Can brain cells move?

Can brain cells move?

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I was discussing this with my brother. I'm pretty sure I read somewhere that they can move.


EDIT: By movement I mean long distance migration (preferably within the brain only).

The question is relatively broad and one should take into account that the brain not only consists of neurons, but also glial cells (supportive cells) and pre-mitotic neuronal stem cells. Furthermore, as critical fellow-scientists have indicated, developmental stage is very important, as the developing embryonic brain is very different from the adult brain.

However, after sifting through various publications, the answer to the question is actually remarkably simple: Yes, brain cells migrate.

In the adult brain glial cells migrate in the brain (Klämbt, 2009). Glial cells are involved in a myriad of functions, but a notable example of migrating glial cells are the oligodendrocytes that migrate relative long distances to find their target axons onto which they wrap themselves to form the insulating myelin sheath (Tsai and Miller, 2002).

Neuronal stem cells migrate over long distances in response to injury (Imitola et al., 2004) and they migrate from specific stem-cell locations (e.g., hippocampus and subventricular zone) to other regions (Clarke, 2003).

Interestingly, post-mitotic (fully differentiated, not-dividing) neurons can also be migratory in the adult brain. Specifically, newly formed neurons can migrate over hundreds of microns in fish (Scott et al., 2012) and neuronal migration has been shown in the human cortex as well (Fox et al., 1998).

Not surprisingly, glial cells, stem cells and neurons also migrate during embryonic development. Most notably, post-mitotic neurons destined to fulfill peripheral functions have to migrate over relatively long distances from the neural crest to their target locations (Neuroscience, 2nd ed, Neuronal Migration).

To add to Christiaan's answer, I'll mention one striking example of long-distance neuronal migration in the adult mammalian brain: the so-called Rostral Migratory Stream found in rodents, in rabbits and both the squirrel and rhesus monkey.

Neuronal precursors originating in the subventricular zone (SVZ) of the brain migrate to reach the main olfactory bulb (OB), and it's quite a distance for the small cells.

Keeping brain development untangled

The hippocampus—the brain region associated with memory—is named after its seahorse-like shape. Here, a crystal seahorse with yellow and blue oil repelling colored water symbolizes the attractive and repulsive forces between the molecules, teneurin-3 (in blue) and latrophilin-2 (in yellow), that direct neural network assembly in the mouse brain.

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Multitasking molecules may be the key to solving the riddle of how the brain makes trillions of specifically coded connections between the brain cells known as neurons.

In mice, two molecules that stud cell surfaces can create attractive or repulsive forces between the brain cells they’re displayed on, a new Stanford University study has found. By attracting or repelling other brain cells questing for neural connections, the magnet-like molecules called teneurin-3 and latrophilin-2 play an important role in wiring the part of the brain that helps mice navigate and process information about the objects around them.The findings help explain how multitudes of neurons can connect in an ordered way using relatively few molecular “tags,” according to a study led by Stanford biologist Liqun Luo, the Ann and Bill Swindells Professor of Biology, and Daniel Pederick, lead author and postdoctoral research fellow with Biology. The study also reveals the architecture of brain development in one segment of the hippocampus, the part of the brain that encodes, stores, and retrieves memories.

The research was published June 4 in the journal Science.

Pederick worked with Luo lab research scientist Jan Lui to search for a cell surface molecule that was present in the opposite places teneurin-3 was found in the two parallel networks in the mouse hippocampus.


When you think of the brain, you probably think of neurons. Neurons are the cells in the brain that send and receive electrical and chemical signals. They are building blocks of your brain, and transmit information to other neurons, muscles, and tissues throughout the body. They allow you to think, feel, move, and comprehend the world around you.

A neuron is made up of three basic parts: the cell body, or soma branching dendrites that receive signals from other neurons and the axon, which sends signals out to surrounding neurons through the axon terminal. When a neuron fires an action potential, electric and chemical signals spread from the axon of one neuron to the dendrites of another neuron across a small gap called the synapse. (Read our fact sheet “How Does the Brain Work?” to learn more.)

Like neurons, glia are important cells of the nervous system. Scientists used to think that glia were like glue, only for holding the neurons in place. The name “glia” is Latin for “glue.” However, we now know that glial cells are not just brain glue. In fact, glia actively participate in brain signaling, and are necessary for the healthy function of neurons.

Unlike neurons, glial cells cannot fire action potentials to communicate messages, but that does not mean they are inactive. Glia communicate to each other and to neurons using chemical signals, and can even respond to many of the same chemicals that neurons can, such as ions and neurotransmitters. This means that glia can eavesdrop on the neurons, to help strengthen the messages that are passed between them.

There are many types of glial cells in the brain. Here are three important glial cell types:

Oligodendrocytes: A special type of glial cell known as an oligodendrocyte wraps around the axons of neurons, making up what is known as the myelin sheath. Like insulation around an electrical wire, oligodendrocytes insulate the axon and help neurons pass electrical signals at incredible speed and over long distances.

Microglia: Microglia are the immune cells of the central nervous system. They move around within the brain and constantly communicate with other glia. In a healthy adult brain, microglia are constantly testing the environment for signs of trouble. For example, if an infection or disease causes neurons to die or become damaged, these neurons will release chemical “danger signals.” Microglia recognize these signals, and alert other nearby microglia of potential danger. This causes the surrounding microglia to swarm to the dangerous area, where they begin to clean up the mess. This prevents the spread of buildup or debris in the brain, and protects the brain from long term inflammation. Once the danger has passed, microglia go back to their resting state, continuing to survey the brain.

Astrocytes: Astrocytes are star-shaped cells that surround neurons and support neuron function. Astrocytes mainly help regulate the brain’s environment. Astrocytes also help neurons signal to other neurons by passing chemicals from one neuron to another. Although microglia are the primary immune cells of the brain, astrocytes can also help microglia when the brain is in trouble.

Research highlight

Recently, scientists are discovering new roles for glial cells in disease. Normally, glia protect and help neurons, but when they malfunction, they can cause serious damage.

Animal studies have shown that inflammation caused by glia is associated with many diseases such as Parkinson’s, Alzheimer’s, and multiple sclerosis. This type of research is important because it allows scientists to examine human diseases in animal models. As we continue to learn more about glia, we will be able to use this information to treat these diseases.

Find out more:

Go to to check out a 3-D model of the brain

Beth Stevens, Ph.D., and Staci Bilbo, Ph.D., wrote an article for us called “Microglia: The Brain’s First Responders.” They also participated in a podcast interview with us, where they talked more about microglia and about working in science.


Aamodt S. (2007) Focus on glia and disease. Nature Neuroscience 10:1349-1349.

COVID-19 can affect the brain. New clues hint at how

COVID-19 can come with brain-related problems, but just how the virus exerts its effects isn’t clear.

Roxana Wegner/Moment/Getty Images

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For more than a year now, scientists have been racing to understand how the mysterious new virus that causes COVID-19 damages not only our bodies, but also our brains.

Early in the pandemic, some infected people noticed a curious symptom: the loss of smell. Reports of other brain-related symptoms followed: headaches, confusion, hallucinations and delirium. Some infections were accompanied by depression, anxiety and sleep problems.

Recent studies suggest that leaky blood vessels and inflammation are somehow involved in these symptoms. But many basic questions remain unanswered about the virus, which has infected more than 145 million people worldwide. Researchers are still trying to figure out how many people experience these psychiatric or neurological problems, who is most at risk, and how long such symptoms might last. And details remain unclear about how the pandemic-causing virus, called SARS-CoV-2, exerts its effects.

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“We still haven’t established what this virus does in the brain,” says Elyse Singer, a neurologist at the University of California, Los Angeles. There are probably many answers, she says. “It’s going to take us years to tease this apart.”

Getting the numbers

For now, some scientists are focusing on the basics, including how many people experience these sorts of brain-related problems after COVID-19.

A recent study of electronic health records reported an alarming answer: In the six months after an infection, one in three people had experienced a psychiatric or neurological diagnosis. That result, published April 6 in Lancet Psychiatry, came from the health records of more than 236,000 COVID-19 survivors. Researchers counted diagnoses of 14 disorders, ranging from mental illnesses such as anxiety or depression to neurological events such as strokes or brain bleeds, in the six months after COVID-19 infection.

“We didn’t expect it to be such a high number,” says study coauthor Maxime Taquet of the University of Oxford in England. One in three “might sound scary,” he says. But it’s not clear whether the virus itself causes these disorders directly.

The vast majority of those diagnoses were depression and anxiety, “disorders that are extremely common in the general population already,” points out Jonathan Rogers, a psychiatrist at University College London. What’s more, depression and anxiety are on the rise among everyone during the pandemic, not just people infected with the virus.

Mental health disorders are “extremely important things to address,” says Allison Navis, a neurologist at the post-COVID clinic at Icahn School of Medicine at Mount Sinai in New York City. “But they’re very different than a stroke or dementia,” she says.

About 1 in 50 people with COVID-19 had a stroke, Taquet and colleagues found. Among people with severe infections that came with delirium or other altered mental states, though, the incidence was much higher — 1 in 11 had strokes.

Serious neurological damage, such as these strokes caused by blocked blood vessels, turn up in people with COVID-19. K. Thakur et al/Brain 2021

Taquet’s study comes with caveats. It was a look back at diagnosis codes, often entered by hurried clinicians. Those aren’t always reliable. And the study finds a relationship, but can’t conclude that COVID-19 caused any of the diagnoses. Still, the results hint at how COVID-19 affects the brain.

Blood vessels scrutinized

Early on in the pandemic, the loss of smell suggested that the virus might be able to attack nerve cells directly. Perhaps SARS-CoV-2 could breach the skull by climbing along the olfactory nerve, which carries smells from the nose directly to the brain, some researchers thought.

That frightening scenario doesn’t seem to happen much. Most studies so far have failed to turn up much virus in the brain, if any, says Avindra Nath, a neurologist who studies central nervous system infections at the National Institutes of Health in Bethesda, Md. Nath and his colleagues expected to see signs of the virus in brains of people with COVID-19 but didn’t find it. “I kept telling our folks, ‘Let’s go look again,’” Nath says.

That absence suggests that the virus is affecting the brain in other ways, possibly involving blood vessels. So Nath and his team scanned blood vessels in post-mortem brains of people who had been infected with the virus with an MRI machine so powerful that it’s not approved for clinical use in living people. “We were able to look at the blood vessels in a way that nobody could,” he says.

Damage abounded, the team reported February 4 in the New England Journal of Medicine. Small clots sat in blood vessels. The walls of some vessels were unusually thick and inflamed. And blood was leaking out of the vessels into the surrounding brain tissue. “You can see all three things happening at the same time,” Nath says.

Those results suggest that clots, inflamed linings and leaks in the barriers that normally keep blood and other harmful substances out of the brain may all contribute to COVID-related brain damage.

Signs of damage in the brains of people with COVID-19 involve inflammation, including these immune cells around a blood vessel (left), and changes in cells (right) that might have resulted from low oxygen. J. Lou et al/Free Neuropathology 2021

But several unknowns prevent any definite conclusions about how these damaged blood vessels relate to people’s symptoms or outcomes. There’s not much clinical information available about the people in Nath’s study. Some likely died from causes other than COVID-19, and no one knows how the virus would have affected them had they not died.

Inflamed body and brain

Inflammation in the body can cause trouble in the brain, too, says Maura Boldrini, a psychiatrist at Columbia University in New York. Inflammatory signals released after injury can change the way the brain makes and uses chemical signaling molecules, called neurotransmitters, that help nerve cells communicate. Key communication molecules such as serotonin, norepinephrine and dopamine can get scrambled when there’s lots of inflammation.

Neural messages can get interrupted in people who suffer traumatic brain injuries, for example researchers have found a relationship between inflammation and mental illness in football players and others who experienced hits to the head.

Similar evidence comes from people with depression, says Emily Troyer, a psychiatrist at the University of California, San Diego. Some people with depression have high levels of inflammation, studies have found. “We don’t actually know that that’s going on in COVID,” she cautions. “We just know that COVID causes inflammation, and inflammation has the potential to disrupt neurotransmission, particularly in the case of depression.”

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Among the cells that release inflammatory proteins in the brain are microglia, the brain’s version of the body’s disease-fighting immune system. Microglia may also be involved in the brain’s response to COVID-19. Microglia primed for action were found in about 43 percent of 184 COVID-19 patients, Singer and others reported in a review published February 4 in Free Neuropathology. Similar results come from a series of autopsies of COVID-19 patients’ brains 34 of 41 brains contained activated microglia, researchers from Columbia University Irving Medical Center and New York Presbyterian Hospital reported April 15 in Brain.

With these findings, it’s not clear that SARS-CoV-2 affects people’s brains differently from other viruses, says Navis. In her post–COVID-19 clinic at Mount Sinai, she sees patients with fatigue, headaches, numbness and dizziness — symptoms that are known to follow other viral infections, too. “I’m hesitant to say this is unique to COVID,” Navis says. “We’re just not used to seeing so many people getting one specific infection, or knowing what the viral infection is.”

Teasing apart all the ways the brain can suffer amid this pandemic, and how that affects any given person, is impossible. Depression and anxiety are on the rise, surveys suggest. That rise might be especially sharp in people who endured stressful diagnoses, illnesses and isolation.

In a postmortem brain from a person with COVID-19, a clotting protein called fibrinogen (red) indicates that the blood vessels are damaged and leaky. Avindra Nath

Just being in an intensive care unit can lead to confusion. Delirium affected 606 of 821 people — 74 percent — while patients were in intensive care units for respiratory failure and other serious emergencies, a 2013 study found. Post-traumatic stress disorder afflicted about a third of people who had been seriously sick with COVID-19 (SN: 3/12/21).

More specific aspects of treatment matter too. COVID-19 patients who spent long periods of time on their stomachs might have lingering nerve pain, not because the virus attacked the nerve, but because the prone position compressed the nerves. And people might feel mentally fuzzy, not because of the virus itself, but because a shortage of the anesthetic drug, propofol, meant they received an alternative sedative that can bring more aftereffects, says Rogers, the psychiatrist at University College London.

Lingering questions — what the virus actually does to the brain, who will suffer the most, and for how long — are still unanswered, and probably won’t be for a long time. The varied and damaging effects of lockdowns, the imprecision doctors and patients use for describing symptoms (such as the nonmedical term “brain fog”) and the indirect effects the virus can have on the brain all merge, creating a devilishly complex puzzle.

For now, doctors are busy focusing on ways in which they can help, even amid these mysteries, and designing larger, longer studies to better understand the effects of the virus on the brain. That information will be key to helping people move forward. “This isn’t going to be over soon, unfortunately,” Troyer says.

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Passing Along the Message

The center of the nervous system is the brain. The brain takes in what your eyes see and what your ears hear. If you decide that you want to move around, your brain tells your muscles to do it. You can think of your nervous system as a relay team passing a baton from one runner to the next. But instead of runners, you have cells, and instead of a baton, you have information. A neuron in your brain starts the relay, handing its information to the next cell, which passes the information to another cell. In the end, the information reaches its destination and causes a change – maybe a muscle contracts. The "information" baton passed from neuron to neuron is usually a small electrical event called an action potential.

Hirase H, Qian L, Barthó P, Buzsáki G, 2004. Calcium Dynamics of Cortical Astrocytic Networks In Vivo. PLoS Biol 2(4): e96. doi:10.1371/journal.pbio.0020096. Retrieved May 14, 2011 from

Martini, F. H. and Judi Nath. (2008). Fundamentals of Anatomy and Physiology 8th Edition.Saddle River, NJ: Benjamin Cummings.

Reece, J. B. Neil A. Campbell, Michael L. Cain, Lisa A. Urry, Peter V. Minorsky, Robert B. Jackson, Steven A. Wasserman. (2010). Campbell Biology 9th Edition.Saddle River, NJ: Benjamin Cummings.

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Printout: Label a Neuron

The brain and spinal cord are made up of many cells, including neurons and glial cells. Neurons are cells that send and receive electro-chemical signals to and from the brain and nervous system. There are about 100 billion neurons in the brain. There are many more glial cells they provide support functions for the neurons, and are far more numerous than neurons.

There are many type of neurons. They vary in size from 4 microns (.004 mm) to 100 microns (.1 mm) in diameter. Their length varies from a fraction of an inch to several feet.

Neurons are nerve cells that transmit nerve signals to and from the brain at up to 200 mph. The neuron consists of a cell body (or soma) with branching dendrites (signal receivers) and a projection called an axon , which conduct the nerve signal. At the other end of the axon, the axon terminals transmit the electro-chemical signal across a synapse (the gap between the axon terminal and the receiving cell). The word "neuron" was coined by the German scientist Heinrich Wilhelm Gottfried von Waldeyer-Hartz in 1891 (he also coined the term "chromosome").

The axon , a long extension of a nerve cell, and take information away from the cell body. Bundles of axons are known as nerves or, within the CNS (central nervous system), as nerve tracts or pathways. Dendrites bring information to the cell body.

Myelin coats and insulates the axon (except for periodic breaks called nodes of Ranvier), increasing transmission speed along the axon. Myelin is manufactured by Schwann's cells, and consists of 70-80% lipids (fat) and 20-30% protein.

The cell body (soma) contains the neuron's nucleus (with DNA and typical nuclear organelles). Dendrites branch from the cell body and receive messages.

A typical neuron has about 1,000 to 10,000 synapses (that is, it communicates with 1,000-10,000 other neurons, muscle cells, glands, etc.).

  • Sensory neurons or Bipolar neurons carry messages from the body's sense receptors (eyes, ears, etc.) to the CNS. These neurons have two processes. Sensory neuron account for 0.9% of all neurons. (Examples are retinal cells, olfactory epithelium cells.)
  • Motoneurons or Multipolar neurons carry signals from the CNS to the muscles and glands. These neurons have many processes originating from the cell body. Motoneurons account for 9% of all neurons. (Examples are spinal motor neurons, pyramidal neurons, Purkinje cells.)
  • Interneurons or Pseudopolare (Spelling) cells form all the neural wiring within the CNS. These have two axons (instead of an axon and a dendrite). One axon communicates with the spinal cord one with either the skin or muscle. These neurons have two processes. (Examples are dorsal root ganglia cells.)

Unlike most other cells, neurons cannot regrow after damage (except neurons from the hippocampus). Fortunately, there are about 100 billion neurons in the brain.


Glial cells make up 90 percent of the brain's cells. Glial cells are nerve cells that don't carry nerve impulses. The various glial (meaning "glue") cells perform many important functions, including: digestion of parts of dead neurons, manufacturing myelin for neurons, providing physical and nutritional support for neurons, and more. Types of glial cells include Schwann's Cells, Satellite Cells, Microglia, Oligodendroglia, and Astroglia.

Neuroglia (meaning "nerve glue") are the another type of brain cell. These cells guide neurons during fetal development.

Can brain cells move? - Biology

For such an awesome organ, the brain doesn't look like much. It's a ball of gray looking wrinkled tissue about the size of two of your fists put together. The brain sits in our hard, thick skull with membranes and fluid around it to protect it.

How the Brain Communicates

The brain is part of the nervous system. Together with the spinal cord, it makes up the central nervous system. The brain connects to nerves that travel throughout the body. Nerves from our senses (hearing, seeing, touch, etc.) send signals to the brain to let the brain know what is going on in the outside world. The brain also sends signals using nerves to muscles in order to make our body move.

    Cerebrum - The cerebrum is the biggest part of the brain. It's the gray wrinkly upper part. The surface of the cerebrum is called the cerebral cortex. Different parts of the cerebrum deal with different parts of the body. The back part deals with vision while other parts deal with other functions like movement, hearing, language, and touch. Smart or thinking people are sometimes called cerebral.

The brain has two kinds of memory, short term memory and long term memory. Scientists are still learning exactly how memory works, but they know that short term memory allows us to remember something for a very short time without rehearsing or practicing it. We can't remember a lot of things in short term memory though, and, like its name suggests, these memories don't last very long.

The Brain Needs Energy

The brain may not move, but it needs lots of energy. Energy is sent to the brain by our blood. There are lots of blood vessels and blood flowing through the brain at all times. The brain actually uses around twenty percent of the body's energy.

The Brain Has Two Halves

The brain is divided into two halves. Since the nerves cross when they enter the brain, the left side of our brain controls the right half of our body and the right side controls the left. Each half also controls specialized functions. What each half does depends on whether you are left or right handed. In a right handed person the left side of the brain is used for language and numbers while the right side is the more artistic side and is also used for recognizing objects.

Marian Diamond, known for studies of Einstein’s brain, dies at 90

Marian Cleeves Diamond with a preserved human brain. Elena Zhukova photos (2010).

Marian Cleeves Diamond, one of the founders of modern neuroscience who was the first to show that the brain can change with experience and improve with enrichment, and who discovered evidence of this in the brain of Albert Einstein, died July 25 at the age of 90 at her home in Oakland.

A professor emerita of integrative biology at the University of California, Berkeley, Diamond achieved celebrity in 1984 when she examined preserved slices of Einstein’s brain, finding that he had more support cells in the brain than average.

Her main claim to fame, however, came from work on rats, in which she showed that an enriched environment — toys and companions — changed the anatomy of the brain. The implication was that the brains of all animals, including humans, benefit from an enriched environment, and that impoverished environments can lower the capacity to learn.

Diamond was awed that a small, three-pound mass of protoplasm like the brain was the most complex structure known to humankind.

“Her research demonstrated the impact of enrichment on brain development — a simple but powerful new understanding that has literally changed the world, from how we think about ourselves to how we raise our children,” said UC Berkeley colleague George Brooks, a professor of integrative biology. “Dr. Diamond showed anatomically, for the first time, what we now call plasticity of the brain. In doing so she shattered the old paradigm of understanding the brain as a static and unchangeable entity that simply degenerated as we age. ”

Her results were initially resisted by some neuroscientists. At one meeting, she later recalled, a man stood up after her talk and said loudly, “Young lady, that brain cannot change!”

“It was an uphill battle for women scientists then — even more than now — and people at scientific conferences are often terribly critical,” she wrote in her 1998 book, Magic Trees of the Mind: How to Nurture your Child’s Intelligence, Creativity, and Healthy Emotions from Birth through Adolescence, co-authored with Janet Hopson. “But I felt good about the work, and I simply replied, ‘I’m sorry, sir, but we have the initial experiment and the replication experiment that shows it can.'”

She subsequently demonstrated that the brain can continue to develop at any age, emphasizing the importance of growth and learning throughout life, that male and female brains are structured differently and that stimulating the brain even enhances our immune system.

Diamond was not only a pioneer in neuroscience and anatomical and behavioral research, but a beloved teacher and mentor who was dedicated to university and public service. For decades she could be seen walking through campus to her anatomy class carrying a flowered hat box containing a preserved human brain.

In her typically packed classes, she would gently lift the brain from its wrapping and express her awe that such a small, three-pound mass of protoplasm was the most complex structure known to humankind.

One of those students was Wendy Suzuki, who said in a 2011 TEDx talk that the day she first saw Diamond unveil the brain was “the day I wanted to become a neuroscientist.” Suzuki is now a neuroscientist at New York University and author of the 2015 book Healthy Brain, Happy Life: A Personal Program to Activate Your Brain and Do Everything Better.

Diamond’s anatomy lectures remain on YouTube to inspire another generation: One has received more than 1 million views over 10 years.

Worldwide, Diamond’s ideas fortified efforts of physicians and educators in promoting early nurturing and educational enrichment of children. Her scholarship and personal efforts led to the building and management of orphanages, including one in Cambodia, where she worked to enrich the minds of impoverished children. Her work on environmental enrichment has been so widely accepted that it even led to significant improvements in laboratory and zoo animal care, said Daniela Kaufer, a UC Berkeley professor of integrative biology.

She took every opportunity to encourage activities, both mental and physical, that enrich the brain, and she herself continued to conduct research and teach until 2014, when she retired at the age of 87.

Her life was memorialized in the 2016 documentary film My Love Affair with the Brain: The Life and Science of Dr. Marian Diamond, by Catherine Ryan and Gary Weimberg.

Among her last words were, “If you’re going to live life, you’ve got to be all in.”

Growing up in an enriched environment

Marian Cleeves was born Nov. 11, 1926, in Glendale, California, the youngest of six children of Dr. Montague Cleeves, an immigrant from northern England, and Rosa Marian Wamphler, a UC Berkeley graduate who abandoned her Ph.D. studies to raise her children in La Crescenta. Like her siblings, Marian attended La Crescenta grammar school, Clark Junior High and Glendale High School. She enrolled in Glendale Community College before transferring to UC Berkeley in 1946, where she played and lettered in tennis. Her interest in in sports and exercise continued into her 80s as Diamond swam daily on the Berkeley campus before turning to teaching and laboratory activities.

After obtaining a bachelor’s degree in 1948, she continued her studies at UC Berkeley as the first female graduate student in the Department of Anatomy. Her doctoral dissertation thesis, “Functional Interrelationships of the Hypothalamus and the Neurohypophysis,” was published in 1953. While working on her Ph.D., Diamond also began to teach, developing a lifelong passion.

After working as a research assistant at Harvard University (1952-53), Diamond was appointed the first woman science instructor at Cornell University (1955-58), where she taught human biology and comparative anatomy. She subsequently moved west to teach anatomy to medical students at UC San Francisco.

She returned to UC Berkeley in 1960 as a lecturer, continuing her studies of brain anatomy. By 1964, Diamond had the first actual evidence — actual anatomical measurements — “showing the plasticity of the anatomy of the mammalian cerebral cortex.”

Her aptitude as a teacher and her revolutionary research findings led to her appointment in 1965 as an assistant professor of anatomy — a department since rolled into the Department of Integrative Biology — and later elevation to full professor. She subsequently served as the assistant and associate dean of the College of Letters and Science and director of the Lawrence Hall of Science from 1990 to 1996, where she was able to use her findings on enriched environments to develop educational programs in science and mathematics for students in preschool through high school.

In seminal studies during the 1960s, Diamond demonstrated that enriched environments like this rat cage with toys and companions enhance learning. Marian Diamond photo, 1964.

Brooks said that several landmark publications by Diamond shaped the field of neuroplasticity. In a 1964 paper, Diamond first showed that the structure of the cerebral cortex of young animals could change in response to environmental input. In a 1983 paper, she first showed sexual dimorphism, that is, differences between male and female animals in the structure of the cerebral cortex of young and old animals.

In a 1985 paper, she first showed that the structure of the cerebral cortex of older animals could change in response to environmental input, and influenced learning capacity.

“Her seminal work on environmental enrichment and neural plasticity spawned an entirely new field in modern neuroscience,” said neuroscientist Robert Knight, a UC Berkeley professor of psychology.

Along the way, in 1984 Diamond received four blocks of the preserved brain of Albert Einstein the work on Einstein’s brain was to make her a media celebrity. By comparing results with previous analyses on control brains, the Diamond lab learned that the frontal cortex had more non-neuronal, or glial cells, per neuron than the parietal cortex. After many years of research, Diamond and her team discovered that the big difference in all four areas was in glial cells: Einstein had more glial cells per neuron in the inferior parietal area than the average male brains of the control group. This seminal work put a spotlight on this understudied cellular population and paved the way to a new area of neuroscience study — glial biology.

In a career at UC Berkeley spanning half a century, Diamond inspired thousands of students over generations. In her course Integrative Biology 131 (IB131, Human Anatomy), Diamond annually filled Wheeler Auditorium with her stunning lectures.

Another of her innovative courses was the Anatomy Enrichment Program, which for more than three decades functioned as both a teaching opportunity and an outreach effort to elementary school children in Berkeley and Albany. The spring 2017 semester marked the 40th year of anatomy students teaching elementary school children.

Diamond with her signature hatbox, in which she carried a preserved human brain.

“Marian Diamond (will be) remembered as an esteemed colleague, a friend and a gentle soul who by nature and nurture sought to extend happiness and accomplishment to her students, colleagues and others,” Brooks said.

Diamond was a fellow of the American Association for the Advancement of Science, a California Professor of the Year and National Gold Medalist from the Council for Advancement & Support of Education, a UC Berkeley Alumna of the Year, recipient of the 2012 Clark Kerr Award for Distinguished Leadership in Higher Education and a 1975 Distinguished Teaching Award recipient from UC Berkeley.

She also authored the book Enriching Heredity: The Impact of the Environment on the Anatomy of the Brain (1988) and co-authored The Human Brain Coloring Book (1985).

Diamond was preceded in death by her husband of 35 years, Arnold (“Arne”) Scheibel, who passed away April 3. She is survived by Catherine Theresa Diamond of Taipei, Taiwan, Richard Cleeves Diamond and Jeff Barja Diamond of Berkeley, and Ann Diamond of Mazama, Washington, all children of her first marriage to the late Richard M. Diamond.

Cell Biology 02: The Plasma Membrane

This semester I’m taking a Cell Biology class at Harvard Extension. My plan is to turn my notes from each lecture into a blog post, figuring out how everything we learned relates to PrP (and maybe huntingtin) along the way. The first class was just review and syllabus, so I’m starting on lecture 2: the plasma membrane.

The plasma membrane refers both to the membrane that surrounds cells and also to the membranes that surround organelles within the cell. The functions of the plasma membrane are held to be as follows:

  • Compartmentalization (separate organelles from other stuff)
  • Scaffolding (give the cell shape)
  • Barrier (keep some things out and others in)
  • Gatekeeper (do let some things through but not others)
  • Monitoring outside signals (receptors on the membrane signal to other proteins inside the cell)
  • Energy transduction (transferring energy across the membrane?)

The membrane is made of a lipid bilayer (the red/orange/yellow stuff in the above diagram). It’s made predominantly of phospholipid molecules, which are amphipathic – part hydrophobic and part hydrophilic:

They contain, from top to bottom:

  1. A polar head group. This can be charged: serine (-), inositol (-), or it can be neutral, with both positively and negatively charged groups: choline, ethanolamine.
  2. A glycerol linker.
  3. A phosphate group.
  4. Two fatty acid chains.

The polar head group faces outward into the aqueous intracellular or extracellular space, while the hydrophobic interior of the membrane is the fatty acid chains. The phospholipids are named after their head groups, thus phosphatidylserine (PS), phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI). Then, randomly, there is also sphingomyelin which has an ethanolamine head group but differs from the others in that it has sphingosine (a long carbon chain amino alcohol) instead of one of the fatty acid chains, and an amide linker instead of glycerol.

The fatty parts – the lipids – make up about 50% of the total mass of the membrane. The fatty acid chains can be either saturated or unsaturated, which accounts for some variety in membrane properties. The saturated chains have no double bonds (all the carbons’ bonding capacities are used up by hydrogens), so the chains lie straight, pack tightly and interact much with each other. The unsaturated chains form kinks due to double bonds – most fatty acids in nature are cis fatty acids, meaning all the hydrogens are on one side, so the chain kinks trans fats, which are abundant in fast food but rare in nature, lie more straight like saturated fats. The kinks in unsaturated cis fatty acids makes them pack less tightly, and the greater amount of space makes for a more ‘fluid’ membrane. Here, ‘fluid’ means it is easier for other things (like transmembrane proteins) to move in two dimensions along the plane of the membrane.

Phospholipids are just most – not all – of the lipid bilayer. There are also glycolipids, which have a glycerol (which is a sugar) instead of phosphate. These make up 2-10% of membrane mass, and are more abundant in the nervous system than elsewhere. Cholesterol is also an important part of the membrane. Here’s what cholesterol looks like:

The OH makes it polar on that end, while the rings and carbon chain on the other end is hydrophobic. So this is also an amphipathic molecule, though it can’t form lipid bilayers on its own. Cholesterol is a steroid, which apparently is a chemical designation referring to that four-ring core, and not a functional designation. Cholesterol is found mostly in eukaryotes and not in bacterial membranes. Its bulky four-ring structure makes the membrane less flexible, the OH head group interacts strongly with other phospholipid head groups thus holding them in place, and the hydrocarbon chain interacts strongly with the phospholipids’ fatty acid chains, making them pack more tightly. For all of these reasons, cholesterol reduces membrane fluidity, though in a temperature-dependent matter (higher temperature means more fluidity).

The two halves of the lipid bilayer are called leaflets: the cytoplasmic leaflet faces (predictably) towards the cytoplasm while the exoplasmic leaflet faces outside the cell or into an organelle. Here is a quick comparison of composition:

    (PS) (-): almost all cytoplasmic (PC) (neutral) found on both sides, esp. exoplasmic (PE) (neutral) found on both sides (PI) (-) almost all cytoplasmic mostly exoplasmic equal on both leaflets

The exoplasmic side tends to be less fluid. But both sides are pretty fluid, with the phospholipids constantly skating around in 2 dimensions (‘lateral diffusion’), rotating, bending tails (‘flection’), and very occasionally, switching from one leaflet to the other (‘flip-flopping’).

A neat laboratory protocol for studying the fluidity of the membrane is fluorescence recovery after photobleaching (FRAP). In this protocol, a molecule of interest is fluorescently tagged – for instance, a membrane protein is tagged with a fluorescently labeled antibody or fused with green fluorescent protein, or an amphipathic molecule is tagged with a fluorophore. Then you ‘bleach’ part of the membrane with a laser which exhausts the fluorescent properties of the fluorescent molecule in that patch. Then you watch as still-fluorescent molecules from elsewhere in the membrane diffuse into the bleached patch. The main goal here is to see how ‘mobile’ the protein you’re studying is. Generally, membrane proteins are less mobile than the phospholipids because they are so much larger. And if the protein is anchored to the cytoskeleton, it won’t move at all, so the bleached patch will recover very slowly if at all. To control for the effects of membrane fluidity you can also tag the phospholipids themselves and compare the mobility of the protein of interest to that of the phospholipids.

There are two kinds of membrane proteins: integral (top) and peripheral (below). Images thanks to Wikimedia Commons user Foobar:

An integral membrane protein (above) has one or more hydrophobic domains anchored in the membrane by simple thermodynamics while the hydrophobic parts stick out into the cytoplasm or extracellular (or intraorganelle) environment). The transmembrane parts might be alpha helices (1 and 2) or beta sheets (3).

The peripheral membrane proteins (above) may have just a segment that buries in the membrane but doesn’t cross it (1, amphipathic alpha helix 2, hydrophobic loop 4, hydrophobic interactions with polar head groups) or be post-translationally modified to add an anchor which buries in the membrane (3) or interact with a transmembrane protein (not pictured). The post-translational modifications might attach a fatty acid chain, oligosaccharide, sugars or farnesyl alcohol group (more common on the cytoplasmic leaflet).

All the different molecules that make up the plasma membrane are not evenly distributed across the whole 2-dimensional surface. Instead, there are patches that are more ordered and tightly packed and have 3-5x the concentration of cholesterol and about 1.5x the concentration of sphingomyelin. These patches are called lipid rafts. In the below image, section 1 is normal plasma membrane and section 2 is a lipid raft:

Lipid rafts have all sorts of highly specialized functions and some particular proteins tend to locate there. People who study membrane proteins often add detergent to their solution to solubilize the glycolipids and bring the proteins into solution. That works less well if the protein of interest is found in lipid rafts, which are harder to dissolve.

The membrane is permeable to gases and small uncharged molecules, which can simply diffuse right through according to their own driving force. Naturally, water, ions, small polar molecules and large, uncharged-but-polar molecules are unable to pass through the membrane on their own. Moving these sorts of things requires some form of transport mediated by membrane proteins: either active (using ATP to fight the transported molecules’ own thermodynamic desires) or passive (allowing molecules to follow their own electrochemical gradient).

Passive transport can take a few different forms. First, it can involve channels that allow ions or molecules to diffuse through. These channels might be highly selective or not at all selective, and might be electrically or chemically gated so they only open under certain conditions. Second, it can involve ‘passive transporters’ (aka ‘porters’), proteins which, upon encountering their substrate ion or molecule, undergo a change in conformation which propels that substrate through to the other side. Predictably, they tend to be more specific than channels, but surprisingly (to me at least), the porters are often faster than just straight-up diffusion would be. Porters are divided into three types:

Uniporters just transport one type of molecule, symporters move two molecules in the same direction and antiporters move two molecules in opposite directions. The trick of the symporters and antiporters is that they allow one of their two substrates to move with its electrochemical gradient, and they harness the energy of that molecule’s thermodynamically favorable movement in order to propel the other molecule against its electrochemical gradient. The symporters and antiporters all require that the multiple substrates bind at the same time – they can’t store energy for later.

GLUT1 is the classic example of a uniporter. It imports glucose into cells when extracellular concentrations are higher then intracellular. It is highly specific for glucose, having limited affinity even for mannose and galactose which differ from glucose in just one carbon atom. Once inside the cell, glucose is immediately modified with a phosphate group so it can’t find its way back out. Red blood cells have tons of GLUT1 because, lacking mitochondria, they rely on anaerobic glycolysis for energy, which is really inefficient (only 2 ATP per glucose as opposed to 36 ATP per glucose via aerobic metabolism).

People who study uniporters use antibodies to pull them down, genetically introduce them into cell types where they are not normally expressed (e.g. GLUT1 in skin cells) or mutate their substrate binding region to see how that changes their function. In spite of this, much is unknown – according to Wikipedia we still don’t know the structure of GLUT1 or how it binds glucose.

A classic antiporter is the Na + /Ca 2+ exchanger (genes: SLC8A1, SLC8A2, SLC8A3). An alternate term for it, ‘sodium-linked calcium antiporter’ tells you more about its energetics: it’s powered by sodium in order to move calcium against its gradient. Specifically, it accepts 3 Na + into the cell in exchange for expelling 1 Ca 2+ . Its affinity to calcium is low enough that it only works at really high calcium concentrations, so it’s useful for preventing excitotoxicity in neurons – getting rid of the excess calcium after repeated stimulus. It’s also found in cardiac muscle cells.

Another classic antiporter is the sodium-hydrogen antiporter (genes: SLC9A1,2,3,5,6,8), which accepts 1 Na + into the cell in order to export 1 H + ion. This maintains the preferred pH of 7.2 inside cells. It also is one step in exporting acid into the stomach, because H + is produced in cells but secreted into the stomach. (But – I had to check – this antiporter is not the target of proton pump inhibitors like omeprazole - those target an active transporter, H + /K + ATPase).

A classic symporter is the sodium glucose symporter (genes: SLC5A1, SLC5A2 & SLC5A4). Remember how GLUT1 uniporter brings glucose into the cell when its extracellular concentration is higher? When the intracellular glucose concentration is higher than extracellular and cells need to import glucose against its concentration gradient, this symporter does so by accepting 2 sodiums into the cell in order to bring one glucose in.

Active transport relies on pumps that couple ATP hydrolysis with movement. You may have noticed that sodium seems to be the common currency of the exampels of symporters and antiporters listed above. They all allow sodium to move into the cell, as is thermodynamically favorable, in order to export something the cell doesn’t want. Predictably, someone has to do the hard work of maintaining that sodium gradient while everyone else is mooching off of it. That someone is Na + /K + -ATPase, which expends 1 ATP in order to export 3 Na + and import 2 K + , both against their respective concentration gradients. This thing is a workhorse, accounting for 20% of energy consumption in most animal cells and 67% in neurons. You don’t get anything for free, so if it just doesn’t feel right to even call the symporters and antiporters ‘passive’ transporters, you can call them by their other name, which is ‘secondary active transporters‘, in recognition of the fact that, while they don’t burn ATP directly, they do use energy by relying on actively maintained sodium gradients.

The active transporters are divided in to F, P, V, and ABC families.

P refers to P-type ATPases which have two catalytic alpha domains (one of which is phosphorylated hence the ‘P’ name) that bind and hydrolyze ATP, and two regulatory beta domains. These include the Na + /K + -ATPase mentioned above as well as SERCA calcium pumps, which stores calcium in the sarcoplasmic reticulum, and the H + /K + ATPase which acidifies your stomach, mentioned above.

ABC refers to the ATP-binding cassette family of hundreds of proteins. They have two transmembrane domains and two ATP-binding domains. Some of them move molecules and not just ions. This class is said to include CFTR, the protein whose loss of function is responsible for cystic fibrosis. But CFTR is a bit weird and, though it evolved from the active transporters, it does not actually pump anything uphill against a concentration gradient. Rather, it allows passive diffusion of chloride and thiocyanate ions along their gradients, but only when opened by an ATP-powered gate. Loss of function mutations in CFTR make it impossible for these ions to diffuse, which in turn eliminates the thermodynamic incentive for water to osmose out of the cell. Without that extra water from osmosis, the extracellular mucus becomes too thick, leading to coughing and chest infections, the hallmarks of cystic fibrosis.

Another important ABC family transporter is MDR1 (gene: ABCB1). MDR stands for multi-drug resistance. This amazing protein found in animal cells is not very specific but somehow can recognize a broad range of ‘xenobiotic‘ molecules – i.e. foreign compounds that we don’t produce and don’t normally have in our cells – and, using energy from ATP, kick them out of the cell. Presumably this keeps the cells from accumulating toxins from the environment. But it also makes treatment difficult because it exports some antiretroviral drugs and chemo drugs – the latter especially in tumor cells that acquire mutations that heighten the action of MDR1. In this way, tumors can sort of evolve resistance to cancer drugs. This is especially a big problem in liver cancers. An old, boring theory about MDR1 was that it was just an ATP-powered channel, but FRAP-like experiments have now shown that it’s in fact something much more interesting: a flipase. That means that rather than just shooting the molecule out of the cell, MDR1 binds the molecule and then flips a section of the membrane, swapping the exoplasmic and cytoplasmic leaflets. It’s like punching a door in a fence in Super Mario World:

The F family are found in bacteria, mitochondria and chloroplasts, and based on their Wikipedia description, don’t sound like active transporters at all.

The V family are found in many other organelles and are responsible mostly for pH maintenance. Lysosomes - one place where misfolded proteins and other cellular waste go to get broken down – have pH 4.8 (compared to 7.2 in the cytosol), which is a clever evolutionary trick. The lysosomes are full of enzymes that could break down everything in the cytosol, which is dangerous, but the enzymes evolved to only function at low pH, so if the lysosome ever ruptures, the enzymes won’t destroy the cell because they won’t function in the cytosol. This pH gradient between lysosome and cytosol is maintained by V ATPases.

PrP and the plasma membrane

PrP in humans is 253 codons long but the final protein is only 208 amino acids. 22 N terminal and 23 C terminal amino acids are signal peptides which direct the protein into the endoplasmic reticulum, where it gets post-translationally modified. That modification cleaves off the signal peptides, replacing the C-terminal segment with a glycosylphosphatidylinositol (GPI) anchor (attached to 231S) which makes PrP technically a peripheral membrane protein (though GPI-anchored proteins have some properties more like integral membrane proteins), with the GPI buried in the exoplasmic leaflet of the plasma membrane and the protein sticking out into the extracellular space. GPI-anchored proteins tend to congregate in lipid rafts. PrP is also a glycoprotein because during post-translational modification it gets glycosylated (has carbohydrate side chains added) at amino acids 181N and 197N.

There has been some debate over whether PrP’s anchoring to the membrane via the GPI anchor is important in prion disease. Experiments seem to suggest that when PrP is not GPI-anchored, it can still misfold but tends not to do so on a large scale: GPI anchorless mice are tough to infect with prions [Klingeborn 2011] and prions don’t propagate well in vitro when the PrP is not GPI-anchored [Priola 2009]. PrP’s localization in lipid rafts and proximity to cholesterol are thought to be somehow important for conversion to PrPSc, which might be part of the explanation for the (albeit limited) therapeutic efficacy of statins and amphotericin B in prion-infected mice. Some people think the N terminus of PrP interacts with another lipid raft protein (possibly Glypican-1 [Taylor 2009]) and that this interaction is necessary (or at least pretty important) for conversion to PrPSc.

About Eric Vallabh Minikel

Eric Vallabh Minikel is on a lifelong quest to prevent prion disease. He is a scientist based at the Broad Institute of MIT and Harvard.

11. Neuropeptide

Neuropeptide is a group of transmitter that is very different and it usually works slowly. In other thing, Neuropeptide is also a little bit different than small molecule transmitter as well. There are about 40 types of peptide that are assumed has function as neurotransmitter.

This list of peptides can be longer due to the discovery of putative neurotransmitter (it’s assumed has function as neurotransmitter based on evidences that being found but it still can’t be proven directly). Neuropeptide has been studied for long time ago but not in its function as neurotransmitter but in its function as hormonal substance.

At first, this type of peptide will be released into the blood stream by endocrine gland. After that, these peptide hormones will lead to the brain tissues. However, these days it’s been proved that peptides that act as neurotransmitter can be synthesized and released by neurons that are located on nerve structure.

Types of Food That Can Improve Chemicals in Brain

There are various types of food that can help improving the activity of chemicals in your brain. Certain types of food might improve certain types of chemical in your brain. For example, there are foods that can improve the activities of dopamine in your brain. Foods such as fruits or foods that are rich of antioxidant and vitamin B6 can improve the dopamine in your brain.

You can also improve serotonin in your brain by consuming certain types of foods as well. Foods that can improve serotonin in your brain are including seafood such as salmon and sardines, whey protein, banana, and chocolate. If you consume these foods, the amount of serotonin in your brain might increase.

Other types of food might increase the amount of nitric oxide in your brain. Watermelon is considered as one of the best types of food that can improve the amount of nitric oxide in your brain. Yolk and lentils are also good for nitric oxide in your brain as well. Other types of food that are good for nitric oxide in your brain are tuna and pistachio.

If you want to improve glycine in your brain, you can consume certain types of foods such as foods that contain high amount of protein. There are so many types of food that came with high amount of protein. Fish, meat, nuts, milk, and cheese are several types of food that are good for glycine in your brain.

There are various types of chemicals that can be found in human’s brain. Each type of these chemicals has its own function and characteristics. These chemicals can give so many benefits for your body. Some of these chemicals might affect your metabolism and the way your body works. However, if you are lack of these chemicals, it might cause some health issues. To maintain and improve the amount of brain chemicals, you can consume certain types of foods.

Watch the video: Neurons How they work in the Human Brain (July 2022).


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