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The sea anemone, a cnidarian, has no brain. It does have a nervous system, and its body has a clear axis, with a mouth on one side and a basal disk on the other. However, there is no organized collection of neurons comparable to the kind of brain found in bilaterians, animals that have both a bilateral symmetry and a top and bottom. Most animals except sponges, cnidarians, and a few other phyla are bilaterians. So an interesting evolutionary question is, which came first, the head or the brain? Do animals such as sea anemones, which lack a brain, have something akin to a head? Chiara Sinigaglia and colleagues reported recently that at least some developmental pathways seen in cnidarians share a common lineage with head and brain development in bilaterians. It might seem intuitive to expect to find genes involved in brain development around the mouth of the anemone, and previous work has suggested that the oral region in cnidarians corresponds to the head region of bilaterians. However, there has been debate over whether the oral or aboral pole of cnidarians is analogous to the anterior pole of bilaterians. At the start of its life cycle a sea anemone exists as a free swimming planula, which then attaches to a surface and becomes a sea anemone. That free-swimming phase contains an apical tuft, a sensory structure at the front of the swimming animal's body. The apical tuft is the part that attaches and becomes the aboral pole --the part distal from the mouth-- of the adult anemone. To test whether genetic expression in the aboral pole of cnidarians does in fact resemble the head patterning seen in bilaterians, researchers analyzed gene expression in Nematostella vectensis, a sea anemone found in estuaries and bays. They focused on the six3 and FoxQ2transcription factors, as these genes are known to regulate development of the anterior-posterior axis in bilaterian species. six3 knockout mice, for example, fail to develop a forebrain, and in humans, six3 is known to regulate the development of forebrain and eyes.
The N. vectensis genome contains one gene from the six3/6 group and four foxQ2 genes. Sinigaglia and colleagues found that Nvsix3/6 and one of the foxQ2 genes, NvFoxQ2a, were expressed predominantly on the aboral pole of the developing cnidarian but, after gastrulation, were excluded from a small spot in that region (NvSix3/6 was also expressed in a small number of other cells of the planula that resembled neurons). Because of this, the authors callNvSix3/6 and NvFoQ2a “ring genes”, and genes that are then expressed in that spot “spot genes.” The spot then develops into the apical tuft.
Through knockdown and rescue experiments, the researchers demonstrate that NvSix3/6 is required for the development of the aboral region; without it, the expression of spot genes is reduced or eliminated and the apical tuft of the planula doesn't form. This suggests that development of the region distal from the cnidarian mouth appears to parallel the development of the bilaterian head.
This research demonstrates that at least a subset of the genes that cause head and brain formation in bilaterians are also differentially expressed in the aboral region of the sea urchin. The expression patterns are not identical to those in all bilaterians; however, the similarities suggest that the patterns of gene expression arose in an ancestor common to bilaterians and cnidarians, and that the process was then modified in bilaterians to produce a brain. So to answer the evolutionary question posed above, it seems that the developmental module that produces a head came first.
Via Sakis Koukouvis
The Human Connectome Project, a five-year endeavor to link brain connectivity to human behavior, has released a set of high-quality imaging and behavioral data to the scientific community. The project has two major goals: to collect vast amounts of data using advanced brain imaging methods on a large population of healthy adults, and to make the data freely available so that scientists worldwide can make further discoveries about brain circuitry. The initial data release includes brain imaging scans plus behavioral information — individual differences in personality, cognitive capabilities, emotional characteristics and perceptual function — obtained from 68 healthy adult volunteers. Over the next several years, the number of subjects studied will increase steadily to a final target of 1,200. The initial release is an important milestone because the new data have much higher resolution in space and time than data obtained by conventional brain scans. The Human Connectome Project (HCP) consortium is led by David C. Van Essen, PhD, Alumni Endowed Professor at Washington University School of Medicine in St. Louis, and Kamil Ugurbil, PhD, Director of the Center for Magnetic Resonance Research and the McKnight Presidential Endowed Chair Professor at the University of Minnesota. “By making this unique data set available now, and continuing with regular data releases every quarter, the Human Connectome Project is enabling the scientific community to immediately begin exploring relationships between brain circuits and individual behavior,” says Van Essen. “The HCP will have a major impact on our understanding of the healthy adult human brain, and it will set the stage for future projects that examine changes in brain circuits underlying the wide variety of brain disorders afflicting humankind.” The consortium includes more than 100 investigators and technical staff at 10 institutions in the United States and Europe (www.humanconnectome.org). It is funded by 16 components of the National Institutes of Health via the Blueprint for Neuroscience Research (www.neuroscienceblueprint.nih.gov).
It is possible to tell who a person is thinking about by analyzing images of his or her brain. Our mental models of people produce unique patterns of brain activation, which can be detected using advanced imaging techniques according to a study by Cornell University neuroscientist Nathan Spreng and his colleagues.
"When we looked at our data, we were shocked that we could successfully decode who our participants were thinking about based on their brain activity," said Spreng, assistant professor of human development in Cornell's College of Human Ecology. Understanding and predicting the behavior of others is a key to successfully navigating the social world, yet little is known about how the brain actually models the enduring personality traits that may drive others' behavior, the authors say. Such ability allows us to anticipate how someone will act in a situation that may not have happened before. To learn more, the researchers asked 19 young adults to learn about the personalities of four people who differed on key personality traits. Participants were given different scenarios (i.e. sitting on a bus when an elderly person gets on and there are no seats) and asked to imagine how a specified person would respond. During the task, their brains were scanned using functional magnetic resonance imaging (fMRI), which measures brain activity by detecting changes in blood flow. They found that different patterns of brain activity in the medial prefrontal cortex (mPFC) were associated with each of the four different personalities. In other words, which person was being imagined could be accurately identified based solely on the brain activation pattern. The results suggest that the brain codes the personality traits of others in distinct brain regions and this information is integrated in the medial prefrontal cortex (mPFC) to produce an overall personality model used to plan social interactions, the authors say. "Prior research has implicated the anterior mPFC in social cognition disorders such as autism and our results suggest people with such disorders may have an inability to build accurate personality models," said Spreng. "If further research bears this out, we may ultimately be able to identify specific brain activation biomarkers not only for diagnosing such diseases, but for monitoring the effects of interventions."
Researchers at Brown University have succeeded in creating the first wireless, implantable, rechargeable, long-term brain-computer interface. The wireless BCIs have been implanted in pigs and monkeys for over 13 months without issue, and human subjects are next. A tether limits the mobility of the patient, and also the real-world testing that can be performed by the researchers. Brown’s wireless BCI allows the subject to move freely, dramatically increasing the quantity and quality of data that can be gathered — instead of watching what happens when a monkey moves its arm, scientists can now analyze its brain activity during complex activity, such as foraging or social interaction. Obviously, once the wireless implant is approved for human testing, being able to move freely — rather than strapped to a chair in the lab — would be rather empowering. Inside the device, there’s a li-ion battery, an inductive (wireless) charging loop, a chip that digitizes the signals from your brain, and an antenna for transmitting those neural spikes to a nearby computer. The BCI is connected to a small chip with 100 electrodes protruding from it, which, in this study, was embedded in the somatosensory cortex or motor cortex. These 100 electrodes produce a lot of data, which the BCI transmits at 24Mbps over the 3.2 and 3.8GHz bands to a receiver that is one meter away. The BCI’s battery takes two hours to charge via wireless inductive charging, and then has enough juice to last for six hours of use.
One of the features that the Brown researchers seem most excited about is the device’s power consumption, which is just 100 milliwatts. For a device that might eventually find its way into humans, frugal power consumption is a key factor that will enable all-day, highly mobile usage. Amusingly, though, the research paper notes that the wireless charging does cause significant warming of the device, which was “mitigated by liquid cooling the area with chilled water during the recharge process and did not notably affect the animal’s comfort.” Another important factor is that the researchers were able to extract high-quality, “rich” neural signals from the wireless implant — a good indicator that it will also help human neuroscience, if and when the device is approved.
A brain-to-brain interface (BTBI) enabled a real-time transfer of behaviorally meaningful sensorimotor information between the brains of two rats. In this BTBI, an “encoder” rat performed sensorimotor tasks that required it to select from two choices of tactile or visual stimuli. While the encoder rat performed the task, samples of its cortical activity were transmitted to matching cortical areas of a “decoder” rat using intracortical microstimulation (ICMS). The decoder rat learned to make similar behavioral selections, guided solely by the information provided by the encoder rat's brain. These results demonstrated that a complex system was formed by coupling the animals' brains, suggesting that BTBIs can enable dyads or networks of animal's brains to exchange, process, and store information and, hence, serve as the basis for studies of novel types of social interaction and for biological computing devices.
In his seminal study on information transfer between biological organisms, Ralph Hartley wrote that “in any given communication the sender mentally selects a particular symbol and by some bodily motion, as his vocal mechanism, causes the receiver to be directed to that particular symbol”. Brain-machine interfaces (BMIs) have emerged as a new paradigm that allows brain-derived information to control artificial actuators and communicate the subject's motor intention to the outside world without the interference of the subject's body. For the past decade and a half, numerous studies have shown how brain-derived motor signals can be utilized to control the movements of a variety of mechanical, electronic and even virtual external devices. Recently, intracortical microstimulation (ICMS) has been added to the classical BMI paradigm to allow artificial sensory feedback signals, generated by these brain-controlled actuators, to be delivered back to the subject's brain simultaneously with the extraction of cortical motor commands. In the present study, a research group took the BMI approach to a new direction altogether and tested whether it could be employed to establish a new artificial communication channel between animals; one capable of transmitting behaviorally relevant sensorimotor information in real-time between two brains that, for all purposes, would from now on act together towards the fulfillment of a particular behavioral task. Previously, the same team reported that specific motor and sensory parameters can be extracted from populations of cortical neurons using linear or nonlinear decoders in real-time. Here, the scientists tested the hypothesis that a similar decoding performed by a “recipient brain” was sufficient to guide behavioral responses in sensorimotor tasks, therefore constituting a Brain-to-Brain Interface (BTBI). To test this hypothesis, they conducted three experiments in which different patterns of cortical sensorimotor signals, coding a particular behavioral response, were recorded in one rat (heretofore named the “encoder” rat) and then transmitted directly to the brain of another animal (i.e. the “decoder” rat), via intra-cortical microstimulation (ICMS). All BTBI experiments described below were conducted in awake, behaving rats chronically implanted with cortical microelectrode arrays capable of both neuronal ensemble recordings and intracortical microstimulation. The scientists demonstrated that pairs of rats could cooperate through a BTBI to achieve a common behavioral goal.
By implanting a tiny microscope in the brain of a mouse Stanford researchers have been able to monitor its brain activity. The study links the observed neuron activity with long-term information storage and could be used to develop treatments and therapies for neurodegenerative conditions in humans. The technique involved genetically engineering the mice to contain a green fluorescent protein. The protein was created to react to the presence of calcium ions so, when the neuron fired and the cell naturally flooded with those ions, the cells fluoresced green. A little microscope positioned just above the hippocampus in the mouse's brain could then capture the activity and send it to a computer screen for near real-time monitoring as the mouse runs around a little arena. "We can literally figure out where the mouse is in the arena by looking at these lights," said biologist Mark Schnitzer, senior author on the paper which has been published in the journal Nature Neuroscience. "The hippocampus is very sensitive to where the animal is in its environment, and different cells respond to different parts of the arena. Imagine walking around your office. Some of the neurons in your hippocampus light up when you're near your desk, and others fire when you're near your chair. This is how your brain makes a representative map of a space." These patterns of firing in the mouse brain were found to stay consistent even after weeks had passed between tests. This consistency is what makes it possible to use the technique as a tool with which to study progressive brain diseases and evaluate the effectiveness of some types of treatment and therapy.
For the first time, Wayne State University researchers have shown brain connectivity in fetuses, a discovery that could lead to new ways to prevent and treat brain disorders. Research has shown that brain disorders such as autism may begin in fetal life but there hasn't been a method for seeing and studying brain development at that stage. But Thomason's study showed that the fetal brain can be studied while in the womb using MRI scans that do not threaten the health of the infant or mother, providing a mechanism for many researchers to study fetal brain connections as they are forming and possibly learn how a lack of connections can result in brain disorders. "By understanding how a lack of (brain) connectivity occurs, the research community can begin to identify what things influence early brain development," Thomason said. "If we know what disrupts or impedes healthy brain development, then we have a better shot at finding a way to treat and possibly prevent it." The research, which began in November, was funded partly by the NIH and WSU. It included 25 fetuses between 24 to 38 weeks of gestation. The findings show that brain connections strengthened between the right and left side as fetuses developed and short-distance connections in the brain network are more strongly connected than long-range connections. It is the first study of a larger project that seeks to define how functional brain networks form in fetuses and examine the environment of the developing child in utero, and factors in the mother's life. The project plans to track the fetuses once they become infants and throughout their life so researchers can compare their neurodevelopment to what was seen in the womb. The hope is to even study the children of these fetuses, if funding allows.
According to new research study from the University of British Columbia and Université Paris Descartes, infants in bilingual environments use pitch and duration cues to discriminate between languages – such as English and Japanese – with opposite word orders. In English, a function word comes before a content word (the dog, his hat, with friends, for example) and the duration of the content word is longer, while in Japanese or Hindi, the order is reversed, and the pitch of the content word higher. “By as early as seven months, babies are sensitive to these differences and use these as cues to tell the languages apart,” says UBC psychologist Janet Werker, co-author of the study. Previous research by Werker and Judit Gervain, a linguist at the Université Paris Descartes and co-author of the new study, showed that babies use frequency of words in speech to discern their significance. “For example, in English the words ‘the’ and ‘with’ come up a lot more frequently than other words – they’re essentially learning by counting,” says Gervain. “But babies growing up bilingual need more than that, so they develop new strategies that monolingual babies don’t necessarily need to use.” “If you speak two languages at home, don’t be afraid, it’s not a zero-sum game,” says Werker. “Your baby is very equipped to keep these languages separate and they do so in remarkable ways.”
US researchers have effectively given laboratory rats a "sixth sense" using an implant in their brains. An experimental device allowed the rats to "touch" infrared light - which is normally invisible to them. The team at Duke University fitted the rats with an infrared detector wired up to microscopic electrodes that were implanted in the part of their brains that processes tactile information. The researchers say that, in theory at least, a human with a damaged visual cortex might be able to regain sight through a device implanted in another part of the brain. The experiment also shows that a new sensory input can be interpreted by a region of the brain that normally does something else (without having to "hijack" the function of that brain region). "We could create devices sensitive to any physical energy," said Prof Nicolelis, from the Duke University Medical Center in Durham, North Carolina. "It could be magnetic fields, radio waves, or ultrasound. We chose infrared initially because it didn't interfere with our electrophysiological recordings." His colleague Eric Thomson commented: "The philosophy of the field of brain-machine interfaces has until now been to attempt to restore a motor function lost to lesion or damage of the central nervous system. "This is the first paper in which a neuroprosthetic device was used to augment function - literally enabling a normal animal to acquire a sixth sense." In their experiments, the researchers used a test chamber with three light sources that could be switched on randomly. They taught the rats to choose the active light source by poking their noses into a port to receive a sip of water as a reward. They then implanted the microelectrodes, each about a tenth the diameter of a human hair, into the animals' brains. These electrodes were attached to the infrared detectors. The scientists then returned the animals to the test chamber. At first, the rats scratched at their faces, indicating that they were interpreting the lights as touch. But after a month - as shown in these videos - the animals learned to associate the signal in their brains with the infrared source. They began to search actively for the signal, eventually achieving perfect scores in tracking and identifying the correct location of the invisible light source. One key finding was that enlisting the touch cortex to detect infrared light did not reduce its ability to process touch signals.
Chimpanzees can far outperform humans in some mental tasks, including rapidly memorising and recalling numbers, Japanese scientists have shown. At the American Association for the Advancement of Science annual meeting, Tetsuro Matsuzawa, of Kyoto University’s Primate Research Institute, showed remarkable videos of chimpanzees displaying mental dexterity that would be way beyond most people. The star performer among the institute’s 14 chimpanzees, a 12-year-old male called Ayumu, has learnt all the numerals from 1 to 19. Several other Kyoto chimpanzees have learnt 1 to 9. When the numbers flash up in random places across a computer screen and in random order, and disappear after less than a second, the apes can point immediately to the exact locations where the numerals had been, in the correct numerical order. Prof Matsuzawa said a few exceptional people, such as those with savant syndrome, might be capable of such memory feats but they are far beyond the average human brain. “One person in several thousand may be able to do this,” he said. “All the chimps I have tested can do it.” Prof Matsuzawa, who combines the study of wild chimpanzees in west Africa with research using the captive colony in Kyoto, said such a good working memory – the ability to take in an accurate, detailed image of a complex scene or pattern – was an important survival tool in the wild. For example, the apes can quickly assess and remember the distribution of edible fruit in a forest canopy. Or, when two rival bands of chimpanzees encounter one another, they can assess the strength of the rival group and decide whether to fight or flee.
A drug-like molecule has been found to let researchers control movements in mice and fish with flashes of light. Unlike similar experiments using a light-based technique known as optogenetics, the new method doesn’t require researchers to genetically engineer animals in order to achieve the neural control. A study published online in today’s Nature Chemical Biology describes a novel approach for controlling neurons and behaviors with light. Such techniques are powerful research tools for understanding the brain, and may one day be used therapeutically. Today’s report describes a method for using light to control neuronal activity in unmodified animals. Fish given a small molecule called “optovin” will move around very quickly in response to a flash of light, report Massachusetts General Hospital’s David Kokel and colleagues. The response is not dependent on the fish perceiving the light—embryonic fish treated with the chemical react to light even before their eyes develop, and decapitated adults respond as well. The compound instead binds to pain sensation receptors on the fish’s body, and when activated by light, it elicits fast movements. The team screened through 10,000 different compounds—each dissolved in a small well with not-yet-hatched zebrafish—before they found one that drastically changed the animals’ behavior in response to light. The compound also works on mice—if optovin is rubbed onto the ears of mice, a flash of light will cause the mice to shake their heads. The team determined that optovin docks onto a specific kind of protein channel that sits in the membrane of nerve cells that are the first to respond to pain. Researchers could use optovin in experiments to study pain; they also think it could be useful in treating pain, says Kokel. “If you over-activate these channels, they become desensitized,” he says. But optovin cannot control the behavior of other kinds of neurons, which is a disadvantage compared to optogenetics. Ed Boyden, a neuroscientist at MIT who has developed optogenetics tools, points out that the genetic engineering-based method gives researchers more flexibility. “A chief utility of our … optogenetic tools is that we can target them to practically any class of neurons, enabling them specifically to be activated and silenced by light,” Boyden says. However, it’s possible, says Kokel, that researchers could identify compounds other than optovin that could regulate the protein channels that control neuron behavior. “You could have a whole tool box of compounds that activate different channels,” he says.
Cognitive decline in old age is linked to decreasing production of new neurons. Scientists from the German Cancer Research Center have discovered in mice that significantly more neurons are generated in the brains of older animals if a signaling molecule called Dickkopf-1 is turned off. In tests for spatial orientation and memory, mice in advanced adult age whose Dickkopf gene had been silenced reached an equal mental performance as young animals. The hippocampus – a structure of the brain whose shape resembles that of a seahorse – is also called the "gateway" to memory. This is where information is stored and retrieved. Its performance relies on new neurons being continually formed in the hippocampus over the entire lifetime. "However, in old age, production of new neurons dramatically decreases. This is considered to be among the causes of declining memory and learning ability", Prof. Dr. Ana Martin-Villalba, a neuroscientist, explains. Martin-Villalba, who heads a research department at the German Cancer Research Center (DKFZ), and her team are trying to find the molecular causes for this decrease in new neuron production (neurogenesis). Neural stem cells in the hippocampus are responsible for continuous supply of new neurons. Specific molecules in the immediate environment of these stem cells determine their fate: They may remain dormant, renew themselves, or differentiate into one of two types of specialized brain cells, astrocytes or neurons. One of these factors is the Wnt signaling molecule, which promotes the formation of young neurons. However, its molecular counterpart, called Dickkopf-1, can prevent this. "We find considerably more Dickkopf-1 protein in the brains of older mice than in those of young animals. We therefore suspected this signaling molecule to be responsible for the fact that hardly any young neurons are generated any more in old age." The scientists tested their assumption in mice whose Dickkopf-1 gene is permanently silenced. Professor Christof Niehrs had developed these animals at DKFZ. The term "Dickkopf" (from German "dick" = thick, "Kopf" = head) also goes back to Niehrs, who had found in 1998 that this signaling molecule regulates head development during embryogenesis. Martin-Villalba's team discovered that stem cells in the hippocampus of Dickkopf knockout mice renew themselves more often and generate significantly more young neurons. The difference was particularly obvious in two-year old mice: In the knockout mice of this age, the researchers counted 80 percent more young neurons than in control animals of the same age. Moreover, the newly formed cells in the adult Dickkopf-1 mutant mice matured into potent neurons with multiple branches. In contrast, neurons in control animals of the same age were found to be more rudimentary already. Blocking Dickkopf improves spatial orientation and memory. Several years ago, Ana Martin-Villalba had shown that mice lose their spatial orientation when neurogenesis in the hippocampus is blocked. Now, is it possible that the young neurons in Dickkopf-deficient mice improve the animals' cognitive performance? The DKFZ researchers used standardized tests to study how the mice orient themselves in a maze. While in the control animals, the younger ones (3 months) performed much better in orienting themselves than the older ones (18 months), the Dickkopf-1-deficient mice showed no age-related decline in spatial orientation capabilities. Older Dickkopf-1 mutant mice also outperformed normal animals in tests determining spatial memory. "Our result proves that Dickkopf-1 promotes age-related decline of specific cognitive abilities," says Ana Martin-Villalba. "Although we had expected silencing of Dickkopf-1 to improve spatial orientation and memory of adult mice, we were surprised and impressed that animals in advanced adult age actually reach the performance levels of young animals." These results give rise to the question whether the function of Dickkopf-1 may be turned off using drugs. Antibodies blocking the Dickkopf protein are already being tested in clinical trials for treating a completely different condition. "It is fascinating to speculate that such a substance may also slow down age-related cognitive decline. But this is still a dream of the future, since we have only just started first experiments in mice to explore this question."
"In movies, we explore landscapes far removed from our day-to-day lives. Whether experiencing the fantastical adventures of Star Wars or the dramatic throes of The English Patient, movies demand that our brains engage in a complex firing of neurons and cognitive processes. We enter into manipulated worlds where musical scores enhance feeling; where cinematography clues us into details we’d normally gloss over; where, like omniscient beings, we voyeuristically peek into others’ lives and minds; and where we can travel from Marrakech to Mars without ever having left our seat. Movies reflect reality, yet are anything but. “Movies are highly complex, multidimensional stimuli,” said Uri Hasson, a neuroscientist and psychologist at Princeton University. “Some areas of the brain analyze sound bites, some analyze word context, some the sentence content, music, emotional aspect, color or motion."
Via Thierry Saint-Paul
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Mice that received transplants of human glial progenitor cells learned much more quickly than normal mice, according to a study published today (March 7) in Cell Stem Cell. The findings support the theory that glial cells made a significant contribution to the evolution of our own enhanced cognitive abilities. “This work is very exciting and surprising because it demonstrates that there may be something special about human glial progenitor cells that contribute to the amazing complexity and computational abilities of the human brain,” said Robert Malenka, a neuroscientist at Stanford University who was not involved in the study, in an email to The Scientist. For many years, glia cells, non-neuronal cells present in the same numbers as neurons in the brain, were thought to play only a supporting role, providing structure, insulation, and nutrients for neurons. But in the past 20 years it has become clear that glia also participate in the transmission of electrical signals. Specifically, astrocytes—a type of glial cell with thousands of tendrils that reach and encase synapses—can modulate signals passing between neurons and affect the strength of those connections over time. Recent studies have also demonstrated that human astrocytes are very different from those found in mouse and rat brains, on which most previous studies of astrocyte physiology were based. Human astrocytes are more numerous, larger, and more complex, and they are capable of far more rapid signaling responses than rodent astrocytes. Together, these results suggest that astrocytes may have been critical to the evolution of enhanced neural processing in humans. Having already transplanted human glial progenitor cells (GPCs) to restore myelination in myelin-deficient mice, Steven Goldman of University of Rochester Medical Center in New York and colleagues realized that they could repeat the trick in normal mice to assess the contribution of human-specific astrocytes to synaptic plasticity and learning. Goldman’s team grafted human GPCs into the brain of baby mice and waited until they became adults, by which time a large proportion of their forebrain glia were replaced by human cells differentiated from the GPCs, including astrocytes with the same structure and functional capabilities as in humans. The researchers then looked at long-term potentiation (LTP)—the strengthening of synaptic connections and a key mechanism underlying learning—in the hippocampus, and found that it was significantly enhanced in mice with human GPCs compared with normal mice and mice engrafted with mouse GPCs. Goldman and colleagues also assessed the performance of the mice on several behavioral tasks that measure leaning and memory—including auditory fear conditioning, a maze test, and object-location memory—and found across the board that mice with human GPCs learned significantly more quickly than normal mice.
Via Luisa Meira
The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Scientists have long known that the young and old brains are very different. Adolescent brains are more malleable or plastic, which allows them to learn languages more quickly than adults and speeds recovery from brain injuries. The comparative rigidity of the adult brain results in part from the function of a single gene that slows the rapid change in synaptic connections between neurons. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity. "These are the molecules the brain needs for the transition from adolescence to adulthood," said Stephen Strittmatter. Vincent Coates Professor of Neurology, Professor of Neurobiology and senior author of the paper. "It suggests we can turn back the clock in the adult brain and recover from trauma the way kids recover." Rehabilitation after brain injuries like strokes requires that patients re-learn tasks such as moving a hand. Researchers found that adult mice lacking Nogo Receptor recovered from injury as quickly as adolescent mice and mastered new, complex motor tasks more quickly than adults with the receptor. "This raises the potential that manipulating Nogo Receptor in humans might accelerate and magnify rehabilitation after brain injuries like strokes," said Feras Akbik, Yale doctoral student who is first author of the study. Researchers also showed that Nogo Receptor slows loss of memories. Mice without Nogo receptor lost stressful memories more quickly, suggesting that manipulating the receptor could help treat post-traumatic stress disorder. "We know a lot about the early development of the brain," Strittmatter said, "But we know amazingly little about what happens in the brain during late adolescence."
The prospect of undergoing surgery while not fully "under" may sound like the stuff of horror movies. But one patient in a thousand remembers moments of awareness while under general anesthesia, physicians estimate. The memories are sometimes neutral images or sounds of the operating room, but occasionally patients report being fully aware of pain, terror, and immobility. Though surgeons scrupulously monitor vital signs such as pulse and blood pressure, anesthesiologists have no clear signal of whether the patient is conscious. But a new study finds that the brain may produce an early-warning signal that consciousness is returning—one that's detectable by electroencephalography (EEG), the recording of neural activity via electrodes on the skull. "We've known since the 1930s that brain activity changes dramatically with increasing doses of anesthetic," says the study's corresponding author, anesthesiologist Patrick Purdon of Massachusetts General Hospital in Boston. "But monitoring a patient's brain with EEG has never become routine practice." Beginning in the 1990s, some anesthesiologists began using an approach called the bispectral (BIS) index, in which readings from a single electrode are connected to a device that calculates, and displays, a single number indicating where the patient's brain activity falls on a scale of 100 (fully conscious) to zero (a "flatline" EEG). Anything between 40 and 60 is considered the target range for unconsciousness. But this index and other similar ones are only indirect measurements, Purdon explains. In 2011, a team led by anesthesiologist Michael Avidan at the Washington University School of Medicine in St. Louis, Missouri, found that monitoring with the BIS index was slightly less successful at preventing awareness during surgery than the nonbrain-based method of measuring exhaled anesthesia in the patient's breath. Of the 2861 patients monitored with the BIS index, seven had memories of the surgery, whereas only two of 2852 patients whose breath was analyzed remembered anything. Despite that, Purdon and his co-workers were hopeful that an "unconsciousness signature" in the brain could be found. Last year, the team worked with three epilepsy patients who'd had electrodes implanted in their brains in preparation for surgery to reduce their seizures. Recording from single neurons in the cortex, where awareness is thought to reside, the researchers gave the patients an injection of the anesthetic propofol. They asked the volunteers to press a button whenever they heard a tone, recording the activity of the neurons. Loss of consciousness, defined as the point when the patients stopped pressing the button, was immediate—40 seconds after injection. Just as immediately, groups of neurons began to emit a characteristic slow oscillation, a kind of ripple in the cells' electrical field. The neurons weren't entirely inactive, but bursts of activity occurred only at specific points in this oscillation, resulting in inconsistent brain cell activity.
Recently, we have witnessed remarkable, fictional-sounding advancements in science and medicine. Using embryos from the African clawed frog (Xenopus laevis), scientists at Tufts’ Center for Regenerative and Developmental Biology were able to transplant eye primordia—cells that will eventually grow into an eye—from one tadpole’s head to another’s posterior, flank, or tail. They didn't connect nerve endings or “wiring” or anything like that. They just cut out the cells from the head, slice open the side or the tail, and jam them in. As the eyes grow, they send out nerve fibesr, or axons. We know this because the “tissue donor” tadpoles were labeled with tdTomato, a red fluorescent protein. This allowed the researchers to watch innervation, or nerve growth, as it happened. Of those eye primordia that sent out axons, nearly half hardwired directly into the spine, while the other half built connections to the nearby stomach. None of the tadpoles grew tdTomato-marked pathways to the brain, however. Before they could test the ectopic eyes for functionality, the native ones had to be severed and removed. Otherwise, how would the scientists know which of the tadpole’s three eyes was truly seeing? Finally, it was time to put the aberrant eyes to the test. Using an underwater arena rigged with blue and red LEDs and electric shock, scientists ran through an exhaustive array of controls and variables. Interestingly, the tadpoles with no eyes at all could still react to LED changes, revealing that they may have other ways of sensing light. However, they proved woefully inadequate at avoiding electro shocks, showing whatever information they were getting was ultimately flawed or unusable. On the other end of the spectrum were the control tadpoles with normal eyes that quickly learned to avoid the shocks through the scientists’ regimen of aversive conditioning. Amazingly, a statistically significant portion of the transplanted one eye tadpoles could not only detect LED changes, but they showed learning behavior when confronted with electric shock. Though eyes have been placed on or near rat brains in previous studies with success, this result marked the first time a vertebrate eye has been able to send visual information to the brain without a direct connection—and from as far away as the other end of the organism. Obviously, many questions remain. For instance, how does the brain know information coming up the spine from the tail is visual? It should have no idea what that aberrant eye is blinking about—and yet it seems to take the information in stride. The paper suggests perhaps different types of data are somehow marked, not altogether different from the way we demarcate files and commands in a computer. Ahead lies everything from better computer brain interfaces to bioengineered organ systems. If we can understand the limits of the brain’s plasticity, we might be able to one day create cybernetic devices that don’t just do what we program, but discover on their own what is required.
Researchers at the University of Pennsylvania School of Medicine estimate that the human retina can transmit visual input at about the same rate as an Ethernet connection, one of the most common local area network systems used today. They present their findings in the July issue of Current Biology. This line of scientific questioning points to ways in which neural systems compare to artificial ones, and can ultimately inform the design of artificial visual systems. Two broad classes of ganglion cell types in the guinea pig retina: brisk cells, which are larger and transmit electrical impulses faster, and sluggish, which are smaller and slower
Much research on the basic science of vision asks what types of information the brain receives; this study instead asked how much. Using an intact retina from a guinea pig, the researchers recorded spikes of electrical impulses from ganglion cells using a miniature multi-electrode array. The investigators calculate that the human retina can transmit data at roughly 10 million bits per second. By comparison, an Ethernet can transmit information between computers at speeds of 10 to 100 million bits per second.
The retina is actually a piece of the brain that has grown into the eye and processes neural signals when it detects light. Ganglion cells carry information from the retina to the higher brain centers; other nerve cells within the retina perform the first stages of analysis of the visual world. The axons of the retinal ganglion cells, with the support of other types of cells, form the optic nerve and carry these signals to the brain. Investigators have known for decades that there are 10 to 15 ganglion cell types in the retina that are adapted for picking up different movements and then work together to send a full picture to the brain. The study estimated the amount of information that is carried to the brain by seven of these ganglion cell types. The guinea pig retina was placed in a dish and then presented with movies containing four types of biological motion, for example a salamander swimming in a tank to represent an object-motion stimulus. After recording electrical spikes on an array of electrodes, the researchers classified each cell into one of two broad classes: “brisk” or “sluggish,” so named because of their speed.
High-order thinking depends upon our ability to generate mental representations in our brains without any sensory stimulation from the environment. These cognitive abilities arise from highly evolved circuits in the prefrontal cortex. Mathematical models by former Yale neurobiologist Xiao-Jing Wang, now of New York University, predicted that in order to maintain these visual representations the prefrontal cortex must rely on a family of receptors that allow for slow, steady firing of neurons. The Yale scientists show that NMDA-NR2B receptors involved in glutamate signaling regulate this neuronal firing. These receptors, studied at Yale for more than a decade, are responsible for activity of highly evolved brain circuits found especially in primates. Earlier studies have shown these types of NMDA receptors are often altered in patients with schizophrenia. The Neuron study suggests that those suffering from the disease may be unable to hold onto a stable view of the world. Also, these receptors seem to be altered in Alzheimer’s patients, which may contribute to the cognitive deficits of dementia. The lab of Dr. John Krystal, chair of the department of psychiatry at Yale, has found that the anesthetic ketamine, abused as a street drug, blocks NMDA receptors and can mimic some of thesymptoms of schizophrenia. The current study in Neuron shows that ketamine may reduce the firing of the same higher-order neural circuits that are decimated in schizophrenia. “Identifying the receptor needed for higher cognition may help us to understand why certain genetic insults lead to cognitive impairment and will help us to develop strategies for treating these debilitating disorders,” Arnsten said.
A team of researchers at UC San Francisco has uncovered the neurological basis of speech motor control, the complex coordinated activity of tiny brain regions that controls our lips, jaw, tongue and larynx as we speak. Described this week in the journal Nature, the work has potential implications for developing computer-brain interfaces for artificial speech communication and for the treatment of speech disorders. It also sheds light on an ability that is unique to humans among living creatures but poorly understood. “Speaking is so fundamental to who we are as humans – nearly all of us learn to speak,” said senior author Edward Chang, MD, a neurosurgeon at the UCSF Epilepsy Center and a faculty member in the UCSF Center for Integrative Neuroscience. “But it’s probably the most complex motor activity we do.” The complexity comes from the fact that spoken words require the coordinated efforts of numerous “articulators” in the vocal tract – the lips, tongue, jaw and larynx – but scientists have not understood how the movements of these distinct articulators are precisely coordinated in the brain. To understand how speech articulation works, Chang and his colleagues recorded electrical activity directly from the brains of three people undergoing brain surgery at UCSF, and used this information to determine the spatial organization of the “speech sensorimotor cortex,” which controls the lips, tongue, jaw, larynx as a person speaks. This gave them a map of which parts of the brain control which parts of the vocal tract. They then applied a sophisticated new method called “state-space” analysis to observe the complex spatial and temporal patterns of neural activity in the speech sensorimotor cortex that play out as someone speaks. This revealed a surprising sophistication in how the brain's speech sensorimotor cortex works. They found that this cortical area has a hierarchical and cyclical structure that exerts a split-second, symphony-like control over the tongue, jaw, larynx and lips. “These properties may reflect cortical strategies to greatly simplify the complex coordination of articulators in fluent speech,” said Kristofer Bouchard, PhD, a postdoctoral fellow in the Chang lab who was the first author on the paper. In the same way that a symphony relies upon all the players to coordinate their plucks, beats or blows to make music, speaking demands well-timed action of several various brain regions within the speech sensorimotor cortex.
A new therapy could help suppress tremors in people with Parkinson's disease, an Oxford University study suggests. The technique – called transcranial alternating current stimulation or TACS – cancels out the brain signal causing the tremors by applying a small, safe electric current across electrodes on the outside of a patient’s head. The preliminary study, conducted with 15 people with Parkinson's disease at Oxford's John Radcliffe Hospital, is published in the journal Current Biology. The researchers showed a 50 per cent reduction in resting tremors among the patients. Physical tremors are a significant and debilitating symptom of Parkinson's disease, but do not respond well to existing drug treatments. Tremors can be successfully treated with deep brain stimulation, a technique that involves surgery to insert electrodes deep into the brain itself to deliver electrical impulses. But this invasive therapy is expensive and carries some health risks, including bleeding in to the brain, which means it is not suitable for all patients. In TACS in contrast, the electrode pads are placed on the outside of the patient's head, so it does not carry the risks associated with deep brain stimulation. Tremors experienced by Parkinson's sufferers can be devastating and any therapy that can suppress or reduce those tremors significantly improves quality of life for patients. Professor Peter Brown of the Nuffield Department of Clinical Neurosciences, who led the study, said: 'Tremors experienced by Parkinson's sufferers can be devastating and any therapy that can suppress or reduce those tremors significantly improves quality of life for patients. 'We are very hopeful this research may, in time, lead to a therapy that is both successful and carries reduced medical risks. We have proved the principle, now we have to optimise it and adapt it so it is able to be used in patients. Often that is the hardest part.'
Babies' brains are highly plastic, meaning they're constantly adapting as they learn and respond to the world and the people around them. It's now known that adult brains can change too, but are far less plastic than very young children's. The challenge is to find ways of unlocking this plasticity when it's needed, say if we've had a brain injury. According to Canadian research, video games may be one way. Daphne Maurer is director of the Visual Development Laboratory at McMaster University in Hamilton Ontario. She has found clues to when plasticity might be locked off in babies and how in some adults it actually may persist unbeknownst to them. The baby is learning 'my people talk that language, my people look like that, my people eat this kind of food'. So the early brain plasticity, the baby's brain starts with an exuberance of connections, it's choosing to reinforce those that match the cultural environment, and those that don't match get pruned away. And that's what neurobiologists call critical periods, periods during which the child must hear language, must have vision, must be exposed to foods in order for that stabilisation to the environment to occur. Instead of being born with connections that process exactly what we need to process in our lives, babies are born with this process of tuning by experience. The brain has to work really hard not to be plastic, and that has allowed us to discover ways to renew plasticity in the adult brain.
In adults with synaesthesia, stimulation of one sensory modality—let's say hearing—causes something extra, typically the perception of color. C sharp might be vermillion and D flat might be turquoise. And it can be across any of our sensory systems, so some people taste words. Some people, it's just within one sensory modality, so when they see black letters they perceive color. Some people when they think of numbers they see them in patterns. They see them in space. So someone might tell you January is here, February is there, March is behind my back.
Before the toddlers start to prune, they're synesthetic. In toddlers, C sharp might be vermillion for one synesthete but turquoise for another synesthete. But they agree that as the pitch gets higher, the colors get lighter. Is there an age where synaesthesia is lost? Probably never. There is underground synaesthesia in all of us. Adults asked to make connections between pitch and surface lightness, or between letters and colors, color associations exactly match the toddlers and the synesthetes. So the pruning is incomplete in everyone, not just in synesthetes. But in those of us without synaesthesia it's been sufficient that the synaesthesia doesn't get to the conscious perception.
A recent study reveals that dogs are much likely to steal food in the dark when humans cannot notice them, indicating they understand a human's perspective. The study, conducted by Dr. Juliane Kaminski of the University of Portsmouth's Department of Psychology, claims that when humans forbid the dog from eating the food, he is four times more likely to steal the food that he was forbidden to eat in the dark. This behavior in dogs reveals that they can change their actions based on what humans think and feel. They take into account what humans can see and what they cannot. "That's incredible because it implies dogs understand the human can't see them, meaning they might understand the human perspective," Dr. Kaminski said in a press statement. This study, funded by the Max Planck Society, is the first that describes how dogs distinguish between different levels of light when they are making strategies to steal food. According to Dr. Kaminski, humans attribute a few qualities and emotions to other living things. It is we who think that the dogs are clever or sensitive, not the dogs themselves. A series of experiments were conducted in different light conditions. In each test, the humans forbade the dog from eating the food. On conducting these tests, she noticed that the dog ate more food in the dark and that too quickly, as compared to when the room was lit. The study had 42 female and 42 male domestic dogs who were 1-year-old or more. She made sure she selected those dogs that were comfortable without their owner, even if it was a dark room. The report states that the tests were complex and involved many variables to rule out that dogs were basing their decisions on simple associative rules, for example, that dark means food. It is not known how well dogs can see in the dark, but the study shows that they can differentiate between light and dark. The researcher concludes saying, "The results of these tests suggest that dogs are deciding it's safer to steal the food when the room is dark because they understand something of the human's perspective." Further studies have to be conducted in order to discover the mechanism that controls the dog's behavior. Previous studies have indicated that dogs consider human's eyes as an important signal in deciding how to behave. For those people who are attentive toward dogs, the animal responds more willingly.
This story begins with a group of people who are expert at looking: the professional searchers known as radiologists. "If you watch radiologists do what they do, [you're] absolutely convinced that they are like superhuman," says Trafton Drew, an attention researcher at Harvard Medical School. About three years ago, Drew started visiting the dark, cavelike "reading rooms" where radiologists do their work. For hours he would stand watching them, in awe that they could so easily see in the images before them things that to Drew were simply invisible. "These tiny little nodules that I can't even see when people point to them — they're just in a different world when it comes to finding this very, very hard-to-find thing," Drew says. In the Invisible Gorilla study, subjects have to count how many times the people in white shirts pass the basketball. By focusing their attention on the ball, they tend to not notice when a guy in a gorilla suit shows up. But radiologists still sometimes fail to see important things, and Drew wanted to understand more. Because of his line of work, he was naturally familiar with one of the most famous studies in the field of attention research, the Invisible Gorilla study. In that groundbreaking study, research subjects are shown a video of two teams of kids — one team wears white; the other wears black — passing two basketballs back and forth between players as they dodge and weave around each other. Before it begins, viewers are told their responsibility is to do one thing and one thing only: count how many times the players wearing white pass the ball to each other. This task isn't easy. Because the players are constantly moving around, viewers really have to concentrate to count the throws. Then, about a half-minute into the video, a large man in a gorilla suit walks on screen, directly to the middle of the circle of kids. He stops momentarily in the center of the circle, looks straight ahead, beats his chest, and then casually strolls off the screen. The kids keep playing, and then the video ends and a series of questions appear, including: "Did you see the gorilla?" "Sounds ridiculous, right?" says Drew. "There's a gorilla on the screen — of course you're going to see it! But 50 percent of people miss the gorilla." This is because when you ask someone to perform a challenging task, without realizing it, their attention narrows and blocks out other things. So, often, they literally can't see even a huge, hairy gorilla that appears directly in front of them. That effect is called "inattentional blindness" — which brings us back to the expert lookers, the radiologists. Drew wondered if somehow being so well-trained in searching would make them immune to missing large, hairy gorillas. "You might expect that because they're experts, they would notice if something unusual was there," he says. He took a picture of a man in a gorilla suit shaking his fist, and he superimposed that image on a series of slides that radiologists typically look at when they're searching for cancer. He then asked a bunch of radiologists to review the slides of lungs for cancerous nodules. He wanted to see if they would notice a gorilla the size of a matchbook glaring angrily at them from inside the slide. But they didn't: 83 percent of the radiologists missed it, Drew says. This wasn't because the eyes of the radiologists didn't happen to fall on the large, angry gorilla. Instead, the problem was in the way their brains had framed what they were doing. They were looking for cancer nodules, not gorillas, so "they look right at it, but because they're not looking for a gorilla, they don't see that it's a gorilla." In other words, what we're thinking about — what we're focused on — filters the world around us so aggressively that it literally shapes what we see. So, Drew says, we need to think carefully about the instructions we give to professional searchers like radiologists or people looking for terrorist activity, because what we tell them to look for will in part determine what they see and don't see.
Differences in the physical connections of the brain are at the root of what make people think and behave differently from one another. Researchers reporting in the February 6 issue of the Cell Press journal Neuron shed new light on the details of this phenomenon, mapping the exact brain regions where individual differences occur. Their findings reveal that individuals' brain connectivity varies more in areas that relate to integrating information than in areas for initial perception of the world. "Understanding the normal range of individual variability in the human brain will help us identify and potentially treat regions likely to form abnormal circuitry, as manifested in neuropsychiatric disorders," says senior author Dr. Hesheng Liu, of the Massachusetts General Hospital. Dr. Liu and his colleagues used an imaging technique called resting-state functional magnetic resonance imaging to examine person-to-person variability of brain connectivity in 23 healthy individuals five times over the course of six months. The researchers discovered that the brain regions devoted to control and attention displayed a greater difference in connectivity across individuals than the regions dedicated to our senses like touch and sight. When they looked at other published studies, the investigators found that brain regions previously shown to relate to individual differences in cognition and behavior overlap with the regions identified in this study to have high variability among individuals. The researchers were therefore able to pinpoint the areas of the brain where variable connectivity causes people to think and behave differently from one another. Higher rates of variability across individuals were also displayed in regions of the brain that have undergone greater expansion during evolution. "Our findings have potential implications for understanding brain evolution and development," says Dr. Liu. "This study provides a possible linkage between the diversity of human abilities and evolutionary expansion of specific brain regions," he adds.
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