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Artistic microscope slides produced in the Victorian era (1840~1900) by arranging hundreds of tiny diatoms into intricate patterns.  This was often accomplished by using a single hair to move the diatoms in a special chamber that prevented disturbance to the slide.  The fabrication of these amazing objects must have required incredible patience, attention to detail, and a steady hand.

Victorian era? Awesome!

(via staceythinx)


Brain activity drives dynamic changes in neural fiber insulation

The brain is a wonderfully flexible and adaptive learning tool. For decades, researchers have known that this flexibility, called plasticity, comes from selective strengthening of well-used synapses — the connections between nerve cells.

Now, researchers at the Stanford University School of Medicine have demonstrated that brain plasticity also comes from another mechanism: activity-dependent changes in the cells that insulate neural fibers and make them more efficient. These cells form a specialized type of insulation called myelin.

“Myelin plasticity is a fascinating concept that may help to explain how the brain adapts in response to experience or training,” said Michelle Monje, MD, PhD, assistant professor of neurology and neurological sciences.

The researchers’ findings are described in a paper published online April 10 in Science Express.

“The findings illustrate a form of neural plasticity based in myelin, and future work on the molecular mechanisms responsible may ultimately shed light on a broad range of neurological and psychiatric diseases,” said Monje, senior author of the paper. The lead authors of the study are Stanford postdoctoral scholar Erin Gibson, PhD, and graduate student David Purger.

Sending neural impulses quickly down a long nerve fiber requires insulation with myelin, which is formed by a cell called an oligodendrocyte that wraps itself around a neuron. Even small changes in the structure of this insulating sheath, such as changes in its thickness, can dramatically affect the speed of neural-impulse conduction. Demyelinating disorders, such as multiple sclerosis, attack these cells and degrade nerve transmission, especially over long distances.

Myelin-insulated nerve fibers make up the “white matter” of the brain, the vast tracts that connect one information-processing area of the brain to another. “If you think of the brain’s infrastructure as a city, the white matter is like the roads, highways and freeways that connect one place to another,” Monje said.

In the study, Monje and her colleagues showed that nerve activity prompts oligodendrocyte precursor cell proliferation and differentiation into myelin-forming oligodendrocytes. Neuronal activity also causes an increase in the thickness of the myelin sheaths within the active neural circuit, making signal transmission along the neural fiber more efficient. It’s much like a system for improving traffic flow along roadways that are heavily used, Monje said. And as with a transportation system, improving the routes that are most productive makes the whole system more efficient.

In recent years, researchers have seen clues that nerve cell activity could promote the growth of myelin insulation. There have been studies that showed a correlation between experience and myelin dynamics, and studies of isolated cells in a dish suggesting a relationship between neuronal activity and myelination. But there has been no way to show that neuronal activity directly causes myelin changes in an intact brain. “You can’t really implant an electrode in the brain to answer this question because the resulting injury changes the behavior of the cells,” Monje said.

The solution was a relatively new and radical technique called optogenetics. Scientists insert genes for a light-sensitive ion channel into a specific group of neurons. Those neurons can be made to fire when exposed to particular wavelengths of light. In the study, Monje and her colleagues used mice with light-sensitive ion channels in an area of their brains that controls movement. The scientists could then turn on and off certain movement behaviors in the mice by turning on and off the light. Because the light diffuses from a source placed at the surface of the brain down to the neurons being studied, there was no need to insert a probe directly next to the neurons, which would have created an injury.

By directly stimulating the neurons with light, the researchers were able to show it was the activation of the neurons that prompted the myelin-forming cells to respond.

Further research could reveal exactly how activity promotes oligodendrocyte-precursor-cell proliferation and maturation, as well as dynamic changes in myelin. Such a molecular understanding could help researchers develop therapeutic strategies that promote myelin repair in diseases in which myelin is degraded, such as multiple sclerosis, the leukodystrophies and spinal cord injury.

“Conversely, when growth of these cells is dysregulated, how does that contribute to disease?” Monje said. One particular area of interest for her is a childhood brain cancer called diffuse intrinsic pontine glioma. The cancer, which usually strikes children between 5 and 9 years old and is inevitably fatal, occurs when the brain myelination that normally takes place as kids become more physically coordinated goes awry, and the brain cells grow out of control.


At TEDxYouth@Manchester, genetics researcher Dan Davis introduces the audience to compatibility genes — key players in our immune system’s functioning, and the reason why it’s so difficult to transplant organs from person to person: one’s compatibility genes must match another’s for a transplant to take.

To learn more about these fascinating genes, watch the whole talk here»

(Images from Davis’s talk, Drew Berry’s animations, and the TED-Ed lessons A needle in countless haystacks: Finding habitable worlds - Ariel Anbar and How we conquered the deadly smallpox virus - Simona Zompi)

(via science-junkie)


A bit of a detour into neuroscience today with a look at the chemical structures of some of the major neurotransmitters in the brain. Inspired in part by this post on the chemicals related to various emotions.

All available to download as free A3 PDFs at the bottom of the accompanying post (

(via neuromorphogenesis)


Meditation as object of medical research

Mindfulness meditation produces personal experiences that are not readily interpretable by scientists who want to study its psychiatric benefits in the brain. At a conference near Boston April 5, 2014, Brown University researchers will describe how they’ve been able to integrate mindfulness experience with hard neuroscience data to advance more rigorous study.

Mindfulness is always personal and often spiritual, but the meditation experience does not have to be subjective. Advances in methodology are allowing researchers to integrate mindfulness experiences with brain imaging and neural signal data to form testable hypotheses about the science — and the reported mental health benefits — of the practice.

A team of Brown University researchers, led by junior Juan Santoyo, will present their research approach at 2:45 p.m on Saturday, April 5, 2014, at the 12th Annual International Scientific Conference of the Center for Mindfulness at the University of Massachusetts Medical School. Their methodology employs a structured coding of the reports meditators provide about their mental experiences. That can be rigorously correlated with quantitative neurophysiological measurements.

“In the neuroscience of mindfulness and meditation, one of the problems that we’ve had is not understanding the practices from the inside out,” said co-presenter Catherine Kerr, assistant professor (research) of family medicine and director of translational neuroscience in Brown’s Contemplative Studies Initiative. “What we’ve really needed are better mechanisms for generating testable hypotheses – clinically relevant and experience-relevant hypotheses.”

Now researchers are gaining the tools to trace experiences described by meditators to specific activity in the brain.

“We’re going to [discuss] how this is applicable as a general tool for the development of targeted mental health treatments,” Santoyo said. “We can explore how certain experiences line up with certain patterns of brain activity. We know certain patterns of brain activity are associated with certain psychiatric disorders.”

Structuring the spiritual

At the conference, the team will frame these broad implications with what might seem like a small distinction: whether meditators focus on their sensations of breathing in their nose or in their belly. The two meditation techniques hail from different East Asian traditions. Carefully coded experience data gathered by Santoyo, Kerr, and Harold Roth, professor of religious studies at Brown, show that the two techniques produced significantly different mental states in student meditators.

“We found that when students focused on the breath in the belly their descriptions of experience focused on attention to specific somatic areas and body sensations,” the researchers wrote in their conference abstract. “When students described practice experiences related to a focus on the nose during meditation, they tended to describe a quality of mind, specifically how their attention ‘felt’ when they sensed it.”

The ability to distill a rigorous distinction between the experiences came not only from randomly assigning meditating students to two groups – one focused on the nose and one focused on the belly – but also by employing two independent coders to perform standardized analyses of the journal entries the students made immediately after meditating.

This kind of structured coding of self-reported personal experience is called “grounded theory methodology.” Santoyo’s application of it to meditation allows for the formation of hypotheses.

For example, Kerr said, “Based on the predominantly somatic descriptions of mindfulness experience offered by the belly-focused group, we would expect there to be more ongoing, resting-state functional connectivity in this group across different parts of a large brain region called the insula that encodes visceral, somatic sensations and also provides a readout of the emotional aspects of so-called ‘gut feelings’.”

Unifying experience and the brain

The next step is to correlate the coded experiences data with data from the brain itself. A team of researchers led by Kathleen Garrison at Yale University, including Santoyo and Kerr, did just that in a paper in Frontiers in Human Neuroscience in August 2013. The team worked with deeply experienced meditators to correlate the mental states they described during mindfulness with simultaneous activity in the posterior cingulate cortex (PCC). They measured that with real-time functional magnetic resonance imaging.

They found that when meditators of several different traditions reported feelings of “effortless doing” and “undistracted awareness” during their meditation, their PCC showed little activity, but when they reported that they felt distracted and had to work at mindfulness, their PCC was significantly more active. Given the chance to observe real-time feedback on their PCC activity, some meditators were even able to control the levels of activity there.

“You can observe both of these phenomena together and discover how they are co-determining one another,” Santoyo said. “Within 10 one-minute sessions they were able to develop certain strategies to evoke a certain experience and use it to drive the signal.”

Toward therapies

A theme of the conference, and a key motivator in Santoyo and Kerr’s research, is connecting such research to tangible medical benefits. Meditators have long espoused such benefits, but support from neuroscience and psychiatry has been considerably more recent.

In a February 2013 paper in Frontiers in Human Neuroscience, Kerr and colleagues proposed that much like the meditators could control activity in the PCC, mindfulness practitioners may gain enhanced control over sensory cortical alpha rhythms. Those brain waves help regulate how the brain processes and filters sensations, including pain, and memories such as depressive cognitions.

Santoyo, whose family emigrated from Colombia when he was a child, became inspired to investigate the potential of mindfulness to aid mental health beginning in high school. Growing up in Cambridge and Somerville, Mass., he observed the psychiatric difficulties of the area’s homeless population. He also encountered them while working in food service at Cambridge hospital.

“In low-income communities you always see a lot of untreated mental health disorders,” said Santoyo, who meditates regularly and helps to lead a mindfulness group at Brown. He is pursuing a degree in neuroscience and contemplative science. “The perspective of contemplative theory is that we learn about the mind by observing experience, not just to tickle our fancy but to learn how to heal the mind.”

It’s a long path, perhaps, but Santoyo and his collaborators are walking it with progress.


New respect for primary visual cortex

In the context of learning and memory, the primary visual cortex is the Rodney Dangerfield of cortical areas: It gets no respect. Also known as “V1,” this brain region is the very first place where information from the retina arrives in the cerebral cortex.

Many existing models of visual processing have dismissed V1 as a static filter, capable only of detecting objects’ edges and passively conveying this information to higher-order visual areas that do the hard work of learning, recognition, prediction, and cognition. But a new MIT study brings fresh respect for the lowly visual cortex: Building on growing evidence that V1 can do more than detect edges, neuroscientist Mark Bear and his postdoc Jeffrey Gavornik have shown that V1 is the site of a complex type of learning involving spatial-temporal sequences.

“We rely on spatial-temporal sequence learning for everything we do,” says Bear, the Picower Professor of Neuroscience at MIT, a Howard Hughes Medical Institute investigator, and the senior author of the study, which appeared in the March 23 online edition of Nature Neuroscience. “It is how we predict what is coming next so that we can modify our behavior accordingly.”

Sequence learning — or a lack thereof — explains why driving on an unfamiliar road at night, with sparse visual information, is such a white-knuckle experience compared with driving more familiar routes that offer visual cues to predict the road ahead. It is also what allows baseball batters to hit balls traveling too fast to actually see: They do so using visual cues from the pitcher’s throw to predict the arc, trajectory, and timing based on past experience.

The value of V1

In the past decade, researchers have begun to chip away at the view of V1 as an immutable, passive brain region. Studies have shown, for example, that V1 can change in response to experience, a hallmark of plasticity. “Every new discovery allowed us to ask a new question that would have seemed outlandish before,” Bear says.

For the new study, the outlandish question was whether V1 could learn to recognize sequences. To find out, Gavornik designed experiments using gratings of black and white stripes in different orientations — the type of stimuli known to cause responses in V1 neurons. For a training sequence, he showed mice gratings in four different orientations — a combination labeled “ABCD” — in the same order 200 times a day for four days. Control mice saw randomly ordered sequences.

On the fifth day, Gavornik presented the training sequences and random sequences, and measured the V1 neural responses. Among mice that had seen the learned sequence, ABCD, that sequence elicited a more powerful response than unfamiliar sequences — indicating the V1 had changed in response to experience.

Bear then altered the timing of the sequences and found that V1 also detected very precise temporal alternations. That makes sense, he notes: In real life, sequencing and timing are always coupled, so the brain must have a mechanism to respond to this pairing.

Implications for human disease

The most “mind-blowing” results of the study, Bear says, came from experiments testing the neural response when the second visual stimulus, “B,” was replaced with a gray screen following the first stimulus, “A.”

“The primary visual cortex responded as if B were there,” Bear says. “The recordings did not report on what the animal was seeing, but on what the animal was expecting to see.”

“V1 had formed a memory that B follows A, and it used that memory to predict what would happen next, after A,” Gavornik adds. “It is as if the mouse were [acting] based on previously learned visual cues.”

But did the experience-dependent plasticity evident in V1 actually arise there, or did it reflect feedback from a higher brain region that underwent a change? To find out, Gavornik injected a blocker of receptors for the neurotransmitter acetylcholine, which is also known to be important for memory formation in the brain. He found that this treatment prevented learning in the targeted V1 region.

“A disruption in acetylcholine signaling is one of the first things to go wrong in Alzheimer’s disease, and one of the few approved treatments for this disease are drugs that promote the action of acetylcholine,” Bear says. “Our study raises the possibility of using visual sequence learning as a sensitive assay for earlier diagnosis of Alzheimer’s, when therapeutic interventions have a better chance of slowing the disease.”

Spatial-temporal sequence learning is also impaired in schizophrenia and dyslexia, but the origins of this impairment remain a mystery. “When we discover what is going on at a neural and molecular level, maybe we can understand better what happens in human disorders and look for new therapeutic approaches,” Gavornik says.

On a broader scale, the involvement of V1 in higher-level cognitive functions might have intrigued the renowned Spanish neuroscientist (and future Nobel laureate) Santiago Ramón y Cajal, who in 1899 speculated that despite significant heterogeneity, different regions of cortex still follow general principles. “Our study supports Cajal’s theory,” Bear says, “because we show that basic cortical computations may be fundamentally similar in higher and lower regions, even if they are used to serve different functions.”


The circadian clock is like an orchestra with many conductors

You’ve switched to the night shift and your weight skyrockets, or you wake at 7 a.m. on weekdays but sleep until noon on weekends—a social jet lag that can fog your Saturday and Sunday.

Life runs on rhythms driven by circadian clocks, and disruption of these cycles is associated with serious physical and emotional problems, says Orie Shafer, a University of Michigan assistant professor of molecular, cellular and developmental biology.

Now, new findings from Shafer and U-M doctoral student Zepeng Yao challenge the prevailing wisdom about how our body clocks are organized, and suggest that interactions among neurons that govern circadian rhythms are more complex than originally thought.

Yao and Shafer looked at the circadian clock neuron network in fruit flies, which is functionally similar to that of mammals, but at only 150 clock neurons is much simpler. Previously, scientists thought that a master group of eight clock neurons acted as pacemaker for the remaining 142 clock neurons—think of a conductor leading an orchestra—thus imposing the rhythm for the fruit fly circadian clock. It is thought that the same principle applies to mammals.

Interactions among clock neurons determine the strength and speed of circadian rhythms, Yao says. So, when researchers genetically changed the clock speeds of only the group of eight master pacemakers they could examine how well the conductor alone governed the orchestra. They found that without the environmental cues, the orchestra didn’t follow the conductor as closely as previously thought.

Some of the fruit flies completely lost sense of time, and others simultaneously demonstrated two different sleep cycles, one following the group of eight neurons and the other following some other set of neurons.

"The finding shows that instead of the entire orchestra following a single conductor, part of the orchestra is following a different conductor or not listening at all," Shafer said.

The findings suggest that instead of a group of master pacemaker neurons, the clock network consists of many independent clocks, each of which drives rhythms in activity. Shafer and Yao suspect that a similar organization will be found in mammals, as well.

"A better understanding of the circadian clock mechanisms will be critical for attempts to alleviate the adverse effects associated with circadian disorders," Yao said.

Disrupting the circadian clock through shift work is associated with diabetes, obesity, stress, heart disease, mood disorders and cancer, among other disorders, Yao says. The International Agency for Research on Cancer classified shift work that disrupts circadian rhythms as a human carcinogen equal to cancer-causing ultraviolet radiation.


Photographer Rachel Sussman has been documenting the world’s oldest organisms for a personal project she’s been working on for almost a decade. Now you can see the results of her epic journey around the globe in her upcoming book The Oldest Living Things in the World which you can pre-order here.

About the book:

Since 2004 artist Rachel Sussman has been researching, working with biologists, and traveling all over the world to photograph continuously living organisms 2,000 years old and older. The work spans disciplines, continents, and millennia: it’s part art and part science, has an innate environmentalism, and is driven by existential inquiry. She begins at ‘year zero,’ and looks back from there, photographing the past in the present. Together, her portraits capture the living history of our planet – and what we stand to lose in the future.


Sapwood Acts as Water Filter

If you’ve run out of drinking water during a lakeside camping trip, there’s a simple solution: break off a branch from the nearest pine tree, peel away the bark and slowly pour lake water through the stick. The improvised filter should trap any bacteria, producing fresh, uncontaminated water.

In fact, an MIT team has discovered that this low-tech filtration system can produce up to four liters of drinking water a day — enough to quench the thirst of a typical person.

Read more:

(via scinerds)