myelination

How the brain makes myelination activity-dependent

A major question regarding how axons acquire a coat of myelin, is the role of spiking activity. It is known that in culture systems oligodendrocytes will at least try to wrap anything that feels like an axon—even dead axons and artificial tubes. As axons acquire additional layers of myelin they conduct signals faster, and presumably become more efficient. It would therefore seem logical that the nervous system should apportion the most myelin to those neurons that are seeing the greatest activity. In that way the brain gets the most bang for its buck, energetically speaking. A new study in PLOS Biology suggests that while myelination is in many cases activity-independent at first, neurons can significantly ramp things up by flipping various molecular switches, one which appears to be Neuregulin (NRG).

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Your Internal Fiber Optic Network

The above image is an SEM of a section through the sciatic nerve, showing Myelinated Nerve Fibers (axons). Myelin (blue) is an insulating fatty layer that surrounds the nerve fiber (brown). This increases the speed at which nerve impulses travel. Much like the insulation on household wiring, myelination helps prevent the electrical current from leaving the axon. It has been suggested that myelin helped permit the existence of larger organisms (like humans) by maintaining agile communication between distant body parts.

Click to see more Myelinated Nerve Fibers

Myelin is formed when Schwann cells wrap around fibers, depositing layers of myelin between each coil. The outermost layer consists of the Schwann cell’s cytoplasm and is known as the neurolemma or sheath of Schwann. During human infancy, myelination occurs quickly, leading to a child’s fast development, including crawling and walking in the first year. Myelination continues through the adolescent stage of life.

View scans showing Multiple Sclerosis

Multiple Sclerosis is an autoimmune disease where the protective myelin sheath is attacked by the immune system, due to what is thought to be a virus or defective gene. When this myelin covering is damaged, nerve signals slow down or stop. This results in a variety of symptoms including muscle spasms, loss of balance and coordination, numbness, and muscle weakness.  

Image above © Steve Gschmeissner / Science Source

This picture shows the architecture of white matter in your brain.

The nervous system is made up of two types of matter; white and grey. They get their colour from when the axons are covered in a fatty white coloured substance called myelin.
Essentially, the grey matter is composed of the neuron’s cell bodies whilst white matter is composed of the myelinated axons which connects areas of grey matter together.
It can be compared to a computer network; the grey matter as the computers, whereas the white matter represents the network cables connecting the computers together.

Insomnia could be caused by loose connections in the brain

Feel like you haven’t slept in ages? If you’re one of the 5 per cent of the population who has severe insomnia – trouble sleeping for more than a month – then your brain’s white matter might be to blame.

The cell bodies and synapses of our brain cells make up our brain’s grey matter, while bundles of their tails that connect one brain region to another make up the white matter. These nerve cell tails – axons – are cloaked in a fatty myelin sheath that helps transmit signals.

Radiologist Shumei Li from Guangdong No. 2 Provincial People’s Hospital in Guangzhou, China, and her team, scanned the brains of 30 healthy sleepers and 23 people with severe insomnia using diffusion tensor imaging MRI. This imaging technique lights up the white matter circuitry.

Axons unsheathed

They found that in the brains of the people with severe insomnia, the regions in the right hemisphere that support learning, memory, smell and emotion were less well connected compared with healthy sleepers. They attribute this break down in circuitry to the loss of the myelin sheath in the white matter. A study in November 2015 suggested that smoking could be one cause for myelin loss.

The team also found that the insomniacs had poorer connections in the white matter of the thalamus, a brain region that regulates consciousness, alertness and sleep.

The study proposes a potential mechanism for insomnia but there could be other factors, says Max Wintermark, a radiologist at Stanford. He says it’s not possible to say whether the poor connections are the cause of result of insomnia.

“This study takes us one step further in understanding insomnia and a step closer to a potential treatment,” says Wintermark. Knowing what the brains of people with insomnia look like is important if we are ever to understand the condition, he says.

Journal reference: Radiology, DOI: 10.1148/radiol.2016152038

Source: New Scientist (by Vijay Shankar)

Wii Balance Board Induces Changes in the Brains of MS Patients

A balance board accessory for a popular video game console can help people with multiple sclerosis (MS) reduce their risk of accidental falls, according to new research published online in the journal Radiology. Magnetic resonance imaging (MRI) scans showed that use of the Nintendo Wii Balance Board system appears to induce favorable changes in brain connections associated with balance and movement.

Balance impairment is one of the most common and disabling symptoms of MS, a disease of the central nervous system in which the body’s immune system attacks the protective sheath around nerve fibers. Physical rehabilitation is often used to preserve balance, and one of the more promising new tools is the Wii Balance Board System, a battery-powered device about the size and shape of a bathroom scale. Users stand on the board and shift their weight as they follow the action on the television screen during games like slalom skiing.

While Wii balance board rehabilitation has been reported as effective in patients with MS, little is known about the underlying physiological basis for any improvements in balance.

Researchers recently used an MRI technique called diffusion tensor imaging (DTI) to study changes in the brains of 27 MS patients who underwent a 12-week intervention using Wii balance board-based visual feedback training. DTI is a non-conventional MRI technique that allows detailed analysis of the white matter tracts that transmit nervous signals through the brain and body.

MRI scans of the MS patients showed significant effects in nerve tracts that are important in balance and movement. The changes seen on MRI correlated with improvements in balance as measured by an assessment technique called posturography.

These brain changes in MS patients are likely a manifestation of neural plasticity, or the ability of the brain to adapt and form new connections throughout life, according to lead author Luca Prosperini, M.D., Ph.D., from Sapienza University in Rome, Italy.

“The most important finding in this study is that a task-oriented and repetitive training aimed at managing a specific symptom is highly effective and induces brain plasticity,” he said. “More specifically, the improvements promoted by the Wii balance board can reduce the risk of accidental falls in patients with MS, thereby reducing the risk of fall-related comorbidities like trauma and fractures.”

Dr. Prosperini noted that similar plasticity has been described in persons who play video games, but the exact mechanisms behind the phenomenon are still unknown. He hypothesized that changes can occur at the cellular level within the brain and may be related to myelination, the process of building the protective sheath around the nerves.

The rehabilitation-induced improvements did not persist after the patients discontinued the training protocol, Dr. Prosperini said, most likely because certain skills related to structural changes to the brain after an injury need to be maintained through training.

“This finding should have an important impact on the rehabilitation process of patients, suggesting that they need ongoing exercises to maintain good performance in daily living activities,” Dr. Prosperini said.

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Histology Look-a-like #211

Schwaan cell (EM) v Cookie monster

This electron micrograph shows a cross-section through a nerve that contains non-myelinated axons. 

Schwaan cells wrap around axons many, many times to form the myelin sheath of a myelinated axon. But, perhaps you didn’t know that Schwaan cells are also associated with non-myelinated axons. In these non-myelinated axons the Schwaan cells don’t wrap around the axons multiple times, they simply engulf them.

This Schwaan cell (nucleus; mouth) was clearly hungry (axons; eyes).

Now me want cookie. 

i♡histo

The Truth About MS

The truth about MS is that this stupid disease is stupid in different ways for each person that has it.

The truth about MS is that it’s like Whack-A-Mole— every time you think you understand it, something else pops up. Unlike Whack-A-Mole, there is no satisfaction of hitting something or winning prizes.

The truth about MS is that there are bad days. And good days. And bad days intertwined with good. But you really appreciate the good days because you don’t know when the bad ones are coming.

The truth about MS is that it comes with profound sadness. I can post a million funny anecdotes about having the disease but there is always this sadness lurking behind the words. It’s sad to have a disease. It’s sad to have a body that fails you.

The truth about MS is that it changes your life. Find supportive people. Meditate. Breathe. Hug an animal. Do nice things for yourself. Read. Live presently. Sing karaoke. Play laser tag. Okay, the last two are for me.

The truth about MS is that it sucks but I try every day to be okay even though things aren’t.

How Infections in Newborns are Linked to Later Behavior Problems

In animal study, inflammation stops cells from accessing iron needed for brain development

Researchers exploring the link between newborn infections and later behavior and movement problems have found that inflammation in the brain keeps cells from accessing iron that they need to perform a critical role in brain development.

Specific cells in the brain need iron to produce the white matter that ensures efficient communication among cells in the central nervous system. White matter refers to white-colored bundles of myelin, a protective coating on the axons that project from the main body of a brain cell.

The scientists induced a mild E. coli infection in 3-day-old mice. This caused a transient inflammatory response in their brains that was resolved within 72 hours. This brain inflammation, though fleeting, interfered with storage and release of iron, temporarily resulting in reduced iron availability in the brain. When the iron was needed most, it was unavailable, researchers say.

“What’s important is that the timing of the inflammation during brain development switches the brain’s gears from development to trying to deal with inflammation,” said Jonathan Godbout, associate professor of neuroscience at The Ohio State University and senior author of the study. “The consequence of that is this abnormal iron storage by neurons that limits access of iron to the rest of the brain.”

The research is published in the Oct. 9, 2013, issue of The Journal of Neuroscience.

The cells that need iron during this critical period of development are called oligodendrocytes, which produce myelin and wrap it around axons. In the current study, neonatal infection caused neurons to increase their storage of iron, which deprived iron from oligodendrocytes.

In other mice, the scientists confirmed that neonatal E. coli infection was associated with motor coordination problems and hyperactivity two months later – the equivalent to young adulthood in humans. The brains of these same mice contained lower levels of myelin and fewer oligodendrocytes, suggesting that brief reductions in brain-iron availability during early development have long-lasting effects on brain myelination. 

The timing of infection in newborn mice generally coincides with the late stages of the third trimester of pregnancy in humans. The myelination process begins during fetal development and continues after birth.

Though other researchers have observed links between newborn infections and effects on myelin and behavior, scientists had not figured out why those associations exist. Godbout’s group focuses on understanding how immune system activation can trigger unexpected interactions between the central nervous system and other parts of the body.

“We’re not the first to show early inflammatory events can change the brain and behavior, but we’re the first to propose a detailed mechanism connecting neonatal inflammation to physiological changes in the central nervous system,” said Daniel McKim, a lead author on the paper and a student in Ohio State’s Neuroscience Graduate Studies Program.

The neonatal infection caused several changes in brain physiology. For example, infected mice had increased inflammatory markers, altered neuronal iron storage, and reduced oligodendrocytes and myelin in their brains. Importantly, the impairments in brain myelination corresponded with behavioral and motor impairments two months after infection.

Though it’s unknown if these movement problems would last a lifetime, McKim noted that “since these impairments lasted into what would be young adulthood in humans, it seems likely to be relatively permanent.”

The reduced myelination linked to movement and behavior issues in this study has also been associated with schizophrenia and autism spectrum disorders in previous work by other scientists, said Godbout, also an investigator in Ohio State’s Institute for Behavioral Medicine Research (IBMR).

“More research in this area could confirm that human behavioral complications can arise from inflammation changing the myelin pattern. Schizophrenia and autism disorders are part of that,” he said.

This current study did not identify potential interventions to prevent these effects of early-life infection. Godbout and colleagues theorize that maternal nutrition – a diet high in antioxidants, for example – might help lower the inflammation in the brain that follows a neonatal infection.

“The prenatal and neonatal period is such an active time of development,” Godbout said. “That’s really the key – these inflammatory challenges during critical points in development seem to have profound effects. We might just want to think more about that clinically.”

Researchers Present New Findings About Human Brain Plasticity

Read the full article Researchers Present New Findings About Human Brain Plasticity at NeuroscienceNews.com.

The brain’s plasticity and its adaptability to new situations do not function the way researchers previously thought, according to a new study published in the journal Cell. Earlier theories are based on laboratory animals, but now researchers at Karolinska Institutet in Sweden have studied the human brain. The results show that a type of support cell, the oligodendrocyte, which plays an important role in the cell-cell communication in the nervous system, is more sophisticated in humans than in rats and mice – a fact that may contribute to the superior plasticity of the human brain.

The research is in Cell. (full open access)

Research:  “Dynamics of Oligodendrocyte Generation and Myelination in the Human Brain” by Maggie S.Y. Yeung, Sofia Zdunek, Olaf Bergmann, Samuel Bernard, Mehran Salehpour, Kanar Alkass, Shira Perl, John Tisdale, Göran Possnert, Lou Brundin, Henrik Druid, and Jonas Frisén in Cell. doi:10.1016/j.cell.2014.10.011

Image: In humans, oligodendrocyte generation is very low but despite this, myelin production can be modulated and increased if necessary. In other words, the human brain appears to have a preparedness for it, while in mice and rats, increased myelin production relies on the generation of new oligodendrocytes. This image is for illustrative purposes only. Credit Holly Fischer.

Mending Myelin

The cable-like axons of nerve cells can carry electrical signals long distances. To speed up transmission in the central nervous system, support cells called oligodendrocytes wrap axons in an insulating material called myelin. But in diseases like multiple sclerosis, myelin is destroyed, making it difficult for nerve cells to carry messages.

In an effort to repair damaged myelin, scientists are searching for ways to nudge immature oligodendrocytes to become mature, myelin-producing cells. The image above shows a single oligodendrocyte (green) growing on a special plate with tiny, cone-shaped projections. Scientists use these plates — called micropillar arrays — because they can test whether various compounds will help oligodendrocytes grow and wrap around the cones in the same way they wrap around axons. This research may open the door for new therapies to regrow myelin in people with multiple sclerosis and other disorders where it is destroyed.  

Source: Brain Facts

Image Credit: Mei, et al. The Journal of Neuroscience, 2016.

Turning science on its head

Harvard neuroscientists have made a discovery that turns 160 years of neuroanatomy on its head.

Myelin, the electrical insulating material in the body long known to be essential for the fast transmission of impulses along the axons of nerve cells, is not as ubiquitous as thought, according to new work led by Professor Paola Arlotta of the Harvard Stem Cell Institute (HSCI) and the University’s Department of Stem Cell and Regenerative Biology, in collaboration with Professor Jeff Lichtman of Harvard’s Department of Molecular and Cellular Biology.

“Myelin is a relatively recent invention during evolution,” says Arlotta. “It’s thought that myelin allowed the brain to communicate really fast to the far reaches of the body, and that it has endowed the brain with the capacity to compute higher-level functions.”

In fact, loss of myelin is a feature in a number of devastating diseases, including multiple sclerosis and schizophrenia.

But the new research shows that despite myelin’s essential roles in the brain, “some of the most evolved, most complex neurons of the nervous system have less myelin than older, more ancestral ones,” said Arlotta, co-director of the HSCI neuroscience program.

What this means, she said, is that the higher one looks in the cerebral cortex — closer to the top of the brain, which is its most evolved part — the less myelin one finds.  Not only that, but “neurons in this part of the brain display a brand-new way of positioning myelin along their axons that has not been previously seen. They have ‘intermittent myelin’ with long axon tracts that lack myelin interspersed among myelin-rich segments.”

“Contrary to the common assumptions that neurons use a universal profile of myelin distribution on their axons, the work indicates that different neurons choose to myelinate their axons differently,” Arlotta said. “In classic neurobiology textbooks, myelin is represented on axons as a sequence of myelinated segments separated by very short nodes that lack myelin. This distribution of myelin was tacitly assumed to be always the same, on every neuron, from the beginning to the end of the axon. This new work finds this not to be the case.”

The results of the research by Arlotta and postdoctoral fellow Giulio Srubek Tomassy, the first author on the report, are published in the latest edition of the journal Science.

The paper is accompanied by a “perspective” by R. Douglas Fields of the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institutes of Health, who said that Arlotta and Tomassy’s findings raise important questions about the purpose of myelin, and “are likely to spark new concepts about how information is transmitted and integrated in the brain.”

Arlotta and Tomassy collaborated closely on the new work with postdoctoral fellow Daniel Berger of the Lichtman lab, which generated one of the two massive electron microscopy databases that made the work possible.

“The fact that it is the most evolved neurons, the ones that have expanded dramatically in humans, suggest that what we’re seeing might be the ‘future.’ As neuronal diversity increases and the brain needs to process more and more complex information, neurons change the way they use myelin to achieve more,” said Arlotta.

Tomassy said it is possible that these profiles of myelination “may be giving neurons an opportunity to branch out and ‘talk’ to neighboring neurons.” For example, because axons cannot make synaptic contacts when they are myelinated, one possibility is that these long myelin gaps may be needed to increase neuronal communication and synchronize responses across different neurons. He and Arlotta postulate that the intermittent myelin may be intended to fine-tune the electrical impulses traveling along the axons, in order to allow the emergence of highly complex neuronal behaviors.

Tuning of Timing in Auditory Axons

An LMU team has shown that the axons of auditory neurons in the brainstem which respond to low and high-frequency sounds differ in their morphology, and that these variations correlate with differences in the speed of signal conduction.

The research is in Nature Communications. (full open access)

Research: “Tuning of Ranvier node and internode properties in myelinated axons to adjust action potential timing” by Marc C. Ford, Olga Alexandrova, Lee Cossell, Annette Stange-Marten, James Sinclair, Conny Kopp-Scheinpflug, Michael Pecka, David Attwell and Benedikt Grothe in Nature Communications doi:10.1038/ncomms9073

Image: Along the axons, the myelin sheath is regularly interrupted by structures referred to as the nodes of Ranvier, and its insulating effect ensures that action potentials can be built up (i.e. signal transmission can occur) only at these sites. Image is for illustrative purposes only.

A scanning electron micrograph (SEM) of a freeze-fractured cross section through a nerve bundle. 

Axons (brown) of nerve cells are surrounded by insulating cells called the myeline sheet (purple). These allow for more efficient conduction of nerve impulses along these huge cells. The sciatic nerve in mammals goes from the base of the spine, to the bottom of your feet. These cells can reach up to more than a meter depending on how tall you are. The perinuerium is the connective tissue (blue) that surrounds the structure.

(Source: Facebook - NeuronsWantFood)

For more information on neurons, feel free to check out this wiki page on them!