed by Gord's resilience and courage," Downie's neuro-oncologist, Dr. James Perry of Sunnybrook Health Sciences Centre, told a news conference. Perry said it's daunting for many of his patients to reveal the diagnosis to their family, children and co-workers. "The news today, while sad, also creates for us in brain tumour research an unprecedented opportunity to create awareness and to create an opportunity for fundraising for research that's desperately needed to improve the odds for all people with this disease," Perry said. Dr. James Perry, head of neurology at Toronto's Sunnybrook Health Sciences Centre, calls Gord Downie's sad news an unprecedented opportunity to fundraise for brain tumour research. (Aaron Vincent Elkaim/Canadian Press) "Gord's courage in coming forward with his diagnosis will be a beacon for all patients with glioblastoma in Canada. They will see a survivor continuing with his craft despite its many challenges." ©2016 CBC/Radio-Canada.

Related chapters from BN8e: Chapter 1: Introduction: Scope and Outlook; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior; Chapter 14: Attention and Consciousness
Link ID: 22251 - Posted: 05.26.2016

By Diana Kwon Microglia, the immune cells of the brain, have long been the underdogs of the glia world, passed over for other, flashier cousins, such as astrocytes. Although microglia are best known for being the brain’s primary defenders, scientists now realize that they play a role in the developing brain and may also be implicated in developmental and neurodegenerative disorders. The change in attitude is clear, as evidenced by the buzz around this topic at this year’s Society for Neuroscience (SfN) conference, which took place from October 17 to 21 in Chicago, where scientists discussed their role in both health and disease. Activated in the diseased brain, microglia find injured neurons and strip away the synapses, the connections between them. These cells make up around 10 percent of all the cells in the brain and appear during early development. For decades scientists focused on them as immune cells and thought that they were quiet and passive in the absence of an outside invader. That all changed in 2005, when experimenters found that microglia were actually the fastest-moving structures in a healthy adult brain. Later discoveries revealed that their branches were reaching out to surrounding neurons and contacting synapses. These findings suggested that these cellular scavengers were involved in functions beyond disease. The discovery that microglia were active in the healthy brain jump-started the exploration into their underlying mechanisms: Why do these cells hang around synapses? And what are they doing? © 2015 Scientific American

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 21566 - Posted: 10.26.2015

Laura Sanders A type of brain cell formerly known for its supporting role has landed a glamorous new job. Astrocytes, a type of glial cell known to feed, clean and guide the growth of their flashier nerve cell neighbors, also help nerve cells send electrical transmissions, scientists report in the Aug. 5 Journal of Neuroscience. The results are the latest in scientists’ efforts to uncover the mysterious and important ways in which cells other than nerve cells keep the nervous system humming. Astrocytes deliver nutrients to nerve cells, flush waste out of the brain (SN: 9/22/12) and even help control appetite (SN: 6/28/14). The latest study suggests that these star-shaped cells also help electrical messages move along certain nerve cells’ message-sending axons, a job already attributed to other glial cells called oligodendrocytes and Schwann cells. Courtney Sobieski of Washington University School of Medicine in St. Louis and colleagues grew individual rat nerve cells in a single dish that contained patches of astrocytes. Some nerve cells grew on the patches; others did not. The nerve cells deprived of astrocyte contact showed signs of sluggishness. The researchers think that astrocytes guide nerve cell growth in a way that enables the nerve cells to later fire off quick and precise messages. It’s not clear how the astrocytes do that, but the results suggest that proximity is the key: Astrocytes needed to be close to the nerve cell to help messages move. © Society for Science & the Public 2000 - 2015

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 21264 - Posted: 08.05.2015

By Ashley Yeager The image is made using Brainbow, a technique developed in 2007 that inserts genes for fluorescent proteins into animals. When activated, the proteins illuminate some cells in a range of colors. While most researchers use Brainbow to visualize connections between nerve cells in the brain, Alain Chédotal of the Institut de la Vision in Paris and colleagues customized the technique to trace networks of cells called oligodendrocytes. These cells wrap a material called myelin, the biological equivalent of electrical insulation, around long strands of nerve cells that transmit electrical signals in the brain and throughout the body. How oligodendrocytes work together to wrap nerve fibers in myelin becomes evident in Brainbow photos of the roughly 3-millimeter-long optic nerve, the team reports in the April Glia. The myelin shields the precious link between brain and eyes. Studying interactions among oligodendrocytes as well as the cells’ reactions to various drugs may lead to improved therapies for multiple sclerosis, a disease caused by the destruction of myelin. Citations L. Dumas et al. Multicolor analysis of oligodendrocyte morphology, interactions, and development with Brainbow. Glia. Vol. 63, April 2015, p. 699. doi: 10.1002/glia.22779 © Society for Science & the Public 2000 - 2015.

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20885 - Posted: 05.05.2015

By Dialynn Dwyer @dia_dwyer Warning: The above video contains graphic images. Steven Keating says he fought his cancer with curiosity. The MIT doctoral student was diagnosed in the summer of 2014 with a baseball-sized brain tumor, and during his treatment he gathered his health data in order to understand the science behind what his body was going through. He even filmed his ten hour brain surgery. And though his surgery was performed and filmed last summer, it gained attention recently when Vox wrote about Keating and his surgery. Through his experience, Keating became passionate about more transparent health records. “Healthcare should be a two-way road, patients alongside doctors and researchers as a team,” he says on his website. “The future will be driven by networked healthcare, support communities, and I believe patient curiosity. I do believe learning, understanding, and access can heal.” Keating has given public talks about his experience, and he has shared all his findings, including the condensed video of his surgery, through his website for anyone to study.

Related chapters from BN8e: Chapter 1: Introduction: Scope and Outlook
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior
Link ID: 20884 - Posted: 05.05.2015

Jon Hamilton The simple act of thinking can accelerate the growth of many brain tumors. That's the conclusion of a paper in Cell published Thursday that showed how activity in the cerebral cortex affected high-grade gliomas, which represent about 80 percent of all malignant brain tumors in people. "This tumor is utilizing the core function of the brain, thinking, to promote its own growth," says Michelle Monje, a researcher and neurologist at Stanford who is the paper's senior author. In theory, doctors could slow the growth of these tumors by using sedatives or other drugs to reduce mental activity, Monje says. But that's not a viable option because it wouldn't eliminate the tumor and "we don't want to stop people with brain tumors from thinking or learning or being active." Even so, the discovery suggests other ways to slow down some of the most difficult brain tumors, says Tracy Batchelor, who directs the neuro-oncology program at Massachusetts General Hospital and was not involved in the research. "We really don't have any curative treatments for high-grade gliomas," Batchelor says. The discovery of a link between tumor growth and brain activity "has opened up a window into potential therapeutic interventions," he says. The discovery came from a team of scientists who studied human glioma tumors implanted in mouse brains. The scientists used a technique called optogenetics, which uses light to control brain cells, to increase the activity of cells near the tumors. © 2015 NPR

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20846 - Posted: 04.25.2015

by Helen Thomson KULLERVO HYNYNEN is preparing to cross neuroscience's final frontier. In July he will work with a team of doctors in the first attempt to open the blood-brain barrier in humans – the protective layer around blood vessels that shields our most precious organ against threats from the outside world. If successful, the method would be a huge step in the treatment of pernicious brain diseases such as cancer, Parkinson's and Alzheimer's, by allowing drugs to pass into the brain. The blood-brain barrier (BBB) keeps toxins in the bloodstream away from the brain. It consists of a tightly packed layer of endothelial cells that wrap around every blood vessel throughout the brain. It prevents viruses, bacteria and any other toxins passing into the brain, while simultaneously ushering in vital molecules such as glucose via specialised transport mechanisms. The downside of this is that the BBB also completely blocks the vast majority of drugs. Exceptions include some classes of fat and lipid-soluble chemicals, but these aren't much help as such drugs penetrate every cell in the body – resulting in major side effects. "Opening the barrier is really of huge importance. It is probably the major limitation for innovative drug development for neurosciences," says Bart De Strooper, co-director of the Leuven Institute for Neuroscience and Disease in Belgium. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19748 - Posted: 06.19.2014

by Ashley Yeager A nerve cell's long, slender tentacle isn’t evenly coated with an insulating sheath as scientists had thought. Instead, many nerve cells in the brains of mice have stretches of these tentacles, called axons, that are naked, researchers report April 18 in Science. The unsheathed feeler can be as long as 80 micrometers. Nerve cells can also have specific patterns in the gaps of the insulating layer, called myelin. The differences in the thickness of that coating may control how fast signals travel between nerve cells, the scientists suggest. The finding could have implications for understanding nerve-based diseases, such as multiple sclerosis, and improve scientists’ understanding of how signals are transmitted in the brain. © Society for Science & the Public 2000 - 2013.

Related chapters from BN8e: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 19507 - Posted: 04.19.2014