Tag Archives: neuron

Stress causes physical changes in the brains of mice, and it may help us design medicine to fight it

New research at the Louisiana State University (LSU) Health Sciences Center points the way to a potential treatment against stress.

Image credits Peggy and Marco Lachmann-Anke.

The team shows that stress can physically alter the structures of mouse brains, with long-lasting effects. They also identify a molecular pathway that could be used to prevent or reverse such changes.


“Stress alters brain function and produces lasting changes in human behavior and physiology. The experience of traumatic events can lead to neuropsychiatric disorders including anxiety, depression, and drug addiction,” explains Si-Qiong June Liu, MD, PhD, Professor of Cell Biology and Anatomy at LSU and lead author of the paper.

“Investigation of the neurobiology of stress can reveal how stress affects neuronal connections and hence brain function. This knowledge is necessary for developing strategies to prevent or treat these common stress-related neurological disorders.”

The team found that, for mice, experiencing even a single stressful event was enough to cause quick, long-lasting changes in the structure of astrocytes, brain cells that help feed neurons and maintain synaptic function. Such events cause the outer branches of these cells to shrink away from synapses (the contact spaces between neurons used to transmit impulses via chemical messengers).

Synapses perform the same role in our brains as transistors do in computers — they give us our processing power. And, without astrocytes, they can become clogged with waste ions.

During a stressful event, the team explains, the stress hormone norepinephrine suppresses a molecular pathway that normally produces a protein, GluA1. This protein is essential in allowing nerve cells and astrocytes to communicate with each other.

“Stress affects the structure and function of both neurons and astrocytes,” adds Dr. Liu. “Because astrocytes can directly modulate synaptic transmission and are critically involved in stress-related behavior, preventing or reversing the stress-induced change in astrocytes is a potential way to treat stress-related neurological disorders.”

They explain that the pathway they identified should, in theory, be targeted with medicine to prevent or even potentially reverse stress-induced changes.

For now, the findings only apply to mice. But many signaling pathways are conserved throughout evolution, the team notes. The molecular pathways that lead to astrocyte structural remodeling and suppression of GluA1 production may, therefore, also occur in humans who experience a stressful event — and they could hold the key to fighting stress.

The paper “. Emotional stress induces structural plasticity in Bergmann glial cells via an AC5-CPEB3-GluA1 pathway” has been published in The Journal of Neuroscience.

Neuromorphic chip mimics biological neurons to prevent heart failure

Scientists have devised a solid-state neuron that responds nearly identically to the electrical behavior of biological neurons. The goal is to someday insert bionic chips into the brains of patients to address malfunctioning biological circuits in the nervous system and regulate functions lost to diseases.

The neural chip responds to electrical signals from nerves in the same way as real neurons. This has huge potential for medical devices, like smart pacemakers. Credit: University of Bath.

Alain Nogaret, a professor of physics at the University of Bath, and colleagues designed microcircuits that mimic the activity of ion channels and the neural response of respiratory and hippocampal neurons.

They first analyzed the parameters from a large-scale database of electrophysiological recordings, replicating the dynamics of hippocampal and respiratory neurons.

Getting the membrane voltage of the synthetic chip to oscillate identically to the biological chip was extremely challenging. But, in the end, “enriching cross-disciplinary interactions with colleagues and hard work” paid off, Nogaret told ZME Science.

The researchers performed 60 different current injection protocols on the solid-state neurons, which generated nearly identical electrical responses when compared to biological neurons.

 Prof. Alain Nogaret and Dr. Kamal Abu-Hassan in their lab
 Credit: University of Bath.

“Our approach allows analog hardware including highly nonlinear circuits to be configured to perform specific tasks. A computation that uses the physical properties of the hardware presents enormous advantages in terms of low latency times, low power consumption, ability to read raw nerve signals, etc. but has so far been hindered by the difficulty of finding hardware parameters that condition the behaviour of biocircuits. We expect to be investigating more complex biocomputers than single neurons in the future and to address neuronal disease,” Nogaret said.

The respiratory neurons that were modeled in this study are responsible for regulating respiratory and cardiac rhythms. When this mechanism goes awry, either through age or disease, an individual becomes at risk of developing sleep apnoea and heart failure. Instead of drugs, a device that adapts biofeedback in a similar way to respiratory neurons may prove to be more effective.

“We have evidence that this approach provides a novel therapy for heart failure. Compliance with implant regulations over the certification phase is probably why this technology will take a bit of time before benefiting humans,” Nogaret said.

The findings appeared in the journal Nature Communications.

No Fun Allowed.

Researchers identify neurons that shut down rewards and motivation in the brains of mice

New research is pushing mice to their breaking point to see what our brain does as we give up.

No Fun Allowed.

Image credits Lagrevehumaine / Wikimedia.

A group of cells known as nociceptin neurons get busy when we’re giving up, new research shows. True to their name, these neurons release nociceptin, a complex molecule that suppresses dopamine. Dopamine is a neurotransmitter that underpins the brain’s pleasure and reward networks. The findings offer us a fresh take on the processes that govern motivation.


“We are taking an entirely new angle on an area of the brain known as VTA [ventral tegmental area],” said co-lead author Christian Pedersen, a fourth-year Ph.D. student in bioengineering at the University of Washington School of Medicine and the UW College of Engineering. “The big discovery is that large complex neurotransmitters known as neuropeptides have a very robust effect on animal behavior by acting on the VTA,” said Pedersen.

Nociceptin neurons are located near the VTA, a brain area that houses the hormones that release dopamine during pleasurable activities. This study took four years to complete and, according to the team, is the first one to describe the effects of the nociceptin modulatory system on dopamine neurons. The team hopes their findings will lead to new ways of helping people find motivation when they are depressed or decrease motivation for drug use in substance-abuse disorders.

The team worked with mice that they trained to seek out sucrose (sugar). To do this, the animals had to poke their snout into a port. The team set-up their experiment in such a way that this task was very simple and straight-forward at first: one poke, one reward. Over time, however, it would take exponentially more pokes (two, five, so on) to get the reward — and eventually, the animals just gave up. All the while, the team monitored the mice’s neural activity.

These recordings showed that the nociceptin neurons act as ‘demotivators’ or ‘frustration’ neurons and became most active when mice stopped seeking sucrose — suggesting they put the brakes on motivation.

“We might think of different scenarios where people aren’t motivated like depression and block these neurons and receptors to help them feel better,” says senior author Michael Bruchas, professor of anesthesiology and pain medicine and of pharmacology at the University of Washington School of Medicine.

“That’s what’s powerful about discovering these cells. Neuropsychiatric diseases that impact motivation could be improved.”

The team explains that these neurons exist as a kind of insurance policy for mammals living in the wild. The reward pathways in our brains work to make us mammals maintain homeostasis (i.e. our internal ‘optimal running conditions’). However, in the wild, animals need a safety switch to keep them from pursuing rewards too much, as the environment tends to have limited resources and this pursuit of reward could impact the animal’s survival by expending too much energy, for example. Persistence in seeking uncertain rewards can also be disadvantageous due to risky exposure to predators, the researchers noted.

The paper “A Paranigral VTA Nociceptin Circuit that Constrains Motivation for Reward” has been published in the journal Cell.

New neurons are formed in the brain well into old age — but this stops in Alzheimer’s

The magic happens in the hippocampus.

Image credits: Gerry Shaw.

The majority of our neurons are already in place by the time we are born, although some are still produced during childhood. Traditionally, it was thought that no new neurons are produced during adulthood, but researches are still arguing whether this is truly the case.

Neurogenesis, the production of new neurons, has remained a controversial topic. A recent study found that even if new neurons are produced into adulthood, this process happens early in adulthood, and is very limited. Other studies have claimed that neurogenesis doesn’t happen at all, while some teams have reported evidence of new neurons being formed. The situation is still murky, but a new study tries to clear the waters, reporting that neurons are formed well into old age.

According to a paper published in Nature Medicine, new neurons continuously develop in the healthy human brain up to the ninth decade of life — at least in the hippocampus. Maria Llorens-Martin and colleagues from the Universidad Autónoma de Madrid analyzed tissue samples from 58 human participants.

They found that while neurogenesis can decline with old age, it is still present across the lifespan in the hippocampus, particularly in an area called the dentate gyrus, a region associated with the formation of new episodic memories and the spontaneous exploration of novel environments.

They also find that this process decreases sharply in people suffering from Alzheimer’s.

“By combining human brain samples obtained under tightly controlled conditions and state-of-the-art tissue processing methods, we identified thousands of immature neurons in the dentate gyrus of neurologically healthy human subjects up to the ninth decade of life. These neurons exhibited variable degrees of maturation along differentiation stages. In sharp contrast, the number and maturation of these neurons declined as AD advanced.”

So not only does the study provide new insight on neurogenesis, but it also highlights a mechanism associated with Alzheimer’s.

“The hippocampus is one of the most affected areas in Alzheimer’s disease,” researchers write in the paper. “Moreover, this structure hosts one of the most unique phenomena of the adult mammalian brain, namely, the addition of new neurons throughout life.”

As for the discrepancies between this study and previous results, researchers say it’s owed to methodological differences. Having high-quality samples and processing them properly and quickly is vital, they argue — otherwise, the evidence of neurogenesis can be destroyed. Factors such as tissue fixation techniques or delays in the time between tissue acquisition and processing can alter the results, they explain.

“Our data demonstrate that the prolonged or uncontrolled fixation conditions to which human samples are typically exposed in brain banks worldwide lead to a sharp reduction in the number of [neurons] detected in the adult dentate gyrus,” the paper concludes.

The study “Adult hippocampal neurogenesis is abundant in neurologically healthy subjects and drops sharply in patients with Alzheimer’s disease” has been published in Nature Medicine.


Scientists link properties of individual brain cell size to intelligence

For the very first time, scientists have linked the properties of single cells to intelligence. The study shows that people with larger dendrites — the highly branched extension of a neuron (nerve cell) that receives signals from other neurons and transmits the signals toward the cell body — were also more likely to have a higher IQ. These neural extensions transported information more quickly and were more active the larger they were.

Credit: Shelley Halpain/UC San Diego.

The complexity of the human brain is absolutely staggering, but not all brains are created equal. For instance, previous research has shown that some individuals have a thicker cortex in the frontal and temporal lobes — such people generally have a higher IQ. Other studies have found that variability in brain volume and intelligence may share a common genetic origin. The theory is that certain genes facilitate neuron growth and firing. However, it’s always been challenging to investigate this due to the inaccessibility of the human neuron.

An international team of researchers led by Natalia Goriounova, a neuroscientist at Vrije Universiteit Amsterdam, managed this breakthrough after gaining access to cortical tissue, which was removed as a part of surgical treatment for epilepsy or tumors. While the surgery focused on removing diseased tissue in the brain, undamaged samples from the temporal lobe were also collected. In total, living neurons from 46 people were studied in the lab, where their electrical signaling was measured. Before their surgery, each study participant had to take an IQ test.

According to experiments, people with a higher IQ also had larger dendrites. In addition, the authors used computational modeling to better understand the underlying principles of efficient information transfer in human cortical neurons.

Dendrites play a critical role in integrating synaptic inputs and in determining the extent to which action potentials are produced by the neuron. The researchers believe that their findings can be explained by the idea that “even the slightest change in efficiency of information transfer by neurons may translate into large differences in mental ability.”

Up until now, scientists used to think dendrites only had the modest role of passing down electrical signals received through synapses, which are neural junctions. However, research carried out at UCLA suggests that could also generate electrical pulses. Much to everyone’s surprise, the researchers recorded five times as many electrical spikes in dendrites than in somas (the cell body of the neuron) when the rats were sleeping and up to 10 times as much when these were actively exploring the maze.  And because dendrites are almost 100 times larger in volume this could mean the brain’s computational capacity is 100 times greater than previously thought.

Taken together with previous research — such as the study of brain structure and function, but also that of genes — the new study may explain what exact properties may be linked to intelligence.

“In conclusion, our results provide first evidence that already at the level of individual neurons, such parameters as dendritic size and ability to maintain fast responses link to general mental ability. Multiplied by an astronomical number of cortical neurons in our brain, very small changes in these parameters may lead to large differences in encoding capabilities and information transfer in cortical networks and result in a speed advantage in mental processing and, finally, in faster reaction times and higher cognitive ability,” the authors wrote in the journal eLife.

Digital reconstruction of a rosehip neuron in the human brain. Credit: Tamas Lab, University of Szeged.

Scientists find a new type of neuron that may be unique to humans

Digital reconstruction of a rosehip neuron in the human brain. Credit: Tamas Lab, University of Szeged.

Digital reconstruction of a ‘rosehip neuron’ in the human brain. Credit: Tamas Lab, University of Szeged.

What makes humans so smart? No one’s really sure what makes our brains so special compared to those of other animals, but there are some hints that something special might occur at the cellular level. An intriguing new study supports this idea. In the paper, scientists describe the discovery of a new type of brain cell, one that doesn’t hasn’t been observed in animal models and could very well be unique to humans.

Remarkably, the new neuron was identified by two different research groups working independently from each other, using totally different techniques.

Gábor Tamás, a neuroscientist at the University of Szeged in Szeged, Hungary, along with colleagues conducted detailed examinations of the shape and electrical properties of cells collected from the neocortex.

The neocortex — the most complex part of the brain — is thought to be responsible for human consciousness and many other functions that we think of as unique to our species. It’s much larger, compared to our body size, than in other animals.

Meanwhile, in the United States, at the Allen Institute for Brain Science, researchers uncovered a suite of genes that encode brain cells but couldn’t be found in the genomes of any rodent.

While visiting the Allen Institute to present his latest research on specialized human brain cell types, Tamás was surprised to learn that his American colleagues had hit on the same cell using a very different technique.

“We realized that we were converging on the same cell type from absolutely different points of view,” Tamás said.

The two groups instantly decided to collaborate.

When looking under the microscope, Tamás and colleagues observed some odd-looking, bushy-shaped neurons. Because the dense bundle looked like a rose after it has shed its petals, the scientists named the cells “rosehip neurons”. They knew they had come across a new type of brain cell because the profile of the proteins coating the neuron’s membranes had never been seen in humans before.

These rosehip neurons are what scientists call inhibitory neurons, which interrupt the activity of other neurons in the brain. Much like traffic lights, this class of neurons stand at crossroads, exciting or blocking neural signals. Judging from their density, rosehip neurons make up roughly 10% to 15% of all inhibitory neurons in the outermost layer of the cortex. 

Rosehip neurons form synapses with another type of neuron in a different part of the human cortex, known as pyramidal neurons, which they likely block when the opportunity is right.

Tamás says inhibitory neurons are like the brakes on a car and rosehip neurons, in particular, would be the breaks that only work in a particular stop on your drive.

“This particular cell type — or car type — can stop at places other cell types cannot stop,” Tamás said. “The car or cell types participating in the traffic of a rodent brain cannot stop in these places.”

At the Allen Institute, in collaboration with the J. Craig Venter Institute, researchers found that rosehip neurons activate a unique set of genes that haven’t been seen in any mouse brain cell types they’ve studied before.

“Alone, these techniques are all powerful, but they give you an incomplete picture of what the cell might be doing,” said Rebecca Hodge, Senior Scientist at the Allen Institute for Brain Science and an author on the study. “Together, they tell you complementary things about a cell that can potentially tell you how it functions in the brain.”

We don’t know yet for sure if the newly identified type of neurons is unique to humans but the fact that they don’t exist in rodents is yet another indication of why lab mice aren’t by far the perfect model of human disease.

“Our brains are not just enlarged mouse brains,” said Trygve Bakken, Senior Scientist at the Allen Institute for Brain Science and an author on the study. “People have commented on this for many years, but this study gets at the issue from several angles.”

“Many of our organs can be reasonably modeled in an animal model,” Tamás said. “But what sets us apart from the rest of the animal kingdom is the capacity and the output of our brain. That makes us human. So it turns out humanity is very difficult to model in an animal system.”

In the future, the researchers plan on looking for rosehip neurons in other parts of the brain. They would also like to explore their potential role in brain disorders.

The findings appeared in the journal Nature Neuroscience. 

Credit: Pixabay.

Never skip leg day: study finds hind leg inactivity causes neurological problems in mice

A new study performed by Italian researchers is rewriting medical textbooks. The findings suggest that inactivity in the hind legs of mice alters the rodents’ nervous system, leading to poor health outcomes that may partially explain why some patients with neuron disease, multiple sclerosis, spinal muscular atrophy and other neurological diseases often rapidly decline in cognitive functions when their movement becomes limited.

Credit: Pixabay.

Credit: Pixabay.

For the study, researchers at the Università degli Studi di Milano, Italy, immobilized the hind legs of mice, but not their front legs, for a period of 28 days. Otherwise, the mice were left to themselves, continuing to eat and groom as they normally would. The mice did not exhibit any signs of stress.

At the end of the trial, the team found that limiting physical activity decreased the number of neural stem cells in the subventricular region of the brain by 70 percent compared to the control group. What’s more, both neurons and oligodendrocytes — specialized cells that support and insulate nerve cells — didn’t fully mature when exercise was severely reduced.

“Our study supports the notion that people who are unable to do load-bearing exercises — such as patients who are bedridden, or even astronauts on extended travel — not only lose muscle mass, but their body chemistry is altered at the cellular level and even their nervous system is adversely impacted,” said Dr. Raffaella Adami from the Università degli Studi di Milano, Italy, in a statement.

“It is no accident that we are meant to be active: to walk, run, crouch to sit, and use our leg muscles to lift things,” Adami added. “Neurological health is not a one-way street with the brain telling the muscles ‘lift,’ ‘walk,’ and so on.”

It’s the brain that commands muscles how and when to contract in order to elicit movement. However, the findings show that muscles also send their own signals to the brain, with consequences for neural health.

When the researchers investigated the connection more closely, they found out that lack of physical activity lowers the amount of oxygen in the body, leading to an anaerobic environment and altered metabolism. Furthermore, reduced exercise impacts two genes. One of these, CDK5Rap1, is known to be critical to the health of mitochondria –– rod-shaped organelles that can be considered the power generators of the cell, converting oxygen and nutrients into adenosine triphosphate.

This feedback loop helps explain several health problems, ranging from cardiovascular disease as a result of sedentary lifestyles to more devastating conditions, such as multiple sclerosis and motor neuron disease.

Beyond medicine practice here on Earth, the findings could prove very important when planning future missions in space. The research shows that physical activity is critical in order to grow new neural cells and, as such, astronauts on long-term missions ought to perform load-bearing exercise daily. In the future, the researchers plan on studying the altered genes identified here in more depth.

The take-home message for the general public is that the physical inactivity is detrimental to our mental health,” co-author Dr. Daniele Bottai, also from the Università degli Studi di Milano, told ZME Science. 

“One could say our health is grounded on Earth in ways we are just beginning to understand,” concludes Bottai.

The findings appeared in the journal Frontiers in Neuroscience. 


Scientists reverse damage by key gene involved in Alzheimer’s Disease

Alzheimer’s Disease (AD) is a debilitating neurogenerative disease for which there is no cure. Among the several risk factors for AD, a certain gene called APOE4 seems to play a major role. Now, scientists have reported correcting this gene variant, erasing its harmful effects.


Credit: Pixabay.

The apolipoprotein (APOE) gene plays a very complex role in the development of Alzheimer’s. This gene comes in three variants: APOE2, E3, and E4. Everybody carries two of these three variants, with the most common variant being APOE3. Some people — about 15 percent of the general population — have APOE4, which increases the risk of AD by up to a factor of three. Those extremely unfortunate enough to have two copies of the gene are 12 times likelier to develop the neurodegenerative disorder.

In a new study, researchers at the Gladstone Institutes in San Francisco, CA, set out to find out what makes the E4 variant so dangerous.

The main role of the APOE gene is to code instructions for the production of a certain protein with the same name. When this protein is combined with fats, lipoproteins emerge, which help to transport and regulate levels of cholesterol throughout the bloodstream. The APOE proteins created by the E3 and E4 variants are very similar, with the two differing very little at only one point. However, even such a tiny difference could have important effects on the human body. For instance, the E4 variant may be causing APOE3 to lose some of its functions or it could be the case that APOE4 has some toxic effects.

In order to investigate how the variants might influence AD development, the researchers modeled the disease in human cells, monitoring the effects of APOE4 on human brain cells for the very first time. This, in and of itself, was already a huge step forward in AD research because more often than not work on animal models, such as experimental drugs, is not transferable to humans.

Can Alzheimer’s be reversed?

Researchers collected skin cells from Alzheimer’s patients with two APOE4 genes, as well as some from people with two APOE3 genes who didn’t have Alzheimer’s. Using stem cell technology, the skin cells were turned into induced pluripotent stem cells, which were, in turn, converted into human brain cells. When the neurons from the APOE3 and APOE4 donors were compared, the researchers found that the latter didn’t function as well as they should. Specifically, the proteins break down into the neurons, leading to higher levels of tau phosphorylation a marker for AD. Intriguingly, the “APOE4 increased [amyloid-beta] production in human, but not in mouse, neurons,” once again highlighting the potentially huge discrepancy in results between animal and human studies.

“There’s an important species difference in the effect of apoE4 on amyloid beta,” said Chengzhong Wang, first author of the new study published in Nature Medicine. “Increased amyloid beta production is not seen in mouse neurons and could potentially explain some of the discrepancies between mice and humans regarding drug efficacy. This will be very important information for future drug development.”

The authors of the new study conclude that the APOE4 protein has a “pathogenic conformation” — in other words, the protein’s structure has an abnormal form that prevents it from functioning properly. And it is this abnormality that leads to disease-causing complications.

The good news is that the researchers were able to reverse the damage by applying a class of compounds that turn APOE4 into APOE3. It’s thus reasonable to assume that it may be possible to treat brain cells with such structure-correcting molecules to restore neuron function. This may actually open up an effective treatment route to reverse the signs of Alzheimer’s, which today is impossible to do. In the future, the team plans on testing such a hypothesis in human patients.

“Treatment of APOE4-expressing neurons with a small-molecule structure corrector ameliorated the detrimental effects, thus showing that correcting the pathogenic conformation of APOE4 is a viable therapeutic approach for APOE4-related [Alzheimer’s disease],” the authors concluded.


Scientists reprogram brain cells that store memories about places


Credit: Pixabay.

Without long-term memory, none of us would be functional human beings. In order to make sense of the world, our memory employs all sorts of reference points, anchors if you will. For instance, one very important building block is the memory of places. Scientists think that the memory for a given environment is stored in specific neurons in the hippocampus, which is the memory formation center in the brain. These neurons are called place cells. Now, German researchers have reported an incredible feat — they’ve ‘reprogrammed’ such place cells in free-roaming mice.

Research suggests that memories about particular locations come together in place maps. Each map is stable as long as we are in that particular environment, but it reorganizes its activity patterns with different locations, thus leading to a new place map for each environment.

Dr. Andrea Burgalossi of the University of Tübingen and colleagues investigated the mechanisms that underlie the reorganization of place cell activity. Two years ago, the same team of neuroscientists showed that so-called silent or dormant cells could be reactivated by electrical stimulation, thereby becoming active place cells. The researchers now revisited this work and built upon it, toying with new ways to form place cells. Quite strangely, the new work suggests that place cells aren’t nearly as stable as we used to think — in fact, place cells can be reprogrammed.

The team used a novel method based on juxtacellular recording and stimulation where very fine electrodes as thin as strands of hair measure and induce tiny currents along individual place cells. The researchers performed this procedure on rats freely roaming an arena in the lab. By stimulating individual place cells in the rat’s brain in a different location from where they had originally been active, the activity of the place cells could be reprogrammed. In other words, the cells stopped firing in the original locations and became active in the area where the electrical stimulation occurred.

“We challenged the idea that place cells are stable entities. Even in the same environment, we can reprogram individual neurons by stimulating them at specific places”, says Andrea Burgalossi. “This finding provides insights into the basic mechanisms that lead to the formation of new memories”. I

“So far, we have reprogrammed single neurons, and it would be fascinating to find what influence this has on place maps as a whole. We would very much like to know what is the minimum number of cells we need to reprogram in order to modify an actual memory trace in the brain.”

Scientific reference: Maria Diamantaki, Stefano Coletta, Khaled Nasr, Roxana Zeraati, Sohie Laturnus, Philipp Berens, Patricia Preston-Ferrer, Andrea Burgalossi: Manipulating Hippocampal Cell Activity by Single-Cell Stimulation in Freely-Moving Mice. In: Cell Reports (in press) April 3rd, 2018.

We can’t grow new neurons in adulthood after all, new study says

Previous research has suggested neurogenesis — the birth of new neurons — was able to take place in the adult human brain, but a new controversial study published in the journal Nature seems to challenge this idea.

a. Toluidine-blue-counterstained semi-thin sections of the human Granule Cell Layer (GCL) from fetal to adult ages. Note that a discrete cellular layer does not form next to the GCL and the small dark cells characteristic of neural precursors are not present.

Scientists have been struggling to settle the matter of human neurogenesis for quite some time. The first study to challenge the old theory that humans did not have the ability to grow new neurons after birth was published in 1998, but scientists had been questioning this entrenched idea since the 60’s when emerging techniques for labeling dividing cells revealed the birth of new neurons in rats. Another neurogenesis study was published in 2013, reinforcing the validity of the results from 1998.

Arturo Alvarez-Buylla, a neuroscientist at the University of California, San Francisco, and his team conducted a study to test the neurogenesis theory using immunohistochemistry — a process that applies various fluorescent antibodies on brain samples. The antibodies signal if young neurons as well as dividing cells are present. Researchers involved in this study were shocked by the findings.

“We went into the hippocampus expecting to see many young neurons,” says senior author Arturo Alvarez-Buylla. “We were surprised when we couldn’t find them.”

In the new study, scientists analyzed brain samples from 59 patients of various ages, ranging from fetal stages to the age of 77. The brain tissue samples came from people who had died or pieces were extracted in an unrelated procedure during brain surgery. Scientists found new neurons forming in prenatal and neonatal samples, but they did not find any sustainable evidence of neurogenesis happening in humans older than 13. The research also indicates the rate of neurogenesis drops 23 times between the ages one and seven.

But some other uninvolved scientists say that the study left much room for error. The way the brain slices were handled, the deceased patients’ psychiatric history, or whether they had brain inflammation could all explain why the researchers failed to confirm earlier findings.

The 1998 study was performed on brains of dead cancer patients who had received injections of a chemical called bromodeoxyuridine while they were still alive. The imaging molecule — which was used as a cancer treatment — became integrated into the DNA of actively dividing cells. Fred Gage, a neuroscientist involved in the 1998 study, says that this new paper does not really measure neurogenesis.

“Neurogenesis is a process, not an event. They just took dead tissue and looked at it at that moment in time,” he adds.

Gage also thinks that the authors used overly restrictive criteria for counting neural progenitor cells, thus lowering the chances of seeing them in adult humans.

But some neuroscientists agree with the findings. “I feel vindicated,” Pasko Rakic, a longtime outspoken skeptic of neurogenesis in human adults, told Scientific American. He believes the lack of new neurons in adult primates and humans helps preserve complex neural circuits. If new neurons would be constantly born throughout adulthood, they could interfere with preexisting precious circuits, causing chaos in the central nervous system.

“This paper not only shows very convincing evidence of a lack of neurogenesis in the adult human hippocampus but also shows that some of the evidence presented by other studies was not conclusive,” he says.

Dividing neural progenitors in the granule cell layer (GCL) are rare at 17 gestational weeks (orthogonal views, inset) but were abundant in the ganglionic eminence at the same age (data not shown). Dividing neural progenitors were absent in the GCL from 22 gestational weeks to 55 years.

Steven Goldman, a neurologist at the University of Rochester Medical Center and the University of Copenhagen, said, “It’s by far the best database that has ever been put together on cell turnover in the adult human hippocampus. The jury is still out about whether there are any new neurons being produced.” He added that if there is neurogenesis, “it’s just not at the levels that have been presumed by many.”

The debate still goes on. No one really seems to know the answer yet, but I think that’s a positive — the controversy will generate a new wave of research on the subject.

Skull statue.

Death creeps through the brain as a “spreading wave” of silence and inactivity

New research looks at the neurological processes of death.

Skull statue.

Image credits Alchemilla Mollis.

We’re all afraid of dying — us and (almost) every other bit of life on this planet, as well. Talking about death can get very uncomfortable, but it’s a natural, quite significant part of our lives. Understanding what we can of it might help us come to grips with death; maybe even fear it less.

The roots of the paper we’ll be discussing here stretch as far back as the 1940s, when Harvard biologist Aristides Leão, working with lab rabbits, observed a “spreading depression” in their brains. Leão described this phenomenon as a silencing of electrical activity following injury in the exposed brains of unconscious animals. The silencing began within 5 minutes at the point of injury before extending over more distant parts of the brain. For what should be quite self-evident reasons, Leão never did replicate his study with humans — so we were unsure whether our brains similarly experience this spreading depression or not.

However, new work published by an international team of neurologists builds on Leão’s research and looks at what happens in the brain of a dying human. To gather their data, the researchers worked with hospitals in Berlin and Cincinnati; after getting consent from next of kin or other legal representatives, they recorded the brain activity of nine patients who died with electrodes implanted into their brains. All of the patients had existing conditions that required invasive neural monitoring, meaning the electrodes were already installed before doctors pulled them from life support.

The nine patients all had severe brain injuries. One was a “47-year-old male occupant of a car struck by train,” another, a “57-year-old male who was found at the base of a stairway”. The others were victims of heart attacks or strokes. The team notes that because of their condition, the nine had likely already experienced their first “spreading depression” before the electrodes were applied — their bodies were being kept alive, but ‘they’ were already dead.

The carbon computer

Brains are made up mostly of cells called neurons. These are the ones which handle information processing, the ones doing the thinking, remembering, and everything that has to do with information.

Like everything else in our bodies, they need finely-tuned conditions to survive. That’s called homeostasis. However, unlike most other cells in the body, neurons need to be able to create a lot of electric impulses, and do so on a dime, every time — they do that through careful application of chemical imbalances that create electrical ones. In short, when a neuron wants to fire, it floods itself with charged ions, which spread an electric shock to its neighbors.

Maintaining this imbalance, however, requires a constant and quite significant expenditure of effort and resources. The same electromagnetic forces that form the signals try to wipe the ions’ charge clean off and fix the imbalance — even as the neurons work to maintain it. So, they need to be supplied with a lot of oxygen and chemical fuel from the bloodstream to maintain proper function. When the body dies, and the blood supply is cut, neurons try to save up as many resources as they can, the team writes.

Sending signals back and forth is a huge expenditure of energy, if you happen to be a neuron; so the cells go silent and pool all their efforts into maintaining their internal charges, waiting for the blood to start flowing again.

The authors also report that the first wave of darkness doesn’t spread — rather, it happens everywhere at once, as starving neurons throughout the brain clamp down on signaling. The final, spreading wave comes a few minutes later, after the cells have burned through their limited stores and their ions leach into thee surrounding tissues. This marks the final moments of brain function for dying patients, the authors report.

However, they note that this shouldn’t be used as an end-all marker of death. Past research has shown that if blood and oxygen return to the brain quickly enough after the spreading wave, the neurons resume activity and recover their chemical charge. It takes several minutes for the depolarized neurons, sitting in this chemical cocktail, to reach a “commitment point” beyond which they cannot restart their function.

The paper “Terminal spreading depolarization and electrical silence in death of human cerebral cortex” has been published in the Annals of Neurlogy.

Extra-virgin olive oil might prevent Alzheimer’s and protect your brain

A new study adds even more benefits to the already impressive pile than olive oil can boast — it protects your brain from Alzheimer’s and improves your synapses.

Image credits: Neufal / Pixabay.

Olive oil is good for you

Extra-virgin olive oil is a key component of the Mediterranean Diet, one of the few diets which have been constantly and scientifically proven to yield substantial health benefits. Olive oil itself has substantial benefits and is one of the healthiest types of fats you can consume. Now, a new study focused on the mechanism through which olive oil can protect your brain.

“Consumption of extra virgin olive oil (EVOO), a major component of the Mediterranean diet, has been associated with reduced incidence of Alzheimer’s disease (AD). However, the mechanisms involved in this protective action remain to be fully elucidated,” the study reads.

Lead investigator Dr. Domenico Praticò – a professor in the departments of Pharmacology and Microbiology and the Center for Translational Medicine at the Lewis Katz School of Medicine at Temple University (LKSOM) in Philadelphia, PA believes that this study brings us closer not only to prevention but also to the reversal of Alzheimer’s. He and his colleagues carried this study and mice and found that mice with EVOO-enriched diets had better memories and learning abilities compared to those who didn’t.

At a closer look, researchers also learned that mice who consumed more olive oil had better functioning synapses — connections between neurons. But it gets even better.

Olive oil reduces brain inflammation and activates the autophagy process, cleaning some of the intracellular debris and toxins in the process. This debris is strongly associated with an onset of Alzheimer’s, and this finding indicates that the oil would prevent and tackle the disease directly.

“Thanks to the autophagy activation, memory and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer’s disease were significantly reduced,” Pratico said. “We want to know whether olive oil added at a later time point in the diet can stop or reverse the disease.”

“This is an exciting finding for us. Thanks to the autophagy activation, memory, and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer’s disease were significantly reduced,” the researcher added.

Image credits: G.steph.rocket / Wiki Commons.

Future studies

Next, they want to conduct a similar experiment later in the onset of the disease and see if similar trends are noticed.

The thing is, eating olive oil once or twice does nothing — you need to introduce it firmly into your diet to reap the benefits, but that’s definitely worth it. Not only does it taste good and provide good, healthy fats for your body, but the data presented in the current paper demonstrate that chronic administration of a diet enriched with EVOO results in an amelioration of working memory, spatial learning, and synaptic pathology. The case for olive oil functioning as a prevention tool against Alzheimer’s seems quite strong, so there are solid, scientific reasons to opt for this type of oil.

However, it’s not clear if it could counteract the disease once it’s already set in. As impressive as olive oil is, it might become even more powerful as a therapeutic tool.

“Usually when a patient sees a doctor for suspected symptoms of dementia, the disease is already present,” Dr. Praticò explains. “We want to know whether olive oil added at a later time point in the diet can stop or reverse the disease.”

Considering that over 5 million Americans suffer from Alzheimer’s and the figure is expected to almost triple to 14 million by 2050, having such a simple and effective tool to combat Alzheimer’s could prove immensely useful.

Journal Reference: Elisabetta Lauretti, Luigi Iuliano, Domenico Praticò — Extra-virgin olive oil ameliorates cognition and neuropathology of the 3xTg mice: role of autophagy. DOI: 10.1002/acn3.431

Dendrites generate electrical spikes too — human brain computing capacity might be 100 times larger than thought

A breakthrough study found the human brain is at least 10 times more active than previously thought after a team from UCLA proved dendrites are actually electrically active. Since dendrites make up to 90 percent of the brain’s volume, computational capacity might actually be 100 times greater than the most hopeful estimates. Yet again, science shows that the tangled mess of billions of neurons we house upstairs is of unrivaled complexity — and that we’re still scratching the surface.

Dendrites are no passive electrical conductors and instead actively generate current like the cell’s body. Credit: Shelley Halpain/UC San Diego

What is consciousness? Where does it stem from? Can you create artificial consciousness? These are the ultimate questions neuroscience hopes to one day answer and a recent paper published by a team from the University of California, Los Angeles, is bringing us one step closer by revisiting the basic building block of any brain: the neuron. This tree-like cell is made up of two key regions: the body, also known as the soma, and the dendrites, which are large extensions that look a lot like branches.

Not a conductor but a generator in its own right

Up until now, scientists used to think dendrites only had the modest role of passing down electrical signals received through synapses, which are neural junctions, through the soma. These electrical signals are transmitted by other somas, which were through to be the sole electrical current generators. But UCLA neurophysicist Mayank Mehta and colleagues showed there is much more to it.

Previously, some groups suggested that dendrites aren’t passive at all and that dendrites could also generate electrical pulses based on studies of brain slices. Observing the same effect in nature, however, is far more revealing. It’s also extremely challenging considering the delicate nature of dendrites. For instance, previous attempts to measure electrical activity in dendrites only managed to destroy the cells. The UCLA team managed to get around this issue by developing a new technique in which electrodes are placed near, and not in, the dendrites of live rodents.

Using this novel approach, dendrite electrical activity was measured for four days in rats that were allowed to move freely around a maze. The electrodes were positioned such that dendrite activity would be recorded from the posterior parietal cortex which is where movement is coordinated.

Much to everyone’s surprise, the researchers recorded five times as many electrical spikes in dendrites than in somas when the rats were sleeping and up to 10 times as much when these were actively exploring the maze.  And because dendrites are almost 100 times larger in volume this could mean the brain’s computational capacity is 100 times greater. Previously, estimates suggested the human brain is 30 times faster than the best supercomputer and simulating 1 second of brain activity requires 82,944 processors. It might actually take a conventional computer much more than that to come close to human computational raw power.

There’s much more to it.

Somas fire electricity in short bursts known as somatic spikes. These spikes are binary all-or-nothing events with little variation in voltage. As such, somas seem to be shuttle information binary much like transistors in digital computers operate which is why you’ll see many scientists refer to the human brain as some binary computing machine. The study, however, shows that dendrites not only generate similar electrical bursts to the somas, they also generate large currents of varying voltage that could be even bigger than the spikes themselves.

“We found that dendrites are hybrids that do both analog and digital computations, which are therefore fundamentally different from purely digital computers, but somewhat similar to quantum computers that are analog,” said Mehta, a UCLA professor of physics and astronomy, of neurology and of neurobiology. “

Because of their singular nature, somas were thought to be the primary way through which perception, learning, and memory formation occur. This long-held belief is now toppled by these most recent findings which not only show that there’s more than one decision maker but the brain is far from binary too.

“Many prior models assume that learning occurs when the cell bodies of two neurons are active at the same time,” said Jason Moore, a UCLA postdoctoral researcher and the study’s first author. “Our findings indicate that learning may take place when the input neuron is active at the same time that a dendrite is active — and it could be that different parts of dendrites will be active at different times, which would suggest a lot more flexibility in how learning can occur within a single neuron.”

Due to technical limitations, neuroscience has mostly focused on the cell’s body thus far. Thanks to more sensitive and clever methods, we’re beginning to explore uncharted territories in the human brain and the secret lives of neurons. Now that our understanding of how neurons compute has changed, other fields will follow from medicine (diagnostic) to computers to artificial intelligence.

We sleep to forget things, new study finds

Sleep is as mysterious as it is vital for our wellbeing. Over the decades, researchers have proposed several mechanisms through which sleep rejuvenates us, but we still don’t fully understand the big picture. Now, two recently published studies come up with an interesting explanation: we sleep to forget some of the things we learn during the day.

Image credits: Dagon / Pixabay

We store memories in networks in our brains. Whenever we learn something new, we grow new connections between neurons, called synapses. In 2003, Giulio Tononi and Chiara Cirelli, biologists at the University of Wisconsin-Madison, proposed something very interesting: during the day, we learn so much and develop so many synapses that things sometimes get fuzzy. Since then, the two and their collaborators have made quite a few interesting additions to that study.

For starters, they showed that neurons can prune out some synapses, at least in the lab. But they suspected the same things happens every day, naturally, in our brains — probably during sleep. So they set up a painstaking experiment, in which Luisa de Vivo, an assistant scientist working in their lab, collected 6,920 synapses from mice, both awake and sleeping. Then, they determined the shape and size of all these synapses, learning that the synapses in sleeping mice were 18 percent smaller than in awake ones. That’s quite a big margin. “That there’s such a big change over all is surprising,” Dr. Tononi said. This was a big tell and helped direct their efforts.

After this, they designed a memory test for mice. They placed the animals in a room where they would get a mild electrical shock if they walked over one particular section of the floor. They injected some of the mice with a substance that had been proved to prevent the pruning of new synapses. The mice that experienced this were much more likely to forget about the section and after a good night’s sleep, they tended to walk over the section again, while mice that slept normally remembered better.

Then, Dr. Tononi and his colleagues found that the pruning didn’t strike every neuron. Some 20% were unchanged, likely well-established memories that shouldn’t be tampered with. In other words, we sleep to forget — but in a smart way. Another interesting consequence might concern sleeping pills. These pills might interfere with the brain’s pruning process and might prevent the brain from forming memories properly.

Markus H. Schmidt, of the Ohio Sleep Medicine Institute, said that the studies make a very good point and found one of the benefits of sleep, but he questions whether this is the reason why we sleep.

“The work is great,” he said of the new studies, “but the question is, is this a function of sleep or is it the function?”

Of course, in would be very difficult to replicate this study on humans.

Journal Reference: Luisa de Vivo et al — Ultrastructural evidence for synaptic scaling across the wake/sleep cycle. DOI: 10.1126/science.aah5982



An artistic rendering of a population of stochastic phase-change neurons which appears on the cover of Nature Nanotechnology, 3 August 2016. Credit: IBM Research

IBM Scientists make phase-changing Artificial Neurons to mimic the Computer Power of Human Brain

An artistic rendering of a population of stochastic phase-change neurons which appears on the cover of Nature Nanotechnology, 3 August 2016. Credit: IBM Research

An artistic rendering of a population of stochastic phase-change neurons which appears on the cover of Nature Nanotechnology, 3 August 2016. Credit: IBM Research

Scientists at IBM-Research Zürich and ETH Zürich claim they’ve made a huge leap in neuromimetic research, which ultimately aims to build a computing machine that closely mimics the human brain. The team imitated large populations of neurons for the very first time and used them to carry out complex computational tasks with remarkable efficiency.

Imitating the most complex biological entity in the universe — the human brain

In a confined space of merely two liters, the human brain is able to perform amazing computational feats requiring only 10 to 20 Watts of power. A supercomputer that would barely mimic the human brain’s computational power would be huge and would require diverting an entire river to keep it cool, were it designed using a classic von-Neumann architecture (the kind your laptop or smartphone uses). With such a great example of biological computing, we’re clearly doing awfully inefficient work right now.

[accordion style=”info”][accordion_item title=”The power of the human brain “]The average human brain has about 100 billion neurons (or nerve cells) and many more neuroglia (or glial cells) which serve to support and protect the neurons (although see the end of this page for more information on glial cells).

Each neuron may be connected to up to 10,000 other neurons, passing signals to each other via as many as 1,000 trillion synaptic connections, equivalent by some estimates to a computer with a 1 trillion bit per second processor. Estimates of the human brain’s memory capacity vary wildly from 1 to 1,000 terabytes (for comparison, the 19 million volumes in the US Library of Congress represents about 10 terabytes of data).[/accordion_item][/accordion]

Mimicking the computing power of the brain, the most complex computational ‘device’ in the universe, is a priority for computer science and artificial intelligence enthusiasts. But we’re just beginning to learn how the brain works and what lies within our deepest recesses – the challenges are numerous. But we’re tackling them one at a time.

It all starts with imitating biological neurons and their synapses. In a biological neuron, a thin lipid-bilayer membrane separates the electrical charge encased in the cell, allowing the membrane potential to be maintained. When the dendrites of the neuron are excited, this membrane potential is altered and the neuron, as a whole, “spikes” or “fires”. Emulating these sort of neural dynamics with conventional CMOS hardware like subthreshold transistor circuits is technically unfeasible.

A chip with large arrays of phase-change devices that store the state of artificial neuronal populations in their atomic configuration. In the photograph, individual devices are accessed by means of an array of probes to allow for precise characterization, modeling and interrogation. Credit: IBM Research

A chip with large arrays of phase-change devices that store the state of artificial neuronal populations in their atomic configuration. In the photograph, individual devices are accessed by means of an array of probes to allow for precise characterization, modeling and interrogation. Credit: IBM Research

Instead, research nowadays is following the biomimetic route as close as possible. For instance, the researchers from Zürich made a nanoscale electronic phase-change device from a chalcogenide alloy called germanium antimony telluride (Ge2Sb2Te5). This sort of material can quickly and reliably change between purely amorphous and purely crystalline states when subjected to an electrical or light stimulus. The same alloy is used in applications like Bluray disks to store digital information, however, in this particular instance, the electronic neurons are analog, just like the synapses and neurons in a biological brain.

. Schematic of an artificial neuron that consists of the input (dendrites), the soma (which comprises the neuronal membrane and the spike event generation mechanism) and the output (axon). The dendrites may be connected to plastic synapses interfacing the neuron with other neurons in a network. The key computational element is the neuronal membrane, which stores the membrane potential in the phase configuration of a nanoscale phase-change device. Credit: Nature Nanomaterials.

Schematic of an artificial neuron that consists of the input (dendrites), the soma (which comprises the neuronal membrane and the spike event generation mechanism) and the output (axon). The dendrites may be connected to plastic synapses interfacing the neuron with other neurons in a network. The key computational element is the neuronal membrane, which stores the membrane potential in the phase configuration of a nanoscale phase-change device. Credit: Nature Nanomaterials.

This phase-change material emulates the biological lipid-bilayer membrane and enabled the researchers to devise artificial spiking neurons, consisting of inputs (dendrites), the soma (which comprises the neuronal membrane and the spike-event generation mechanism) and the output (axon). These were assembled in 10×10 arrays. Five such arrays were connected to create a neural population of 500 artificial neurons, more than anyone has come close yet.

“In a von-Neumann architecture, there is a physical separation between the processing unit and memory unit. This leads to significant inefficiency due to the need to shuttle data back and forth between the two units,” said Dr. Abu Sebastian, Research Staff Member Exploratory Memory and Cognitive Technologies, IBM Research – Zurich and co-author of the paper published in Nature Nanotechnology.

“This is particularly severe when the computation is more data-centric as in the case of cognitive computing. In neuromorphic computing, computation and memory are entwined. The neurons are connected to each other, and the strength of these connections, known as synapses, changes constantly as the brain learns. Due to the collocation of memory and processing units, neuromorphic computing could lead to significant power efficiency. Eventually, such neuromorphic computing technologies could be used to design powerful co-processors to function as accelerators for cognitive computing tasks,” Sebastian added for ZME Science.

Prof. David Wright, the head of Nano-Engineering, Science and Technology Group at the University of Exeter, says that just one of these integrate-and-fire phase-change neurons can carry out tasks of surprising computational complexity.

“When applied to social media and search engine data, this leads to some remarkable possibilities, such as predicting the spread of infectious disease, trends in consumer spending and even the
future state of the stock market,” Wright said, who was not involved in the present paper, but is very familiar with the work.

When the GST alloy crystallizes to become conductive, it spikes. What’s amazing and different from previous work, however, is that this firing exhibits an inherently stochastic nature. Scientists use the term stochastic to refer to the randomness or noise biological neurons generate.

“Our main achievements are two fold. First, we have constructed an artificial integrate-and-fire neuron based on phase change materials for the first time. Secondly, we have shown how such a neuron can be used for highly relevant computational tasks such as temporal correlation detection and population coding-based signal representation. For the latter application, we also exploited the inherent stochasticity or randomness of phase change devices. With this we have developed a powerful experimental platform to realize several emerging neural information processing algorithms being developed within the framework of computational neuroscience,” Dr. Sebatian told ZME Science.

The same artificial neurons can sustain billions of switching cycles, signaling they can pass a key reliability test if they’re ever to become useful in the real world, such as embedded in Internet of Things devices or the next generation of parallel computing machines. Most importantly, the energy required for each neuron to operate is awfully low, minuscule even. One neuron update needs only five picojoules of energy to trigger it. In terms of power, it uses less than 120 microwatts or hundreds of thousands of times less than your typical light bulb.

“Populations of stochastic phase-change neurons, combined with other nanoscale computational elements such as artificial synapses, could be a key enabler for the creation of a new generation of extremely dense neuromorphic computing systems,” said Tomas Tuma, a co-author of the paper, in a statement.

The phase-change neurons are still far from capturing the full range of biological neuron traits, but the work is groundbreaking on many levels. Next on the agenda is to make these artificial neurons even more efficient by aggressively scaling down the size of the phase-change devices, Dr. Sebastian said.

Paralyzed man becomes the first person to feel physical sensations through a prosthetic hand directly connected to his brain

A 28-year old who has been paralyzed for more than a decade following a spinal cord injury has become the first person to be able to “feel” physical sensations, through a special prosthetic developed by DARPA – the Defense Advanced Research Projects Agency, a US agency responsible for the development of emerging technologies, mostly for military purposes. The prosthetic hand is connected directly to his brain, allowing him to feel sensations in it.

“We’ve completed the circuit,” said DARPA program manager Justin Sanchez. “Prosthetic limbs that can be controlled by thoughts are showing great promise, but without feedback from signals traveling back to the brain it can be difficult to achieve the level of control needed to perform precise movements. By wiring a sense of touch from a mechanical hand directly into the brain, this work shows the potential for seamless bio-technological restoration of near-natural function.”

This is not the actual prosthetic DARPA used. The volunteer’s identity has been kept secret for privacy reasons. Image via Tech Times.

Electrodes were placed into the volunteer’s cortex, and a special array was placed on his motor cortex, the part of the brain responsible for movements. Then, wires from his motor cortex were connected to a mechanical hand developed by the Applied Physics Laboratory (APL) at Johns Hopkins University. Firstly, this allowed him to move the hand with his thoughts – a remarkable achievement, but something which had already been done.

But then, DARPA breached new ground. They provided the volunteer with a sense of touch! The prosthetic hand contains a vast and sophisticated array of torque sensors that can detect when pressure is being applied, and can convert those physical sensations into electrical signals which are then passed on directly to the brain. In other words, they gave the patient a sense of touch in his 3rd, prosthetic arm.

The feeling, he reported, was as if his own hand was being touched. When blindfolded, the volunteer could determine which finger on the hand was touched with nearly 100% accuracy. Even when the team tried to trick him, he caught on to it.

“At one point, instead of pressing one finger, the team decided to press two without telling him,” said Sanchez, who oversees the Revolutionizing Prosthetics program. “He responded in jest asking whether somebody was trying to play a trick on him. That is when we knew that the feelings he was perceiving through the robotic hand were near-natural.”

Restoring memories

Image via io9

The restoration of sensation is one of several neurotechnology-based advances emerging from DARPA’s 18-month-old Biological Technologies Office, Sanchez said.

“DARPA’s investments in neurotechnologies are helping to open entirely new worlds of function and experience for individuals living with paralysis and have the potential to benefit people with similarly debilitating brain injuries or diseases,” he said.

This is tightly connected to another DARPA project, restoring memories (especially to soldiers and veterans).

“Traumatic brain injury (TBI) is a serious cause of disability in the United States. Diagnosed in more than 270,000 military service members since 2000 and affecting an estimated 1.7 million U.S. civilians each year, TBI frequently results in an impaired ability to retrieve memories formed prior to injury and a reduced capacity to form or retain new memories following injury,” their website reads.

The end goal of this project is to develop a wireless, fully implantable neural-interface medical device that would allow humans to retrieve memories currently inaccessible to them, which to me, is simply mind blowing. We’ve reached a stage where we can not only create prosthetics we can control with our hands, but we can also create sensations in them, and we can tap into how our brain accesses memories. These are truly remarkable times we are living in.


The Brain Wikipedia – Scientists Launch Open-Access Neuron Database

The human brain is one of the biggest and most intriguing mysteries scientists are tackling. It’s an incredibly active, bustling place that keeps us going and effectively makes us the people we are. There are about 100 billion neurons processing and transmitting information through electrical and chemical signals and to make things even more complicated, each of these neurons has about 10,000 different connections to neighboring brain cells. Needless to say, mapping and understanding all these neurons and connections is a gargantuan task – that’s why computer scientists and biologists from Carnegie Mellon University in the US have created an open-access database indexing all the known physiological information about neurons.

Image via CG Trader.

Basically, they’ve developed a wiki-like system called NeuroElectro (website here).

“The goal of the NeuroElectro Project is to extract information about the electrophysiological properties (e.g. resting membrane potentials and membrane time constants) of diverse neuron types from the existing literature and place it into a centralized database”.

I took a look at the website, and I have to say, it’s a fantastic achievement. The design is pleasant, information is easy to access (if you know what you’re looking for), and speaking of information – there’s a LOT of it. The roughly 300 types of neurons are arranged, discussed and presented in an almost exhaustive fashion.

The database was created by computational neuroscientist, Shreejoy J. Tripathy, from the University of British Columbia in Canada, who analyzed almost 10,000 published papers describing how neurons react to various inputs. He then used text-mining algorithms to ‘read’ each of the papers, retrieving information on how they function, how they respond, and how the data was gathered. The work isn’t finished, and until now, he “only” managed to characterize 100 types of neurons; the algorithms he used are also not perfect, so he had to complement it with a lot of manual checking and validation.

“If we want to think about building a brain or re-engineering the brain, we need to know what parts we’re working with,” said Nathan Urban, director of the Carnegie Mellon’s BrainHub neuroscience initiative, in a press release.

“We know a lot about neurons in some areas of the brain, but very little about neurons in others. To accelerate our understanding… we need to be able to easily determine whether what we already know about some neurons can be applied to others we know less about.”

The database, as well as the techniques used to create it (and future plans for improvement) are described in the Journal of NeurophysiologyIt’s a great achievement, and a great tool for many researchers working in the field.

“It’s a dynamic environment in which people can collect, refine and add data,” Urban said of the NeuroElecto database. “It will be a useful resource to people doing neuroscience research all over the world.“

Via Science Alert.

neurons painting

Stunning Neurons on Canvas Painted by a Neuroscientist

neurons painting

The human brain is often described as the most beautiful organism in the Universe. We say this because of the beautiful things the mind, sustained by the brain, can create and imagine. Greg Dunn earned his PhD  in Neuroscience at the University of Pennsylvania in 2011, but while his colleagues are fiddling with microscopes to unravel the inner workings of brain cells, he works with a paintbrush to magnify neurons on a canvas. His work shows a brain whose beauty transcends romanticism and awes in its raw form.


Dunn was always inspired and fascinated by the sumi-e paintbrush style, very popular in Asian works. Simplicity is the most outstanding characteristic of Sumi-e. An economy of brush strokes is used to communicate the essence of the subject.


Driven by passion, the neuroscientist tried to capture the essence of the brain through unconventional art. Of course, he uses microscope images for inspiration, but all the neurons are painted by him.


According to Dunn, the artist first blows some ink around a non-absorbing paper. The turbulence and the paper’s texture causes tree-like ink to splatter, which look like neurons. What makes it so effective is in fact the variance and randomness blowing the ink introduces. If you try to paint neurons by hand, you’ll adhere to some unconscious patterns that will affect the quality of the sumi-e paintings, says Dunn.


Besides paintings, Dunn also etches ink paintings on metal sheets. He first scans the ink painting then uses software to create a high-resolution image out of hatched lines; the angles of these lines determine how light will reflect off the image. Besides photolithography, the artist also adds lights and shadowboxes around the frames of the engravings, to add different colors. The Brainbow Hippocampus below, for instance, is the same work, but under different lights.

neuron artneuron art

For more on Dunn and his work, visit his website.

neuron art

neuron art

When synapses are destroyed, the memories that they foster aren't necessarily erased. Credit: Red Orbit

Long-term memory isn’t stored in synapses, meaning it could be restored even when struck by Alzheimer’s

For a while, the general consensus was that long term memories are stored in synapses. A new  UCLA research topples this paradigm after experiments made on snails suggests that synapses aren’t that crucial storing memories as previously believed, but only facilitate the transfer of information someplace else, most likely in the nucleus of the neurons themselves – though this has yet to be proven.  The findings defy conventional wisdom and shines new hope that people struck by neruodegenerative diseases like Alzheimer’s might have be able to recover part of their memories.

Tabula rasa

When synapses are destroyed, the memories that they foster aren't necessarily erased. Credit: Red Orbit

When synapses are destroyed, the memories that they foster aren’t necessarily erased. Credit: Red Orbit

“Long-term memory is not stored at the synapse,” said David Glanzman, a senior author of the study, and a UCLA professor of integrative biology and physiology and of neurobiology. “The nervous system appears to be able to regenerate lost synaptic connections. If you can restore the synaptic connections, the memory will come back. It won’t be easy, but I believe it’s possible.”

The team led by Glanzman studied a marine snail called  Aplysia, which has a defensive system to protects its gill from potential harm. Namely, it has a withdrawal reflex that causes the sea hare’s delicate siphon and gill to be retracted when the animal is disturbed. This simple and easy to observe behaviour has made it a lab favorite for neuroscientists. Despite what you might think, the cellular and molecular processes seem to be very similar between the marine snail and humans, even though the snail has approximately 20,000 neurons and humans have about 1 trillion. Neurons each have several thousand synapses.

Researchers applied several electric shocks to the snail’s tail to enhance’s the snail’s withdrawal reflex sensibility. After a couple of more series of ‘shock therapy’, the enhancement stayed for days which shows it had been implemented in the snail’s long-term memory. On a neural level, when the shock is applied the hormone serotonin is released in the brain.

When serotonin reaches the nervous system, it promotes growth of new synaptic connections.  As long-term memories are formed, the brain creates new proteins that are involved in making new synapses. When this process is disrupted, by a concussion, some other injury or neurodegenerative disease, the proteins aren’t synthesized and long-term memories can’t form.

“If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn’t remember the training,” Glanzman said.  “However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later.  In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn’t affect long-term memory. That’s true in the Aplysia and in human’s brains.”  (This explains why people’s older memories typically survive following a concussion.)

Brain grown in a jar

This process holds true even when the brain cells are studied in a Petri dish. The researchers placed sensory and motor neurons, involved in the snail’s withdrawal reflex, in a Petri dish and found that neurons re-formed the synaptic connections that were in place when the neurons were placed inside the snail’s body. When serotonin was added to mix, new synaptic connections altogether formed. However, if immediately after serotonin was added a protein synthesis inhibitor was also placed, then the new synaptic growth was blocked and long-term memories couldn’t be formed.

But do memories disappear when synapses do? The researchers wanted to know, so they counted the number of synapses in the dish and then, 24 hours later, they added the protein inhibitor. After the re-count, they found new synapses had grown and the synaptic connections between the neurons had been strengthened, so the inhibitor was of no consequence.

Next, the scientists added serotonin to a Petri dish containing a sensory neuron and motor neuron, waited 24 hours, and then added another brief pulse of serotonin — which served to remind the neurons of the original training — and immediately afterward add the protein synthesis inhibitor.This time, both synaptic growth and memory were erased. This suggests that the “reminder” pulse of serotonin triggered a new round of memory consolidation, and that inhibiting protein synthesis during this “reconsolidation” erased the memory in the neurons.

So, if synapses are indeed storing long term memory, then we should have seen that the lost synapses were the same ones that had grown in response to the serotonin. This wasn’t the case, however.  Instead, they found that some of the new synapses were still present and some were gone, and that some of the original ones were gone, too. Glanzman says that there doesn’t seem to be any pattern to which synapses stayed and disappear, so it must mean that they’re not connected to long-term memory storage.

Moreover, when the scientists repeated the experiment in the snail, and then gave the animal a modest number of tail shocks — which do not produce long-term memory in a naive snail — the memory they thought had been completely erased returned.

“That suggests that the memory is not in the synapses but somewhere else,” Glanzman said. “We think it’s in the nucleus of the neurons. We haven’t proved that, though.”

While in its late stage Alzheimer’s destroys neurons, even in its early stage the disease causes memory loss. So, just because synapses are lost to the disease, it doesn’t necessarily mean that memories are erased as well. By re-activating the synapses, one might be able to tap into the lost memories as well.

Findings appeared in the online journal eLife.


Image: Flickr // angeladellatorre]

Mice with half human brains are smarter, some healthier

Oh, boy. This week’s freaky science story comes from the University of Rochester Medical Center in New York where researchers grafted mouse pups with human glial cells. Within one year, half the brain cells of the by now adult mice were human. A study made last year by the same team suggests that mice whose brains contain human glial cells are smarter, while another experiment seems to indicate that mice with defects like uninsulated nerves can repair these nerves if human brain cells are inserted.

The overlooked glia


Image: Scientific American

It’s important to set one thing straight: the mice still kept their 100% originally sourced neurons. It’s the glial cells that were human. Although there are about 100 billion neurons in the brain – the human one –  there may be about 10 to 50 times that many glial cells. So, why haven’t you heard about them before if they’re so important? You know how fads come and go…

Sure, neurons are the rock stars because they have firing ability and are responsible for all the signaling that goes inside the brain. Without glial cells, however, neurons would never be able to function. There are five types of glia:

  • Astrocyte (Astroglia): Star-shaped cells that provide physical and nutritional support for neurons: 1) clean up brain “debris”; 2) transport nutrients to neurons; 3) hold neurons in place; 4) digest parts of dead neurons; 5) regulate content of extracellular space
  • Microglia: Like astrocytes, microglia digest parts of dead neurons.
  • Oligodendroglia: Provide the insulation (myelin) to neurons in the central nervous system.
  • Satellite Cells: Physical support to neurons in the peripheral nervous system.
  • Schwann Cells: Provide the insulation (myelin) to neurons in the peripheral nervous system.

Steve Goldman of the University of Rochester Medical Center in New York extracted infant glia from donated human embryos and injected these into the brains of mouse pups. Soon enough, the glia started developing into astrocytes, which strengthen the connection between neuron connections called synapses. Human astrocytes are 10 to 20 times the size of mouse astrocytes and carry 100 times as many tendrils.

Taking over

Image: Wikimedia Commons

Image: Wikimedia Commons

Initially, some 300,000 human glia were inserted, but by the end of the year, the mouse had 12 million. This means that nearly all of the mouse’s native glia had been displaced.

“We could see the human cells taking over the whole space,” says Goldman. “It seemed like the mouse counterparts were fleeing to the margins.”

But do the human astrocytes in the mice actually behave as in the human brain or does the environment regulate them?

“That the cells work at all in a different species is amazing, and poses the question of which properties are being driven by the cell itself and which by the new environment,” says Wolfgang Enard of Ludwig-Maximilians University Munich in Germany, who has shown that mice are better at learning if they have the human Foxp2 gene, which has been linked with human language development.

This question will definitely be very interesting to answer. In a parallel experiment, Goldman and team inserted human glia once more into the brains of mice pups, only this time these bore a defect. The mice were poor at making myelin, the protein that insulates nerves.  Once again, the immature glia developed quickly, but this time something amazing happened:  many of the human glial cells matured into oligodendrocytes, brain cells that specialise in making the insulating material. Somehow, the glia recognized the defect and compensated.

[RELATED] Scientists engineer ‘super’ mice 

Multiple sclerosis is a terrible disease in which the myelin sheath is damaged, and the findings suggest that glia therapy might render positive results. In fact, Goldman applied for permission to treat MS patients with the glial progenitor cells, and hopes to start a trial in 12 to 15 months.

Is this still a mouse?

Image: Flickr // angeladellatorre]

Image: Flickr // angeladellatorre]

The same team made a similar experiment last year, only the human glia they inserted were mature. These became integrated into the mouse brain, but didn’t develop further or expanded in numbers. But here’s the interesting part. In a standardized memory test, mice remembered a sound associated with a mild electric shock  for four times as long as other mice when they heard the sound, suggesting their memory was about four times better.

“These were whopping effects,” says Goldman. “We can say they were statistically and significantly smarter than control mice.”

Next, to further determine how human astrocytes affect things like intelligence, memory or learning, Goldman will be grafting the same immature human glia into rat brains. Rats are smarter than mice, so it should be interesting to follow how the humanized rats respond.

Is this a super mouse? Is it a mouse anymore? Is it just a super smart mouse? Well, let’s leave it to Goldman:

“This does not provide the animals with additional capabilities that could in any way be ascribed or perceived as specifically human,” he says. “Rather, the human cells are simply improving the efficiency of the mouse’s own neural networks. It’s still a mouse.

Findings appeared in the Journal of Neuroscience.