Tech time not to blame for teens' mental health problems

Teenagers using smartphones

A new study, published in the journal Clinical Psychological Science, suggests that the time adolescents are spending on their phones and online is not that bad.

The study tracked young adolescents on their smartphones to test whether more time spent using digital technology was linked to worse mental health outcomes. The researchers -- Candice Odgers, professor of psychological science at the University of California, Irvine; Michaeline Jensen, assistant professor of psychology at the University of North Carolina at Greensboro; Madeleine George, postdoctoral researcher at Purdue University; and Michael Russell, assistant professor of behavioral health at Pennsylvania State University -- found little evidence of longitudinal or daily linkages between digital technology use and adolescent mental health.

"It may be time for adults to stop arguing over whether smartphones and social media are good or bad for teens' mental health and start figuring out ways to best support them in both their offline and online lives," Odgers said.

"Contrary to the common belief that smartphones and social media are damaging adolescents' mental health, we don't see much support for the idea that time spent on phones and online is associated with increased risk for mental health problems," Jensen said.

The study surveyed more than 2,000 youth and then intensively tracked a subsample of nearly 400 teens on their smartphones multiple times a day for two weeks. Adolescents in the study were between 10 and 15 years old and represented the economically and racially diverse population of youth attending North Carolina public schools.

The researchers collected reports of mental health symptoms from the adolescents three times a day and they also reported on their daily technology usage each night. They asked whether youth who engaged more with digital technologies were more likely to experience later mental health symptoms and whether days that adolescents spent more time using digital technology for a wide range of purposes were also days when mental health problems were more common. In both cases, increased digital technology use was not related to worse mental health.

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How memories form and fade

Memories in the brain concept

Why is it that you can remember the name of your childhood best friend that you haven't seen in years yet easily forget the name of a person you just met a moment ago? In other words, why are some memories stable over decades, while others fade within minutes?

Using mouse models, Caltech researchers have now determined that strong, stable memories are encoded by "teams" of neurons all firing in synchrony, providing redundancy that enables these memories to persist over time. The research has implications for understanding how memory might be affected after brain damage, such as by strokes or Alzheimer's disease.

The work was done in the laboratory of Carlos Lois, research professor of biology, and is described in a paper that appears in the August 23 of the journal Science. Lois is also an affiliated faculty member of the Tianqiao and Chrissy Chen Institute for Neuroscience at Caltech.

Led by postdoctoral scholar Walter Gonzalez, the team developed a test to examine mice's neural activity as they learn about and remember a new place. In the test, a mouse was placed in a straight enclosure, about 5 feet long with white walls. Unique symbols marked different locations along the walls -- for example, a bold plus sign near the right-most end and an angled slash near the center. Sugar water (a treat for mice) was placed at either end of the track. While the mouse explored, the researchers measured the activity of specific neurons in the mouse hippocampus (the region of the brain where new memories are formed) that are known to encode for places.

When an animal was initially placed in the track, it was unsure of what to do and wandered left and right until it came across the sugar water. In these cases, single neurons were activated when the mouse took notice of a symbol on the wall. But over multiple experiences with the track, the mouse became familiar with it and remembered the locations of the sugar. As the mouse became more familiar, more and more neurons were activated in synchrony by seeing each symbol on the wall. Essentially, the mouse was recognizing where it was with respect to each unique symbol.

To study how memories fade over time, the researchers then withheld the mice from the track for up to 20 days. Upon returning to the track after this break, mice that had formed strong memories encoded by higher numbers of neurons remembered the task quickly. Even though some neurons showed different activity, the mouse's memory of the track was clearly identifiable when analyzing the activity of large groups of neurons. In other words, using groups of neurons enables the brain to have redundancy and still recall memories even if some of the original neurons fall silent or are damaged.

Gonzalez explains: "Imagine you have a long and complicated story to tell. In order to preserve the story, you could tell it to five of your friends and then occasionally get together with all of them to re-tell the story and help each other fill in any gaps that an individual had forgotten. Additionally, each time you re-tell the story, you could bring new friends to learn and therefore help preserve it and strengthen the memory. In an analogous way, your own neurons help each other out to encode memories that will persist over time."

Memory is so fundamental to human behavior that any impairment to memory can severely impact our daily life. Memory loss that occurs as part of normal aging can be a significant handicap for senior citizens. Moreover, memory loss caused by several diseases, most notably Alzheimer's, has devastating consequences that can interfere with the most basic routines including recognizing relatives or remembering the way back home. This work suggests that memories might fade more rapidly as we age because a memory is encoded by fewer neurons, and if any of these neurons fail, the memory is lost. The study suggests that one day, designing treatments that could boost the recruitment of a higher number of neurons to encode a memory could help prevent memory loss.

"For years, people have known that the more you practice an action, the better chance that you will remember it later," says Lois. "We now think that this is likely, because the more you practice an action, the higher the number of neurons that are encoding the action. The conventional theories about memory storage postulate that making a memory more stable requires the strengthening of the connections to an individual neuron. Our results suggest that increasing the number of neurons that encode the same memory enables the memory to persist for longer."

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Genetic diversity couldn't save Darwin's finches

Researchers at the University of Cincinnati found that Charles Darwin's famous finches defy what has long been considered a key to evolutionary success: genetic diversity.

The study of the finches of the Galapagos Islands could change the way conservation biologists think about species with naturally fragmented populations to understand their potential for extinction.

UC graduate Heather Farrington and UC biologists Kenneth Petren and Lucinda Lawson found that genetic diversity was not a good predictor of whether populations of finches would survive. A UC lab analysis of century-old museum specimens found that six of eight extinct populations had more genetic diversity than similar museum specimens from which descendants survive today. In most other species, low genetic diversity is a signal of a population in decline.

Researchers examined 212 tissue samples from museum specimens and living birds. Some of the museum specimens in the study were collected by Darwin himself in 1835. Only one of the extinct populations, a species called the vegetarian finch, had lower genetic diversity compared to modern survivors.

Lawson said the findings are explained by the fact that these birds can migrate in between populations.

Specifically, researchers believe a biological phenomenon called sink-source dynamics is at play in which larger populations of birds from other islands act as a "source" of immigrants to the island population that is naturally shrinking, the "sink." Without these immigrant individuals, the natural population on the island likely would continue to dwindle to local extinction. The immigrants have diverse genetics because they are coming from a variety of healthier islands, giving this struggling "sink" population inflated genetic diversity.

Petren said the findings serve as a warning that the genetics of individuals in fragmented populations might not tell the whole story about a species. And that is important for scientists who increasingly use genetics to account for the flow of genes between populations when determining a threatened species' likelihood of extinction.

"The promise of genetics is to sample a few individuals to understand the whole population. But it's a cautionary note that you might be sampling a fragment. You could be misled," he said.

Petren has been studying the birds for 25 years at UC's McMicken College of Arts and Sciences. He said the island's 18 recognized species of finches are unusual for other reasons. Some finches that look most different are actually closely related, he said. And similar-looking finches that birders might have trouble telling apart are actually far apart on the evolutionary family tree.

"It's a paradox. If Darwin fully understood what was going on, it might have blown his mind," Petren said. "These finches are not the first case you would pick to formulate the notion that species can change over time because the patterns of change are so complicated."

The UC study was published in August in the journal Conservation Genetics after first appearing online in April. It suggests that genetic diversity may not be the best predictor of extinction risk for mobile species like the island-hopping finches. That's because healthier populations may contribute individuals to declining ones.

Lawson said factors such as historical diversity or the possibility of gene flow between populations should be considered in addition to the snapshot view provided by a genetic analysis for a fuller understanding of a species' potential for extinction.

"Typically, we would expect populations with high genetic diversity to have a greater potential for long-term survival," she said. "Meanwhile, the low-diversity populations would be more likely to go extinct because that's a common pattern as populations decline to few individuals. Surprisingly, we found that most of the extinct populations had higher genetic diversity."

The study was sponsored in part by the National Science Foundation, Sigma Xi, the American Ornithologists' Union and UC's Office of Research.

Darwin's "On the Origin of Species" was groundbreaking in our understanding of evolution through natural selection. "Survival of the fittest" is a household phrase and a shorthand description of any competition.

While scientists today know more about how new species are formed, the principles Darwin developed remain the foundation of evolutionary biology, Petren said.

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Here's how early humans evaded immunodeficiency viruses

Mangabey monkeys

For hundreds of thousands of years, monkeys and apes have been plagued by simian immunodeficiency virus (SIV), which still devastates primate groups in Africa.

Luckily, as humans evolved from these early primates, we picked up a mutation that made us immune from SIV -- at least until the early 20th century, when the virus evolved to get around our defenses, giving rise to human immunodeficiency virus (HIV) and an AIDS pandemic that today affects an estimated 38 million people worldwide.

University of California, Berkeley, researchers have now discovered how that long-ago human mutation interfered with SIV infection, a finding that could provide clues for the development of new therapies to thwart HIV and similar viral infections.

"The main importance for this paper is that it tells us what was one of the last major barriers before the crossover to humans happened," said James Hurley, a UC Berkeley professor of molecular and cell biology. "The current paper is an archeological look at how this happened."

The barrier was a mutation in human cells that blocked SIV from forcing these cells to shed thousands more copies of the virus. As a result, humans could not re-infect one another.

This genetic mutation interfered with the ability of an SIV protein to tightly bind two human proteins and send them for destruction within the cell, instead of fighting the virus. The researchers used cryo-electron microscopy, or cryoEM, to determine the structure of this protein complex and discovered that the mutation so effectively disrupted the protein binding sites that it took SIV a long time to find a work-around.

"The binding site involved is structurally very complex, so essentially it is not possible to adapt to it once the tight binding is lost. The virus had to invent a completely different way to do the same thing, which took a long time in evolution," Hurley said. "This conferred an advantage on our prehistoric ancestors: From chimps on down, every primate was susceptible to SIV, but humans were immune. That gave humans probably a grace period of tens to hundreds of thousands of years to develop without having to deal with this disease. I tend to think that really gave a leg up to humans in early evolution."

Though the SIV virus -- in this case, from a monkey called the sooty mangabey, the source of the less virulent HIV-2 strain in humans -- differs in several ways from the HIV strains that afflict humans, the findings could pinpoint targets for drugs as researchers look for "functional" cures for AIDS. These would be one-time treatments that prevent flare-ups of the disease, even if the virus remains in the body.

"The overall strategy in our lab is to try to find regions in the structures of human proteins that are attacked by viruses, but are not needed for normal purposes by the host, so that a drug can be designed to attack that region," Hurley said. "The virus will typically respond by mutating, which means it evolves drug resistance, but this new finding suggests that with the right point of attack, it could take SIV or HIV, in some cases, tens of thousands of years of evolution to catch up."

The work will be published in the Sept. 11 issue of the journal Cell Host & Microbe and was posted online Aug. 22.

Sooty mangabeys

SIV and HIV, which are lentiviruses, are hard to root out the body because they insert their DNA into the genomes of host cells, where it sits like a ticking time bomb, ready at any moment to revive, take over the host cell's machinery to makes copies of itself and send out thousands of these copies -- called virions -- to infect other cells.

These virions are formed when the newly copied viral DNA wraps itself in a piece of the host cell's membrane and buds off, safely ensconced in a bubble until it can reinfect.

Because budding is an important step in the spread of many viruses, primates long ago evolved natural defenses, including proteins on the surface of cells that staple the budding virions to the cell and prevent them from leaving. As they accumulate, the immune system recognizes these unbudded virions as abnormal and destroys the whole cell, virus and all.

In monkey, ape and human cells, the staple is called tetherin, because it tethers the budding virion to the cell membrane.

In the constant arms race between host and pathogen, SIV evolved a countermeasure that exploits another normal cell function: its recycling system. Cells have ways to remove proteins sitting on the surface, through which cells constantly take up and recycle tetherin if there's no indication it is needed to fight an invading virus. It does this by dimpling the membrane inward to form a little bubble inside the cell, capturing tetherin and other surface proteins in this vesicle and then digesting all the contents, including tetherin.

SIV's countermeasure was to produce a protein, called Nef, that revs up the recycling of tetherin, even during an infection. This enables virions to bud off and search for new victims.

Hurley and project scientist Xuefeng "Snow" Ren found that Nef forms a tight wedge between tetherin and a protein in the vesicle called AP-2, preventing tetherin from escaping the vesicle and dooming it to recycling.

"Nef is a bridge between AP2 and tetherin to recruit them into endocytosis, dragging the tetherin into the vesicle," Ren said. "So it tricks our own cells' machinery for getting rid of stuff we don't want into getting rid of stuff the virus doesn't want."

The five amino acids that humans lost in the tetherin protein -- the mutation that gave humans immunity against SIV -- loosened the binding between tetherin, Nef and AP-2, which allowed tetherin to escape recycling. This blocked the crossover of zoonotic virus transmission, Ren said, because the structural rearrangement was so extensive that SIV couldn't fix it by simple mutations in Nef.

SIV developed a new trick

Some variants of SIV did eventually find a way around this hurdle, however. At some point, a few SIVs acquired a second protein, Vpu, to do what Nef also did -- wedge itself between proteins to cement connections helpful to the virus. At some point, perhaps a hundred years ago, this strain of SIV moved into humans from chimpanzees, and a slight mutation in Vpu reignited the recycling of tetherin in humans, unleashing what we know today as group M HIV-1, the most virulent form of HIV worldwide.

"There were probably many crossovers into humans that failed, but eventually, some hunter in Africa, perhaps in the course of butchering a chimp, was exposed to the blood, and the virus then acquired an additional mutation, a small step that turned SIV into HIV," Hurley said.

Next up, Hurley, Ren and their colleagues plan to use cryoEM to determine the structure of the three-protein complex in gorilla variants of SIV, which evolved into the O strain of HIV-1, a less virulent strain that originated in the African country of Cameroon.

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Do single people suffer more?

Researchers at the University of Health Sciences, Medical Informatics and Technology (UMIT, Hall, Austria) and the University of the Balearic Islands (Palma de Mallorca, Spain) have confirmed the analgesic effects of social support -- even without verbal or physical contact.

The short communication, entitled "Dispositional empathy is associated with experimental pain reduction during provision of social support by romantic partners" by Stefan Duschek, Lena Nassauer, Casandra I. Montoro, Angela Bair and Pedro Montoya has recently been published in the Scandinavian Journal of Pain.

The authors assessed sensitivity to pressure pain in 48 heterosexual couples with each participant tested alone and in the passive presence of their partner. Dispositional empathy was quantified by a questionnaire.

In the presence, as compared to the absence, of their partners both men and women exhibited higher pain thresholds and tolerance as well as lower sensory and affective pain ratings on constant pressure stimuli. Partner empathy was positively associated with pain tolerance and inversely associated with sensory pain experience.

"Repeatedly, talking and touching have been shown to reduce pain, but our research shows that even the passive presence of a romantic partner can reduce it and that partner empathy may buffer affective distress during pain exposure," said Professor Stefan Duschek of UMIT, speaking on behalf of the authors.

From Science Daily

Scorpion toxin that targets 'wasabi receptor' may help solve mystery of chronic pain

Black rock scorpion

Researchers at UC San Francisco and the University of Queensland have discovered a scorpion toxin that targets the "wasabi receptor," a chemical-sensing protein found in nerve cells that's responsible for the sinus-jolting sting of wasabi and the flood of tears associated with chopping onions. Because the toxin triggers a pain response through a previously unknown mechanism, scientists think it can be used as a tool for studying chronic pain and inflammation, and may eventually lead to the development of new kinds of non-opioid pain relievers.

The scientists isolated the toxin, a short protein (or peptide) that they dubbed the "wasabi receptor toxin" (WaTx), from the venom of the Australian Black Rock scorpion. The discovery came as the researchers were conducting a systematic search for compounds in animal venom that could activate, and therefore be used to probe and study, the wasabi receptor -- a sensory protein officially named TRPA1 (pronounced "trip A1") that's embedded in sensory nerve endings throughout the body. When activated, TRPA1 opens to reveal a channel that allows sodium and calcium ions to flow into the cell, which can induce pain and inflammation.

"Think of TRPA1 as the body's 'fire alarm' for chemical irritants in the environment," said John Lin King, a doctoral student in UCSF's Neuroscience Graduate Program and lead author of a study published August 22, 2019 in Cell, which describes the toxin and its surprising mode of action. "When this receptor encounters a potentially harmful compound -- specifically, a class of chemicals known as 'reactive electrophiles,' which can cause significant damage to cells -- it is activated to let you know you're being exposed to something dangerous that you need to remove yourself from."

Cigarette smoke and environmental pollutants, for example, are rich in reactive electrophiles which can trigger TRPA1 in the cells that line the surface of the body's airway, which can induce coughing fits and sustained airway inflammation. The receptor can also be activated by chemicals in pungent foods like wasabi, onions, mustard, ginger and garlic -- compounds that, according to Lin King, may have evolved to discourage animals from eating these plants. WaTx appears to have evolved for the same reason.

Though many animals use venom to paralyze or kill their prey, WaTx seems to serve a purely defensive purpose. Virtually all animals, from worms to humans, have some form of TRPA1. But the researchers found that WaTx can only activate the version found in mammals, which aren't on the menu for Black Rock scorpions, suggesting that the toxin is mainly used to ward off mammalian predators.

"Our results provide a beautiful and striking example of convergent evolution, whereby distantly related life forms -- plants and animals -- have developed defensive strategies that target the same mammalian receptor through completely distinct strategies," said David Julius, PhD, professor and chair of UCSF's Department of Physiology, and senior author of the new study.

But what the researchers found most interesting about WaTx was its mode of action. Though it triggers TRPA1, just as the compounds found in pungent plants do -- and even targets the very same site on that receptor -- the way it activates the receptor was novel and unexpected.

First, WaTx forces its way into the cell, circumventing the standard routes that place strict limits on what's allowed in and out. Most compounds, from tiny ions to large molecules, are either ingested by the cell through a complex process known as "endocytosis," or they gain entry by passing through one of the many protein channels that stud the cell's surface and act as gatekeepers.

But WaTx contains an unusual sequence of amino acids that allows it to simply penetrate the cell's membrane and pass right through to the cell's interior. Few other proteins are capable of the same feat. The most famous example is an HIV protein called Tat, but surprisingly, WaTx contains no sequences similar to those found in Tat or in any other protein that can pass through the cell's membrane.

"It was surprising to find a toxin that can pass directly through membranes. This is unusual for peptide toxins," Lin King said. "But it's also exciting because if you understand how these peptides get across the membrane, you might be able to use them to carry things -- drugs, for example -- into the cell that can't normally get across membranes."

Once inside the cell, WaTx attaches itself to a site on TRPA1 known as the "allosteric nexus," the very same site targeted by pungent plant compounds and environmental irritants like smoke. But that's where the similarities end.

Plant and environmental irritants alter the chemistry of the allosteric nexus, which causes the TRPA1 channel to rapidly flutter open and closed. This allows positively charged sodium and calcium ions to flow into the cell, triggering pain. Though both ions are able to enter when TRPA1 is activated by these irritants, the channel exhibits a strong preference for calcium and lets much more of it into the cell, which leads to inflammation. By contrast, WaTx wedges itself into the allosteric nexus and props the channel open. This abolishes its preference for calcium. As a result, overall ion levels are high enough to trigger a pain response, but calcium levels remain too low to initiate inflammation.

To demonstrate this, the researchers injected either mustard oil, a plant irritant known to activate the wasabi receptor, or WaTx into the paws of mice. With mustard oil, they observed acute pain, hypersensitivity to temperature and touch -- key hallmarks of chronic pain -- and inflammation, as evidenced by significant swelling. But with WaTx, they observed acute pain and pain hypersensitivities, but no swelling.

"When triggered by calcium, nerve cells can release pro-inflammatory signals that tell the immune system that something's wrong and needs to be repaired," Lin King said. "This 'neurogenic inflammation' is one of the key processes that becomes dysregulated in chronic pain. Our results suggest that you can decouple the protective acute pain response from the inflammation that establishes chronic pain. Achieving this goal, if only in principle, has been a longstanding aim in the field."

The researchers believe their findings will lead to a better understanding of acute pain, as well as the link between chronic pain and inflammation, which were previously thought to be experimentally indistinguishable. The findings may even lay the groundwork for the development of new pain drugs.

"The discovery of this toxin provides scientists with a new tool that can be used to probe the molecular mechanisms of pain, in particular, to selectively probe the processes that lead to pain hypersensitivity," Lin King said. "And for those interested in drug discovery, our findings underscore the promise of TRPA1 as a target for new classes of non-opioid analgesics to treat chronic pain."

Read more at Science Daily

Mission to Jupiter's icy moon confirmed

A 2016 artist's concept of the Europa Clipper spacecraft. The design is changing as the spacecraft is developed.

An icy ocean world in our solar system that could tell us more about the potential for life on other worlds is coming into focus with confirmation of the Europa Clipper mission's next phase. The decision allows the mission to progress to completion of final design, followed by the construction and testing of the entire spacecraft and science payload.

"We are all excited about the decision that moves the Europa Clipper mission one key step closer to unlocking the mysteries of this ocean world," said Thomas Zurbuchen, associate administrator for the Science Mission Directorate at NASA Headquarters in Washington. "We are building upon the scientific insights received from the flagship Galileo and Cassini spacecraft and working to advance our understanding of our cosmic origin, and even life elsewhere."

The mission will conduct an in-depth exploration of Jupiter's moon Europa and investigate whether the icy moon could harbor conditions suitable for life, honing our insights into astrobiology. To develop this mission in the most cost-effective fashion, NASA is targeting to have the Europa Clipper spacecraft complete and ready for launch as early as 2023. The agency baseline commitment, however, supports a launch readiness date by 2025.

NASA's Jet Propulsion Laboratory in Pasadena, California, leads the development of the Europa Clipper mission in partnership with the Johns Hopkins University Applied Physics Laboratory for the Science Mission Directorate. Europa Clipper is managed by the Planetary Missions Program Office at NASA's Marshall Space Flight Center in Huntsville, Alabama.

From Science Daily

Temperatures of 800 billion degrees in the cosmic kitchen

When two neutron stars collide, the matter at their core enters extreme states. An international research team has now studied the properties of matter compressed in such collisions. The HADES long-term experiment, involving more than 110 scientists, has been investigating forms of cosmic matter since 1994. With the investigation of electromagnetic radiation arising when stars collide, the team has now focused attention on the hot, dense interaction zone between two merging neutron stars.

Simulation of electromagnetic radiation
Collisions between stars cannot be directly observed -- not least of all because of their extreme rarity. According to estimates, none has ever happened in our galaxy, the Milky Way. The densities and temperatures in merging processes of neutron stars are similar to those occurring in heavy ion collisions, however. This enabled the HADES team to simulate the conditions in merging stars at the microscopic level in the heavy ion accelerator at the Helmholtzzentrum für Schwerionenforschung (GSI) in Darmstadt.

As in a neutron star collision, when two heavy ions are slammed together at close to the speed of light, electromagnetic radiation is produced. It takes the form of virtual photons that turn back into real particles after a very short time. However, the virtual photons occur very rarely in experiments using heavy ions. "We had to record and analyze about 3 billion collisions to finally reconstruct 20,000 measurable virtual photons," says Dr. Jürgen Friese, the former spokesman of the HADES collaboration and researcher at Laura Fabbietti's Professorship on Dense and Strange Hadronic Matter at TUM.

Photon camera shows collision zone

To detect the rare and transient virtual photons, researchers at TUM developed a special 1.5 square meter digital camera. This instrument records the Cherenkov effect: the name given to certain light patterns generated by decay products of the virtual photons. "Unfortunately the light emitted by the virtual photons is extremely weak. So the trick in our experiment was to find the light patterns," says Friese. "They could never be seen with the naked eye. We therefore developed a pattern recognition technique in which a 30,000 pixel photo is rastered in a few microseconds using electronic masks. That method is complemented with neural networks and artificial intelligence."

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Brain finds order amidst chaos

How does the brain find order amidst a sea of noise and chaos? Researchers have found the answer by using advanced simulation techniques to investigate the way neurons talk to each other. They found that by working as a team, cortical neurons can respond even to weak input against the backdrop of noise and chaos, allowing the brain to find order.

Neurons communicate with each other by sending out rapid pulses of electrical signals called spikes. At first glance, the generation of these spikes can be very reliable: when an isolated neuron is repeatedly given exactly the same electrical input, we find the same pattern of spikes. Why, then, does the activity of cortical neurons in a live animal fluctuate and actually seem so variable?

There are two reasons for this. Firstly, when transmitting a signal to another neuron, the process can sometimes fail and these failures are unpredictable -- like rolling a die to decide on an outcome. "We estimate the chance of a synapse between two cortical pyramidal neurons passing a chemical neurotransmitter signal can be as low as 10%," explains lead researcher Max Nolte. This uncertainty means that a neuron will hear the same message sent by connected neurons differently every time.

Secondly, when the two fundamental types of cortical neurons (excitatory and inhibitory) are interconnected in a network, small uncertainties in activity patterns become amplified. This leads to unpredictable patterns, a behavior that is called chaos.

This backdrop of noise and chaos suggests that individual cortical neurons cannot find order and fire reliable spikes, and so the brain has to 'average' the activity of many neurons for certainty -- listen to the whole choir instead of individual singers.

Simulation neuroscience finds the answer

The experimental manipulations required to untangle the noise sources in the brain and evaluate their impact on neuronal activity are currently impossible to perform in a live animal in vivo, or even in separated brain tissue in vitro. "For the moment, it is simply not possible to monitor all of the thousands of brain-wide inputs to a neuron in vivo, nor to turn on and off different noise sources," says Nolte. The closest approximation of cortical tissue to date in a model is the Blue Brain Project's biologically detailed digital reconstruction of rat neocortical microcircuitry (Cell 2015). This computer model provided the ideal platform for the researchers to study to what degree the voices of individual neurons can be understood, as it contains data-constrained models of the unreliable signal transmission between neurons.

Using this model, they found that activity that is spontaneously generated from the interconnected neurons is highly noisy and chaotic, depicting very different spike times in each repetition. "We studied the origin and nature of cortical internal variability with a biophysical neocortical microcircuit model with biologically realistic noise sources," reveals Nolte. "We observed that the unreliable neurotransmitter signals are amplified by recurrent network dynamics, causing a rapidly decaying memory of the past -- a sea of noise and chaos."

Reliable responses amidst noise and chaos

But, of course the mammalian brain does not have a rapidly decaying memory. In fact, perhaps the most fascinating insight from the findings is that spike times that were highly unreliable during spontaneous activity became highly reliable when the circuit received external inputs. This phenomenon was not simply a result of strong external input directly driving the neurons to reliable responses. Even weak thalamocortical input could switch the network briefly to a regime of highly reliable spiking. At that point, the interactions between the neurons that otherwise amplify uncertainty and chaos conversely amplify reliability and allow the brain to find order.

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Memory research: Fruit flies learn their body size once for an entire lifetime

In order to orient themselves and survive in their environment, animals must develop a concept of their own body size. Researchers at Johannes Gutenberg University Mainz (JGU) have shown that the fruit fly Drosophila melanogaster develops a very stable long-term memory for its own body size and the reach of its extremities after it has hatched from the pupal case. The fruit fly acquires this memory through visual feedback obtained when walking, but in the first two hours after training the memory is still susceptible to the effects of stress and not yet firmly anchored. "Once the memory has consolidated, it appears from our observations that it remains intact for life," said Professor Roland Strauss of the Institute of Developmental Biology and Neurobiology at JGU. "The insects seem to have calibrated themselves for the rest of their lives." However, it is still puzzling why they are only able to access the acquired knowledge 12 hours after training. The researchers still don't know what happens in the brain in the interim.

The research group of Professor Roland Strauss uses Drosophila melanogaster to investigate memory retention and consolidation processes that are known to occur to some extent also in humans. Earlier studies have shown that the short-term memory of fruit flies declines with age and that a protein is involved in this process which is similar to that playing a role in humans.

In the new study, Tammo Krause and Laura Spindler analyzed the body-size memory of Drosophila. Fruit flies are insects that undergo a complete metamorphosis. They undergo three larval stages, during which they grow. Finally, at the end of pupation, the mature fruit fly emerges. Due to Drosophila's hard exoskeleton, the body size can no longer change; it can vary however, as the actual size of a fly is determined by the availability and the quality of food during the larval stages.

Leg-over-head behavior indicates an intention to climb

"In our recent study, we wanted to find out how the insects acquire information about their body size and remember it later," explained Tammo Krause and Laura Spindler. They observed how, under various conditions, the insects try to overcome a small gap exceeding their step size. Drosophila displays stereotypical behavior in such situations: In order to initiate the attempt to climb, the insect begins by making search movements with its forelegs lifted over the head. If the gap is far too wide, this typical behavior is not observed. The fly just turns away.

Knowledge of body size is gained through visual feedback

The results show that Drosophila learns to estimate the distance across a gap and the reach of its legs by linking visual information from the environment, such as a striped pattern, with their body size. Newly hatched fruit flies raised in the dark overestimate their body size and try to overcome gaps that are far too big significantly more frequently than animals raised in the usual light-dark cycle. The motion parallax created on the retina by structures in the surroundings when walking is used for the learning process. Another experiment in which the motion parallax was manipulated and artificially reduced during the learning process confirmed this. As a result, the flies underestimated their body size and undertook fewer climbing attempts.

"When fruit flies hatch from the pupal case and move through space, the resulting motion is captured by the eye and the fly can calibrate itself," explained Professor Roland Strauss. "Once this calibration has occurred, the knowledge is retained for life." The research team proved this in an additional experiment in which the fruit flies had to spend 21 days in the dark after three days under normal light conditions. Even after this long period, they still undertook the same number of climbing attempts as three-day-old flies. "We therefore assume that memory of their own body size is the most permanent form of recall detected in Drosophila to date," the two lead authors Tammo Krause and Laura Spindler concluded in their article in Current Biology.

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