Glia cells also regulate learning and memory, new Tel Aviv University research finds     

Glia cells, named for the Greek word for "glue," hold the brain's neurons together and protect the cells that determine our thoughts and behaviors, but scientists have long puzzled over their prominence in the activities of the brain dedicated to learning and memory. Now Tel Aviv University researchers say that glia cells are central to the brain's plasticity — how the brain adapts, learns, and stores information. According to Ph.D. student Maurizio De Pittà of TAU's Schools of Physics and Astronomy and Electrical Engineering, glia cells do much more than hold the brain together. A mechanism within the glia cells also sorts information for learning purposes, De Pittà says. "Glia cells are like the brain's supervisors. By regulating the synapses, they control the transfer of information between neurons, affecting how the brain processes information and learns."

De Pittà's research, led by his TAU supervisor Prof. Eshel Ben-Jacob, along with Vladislav Volman of The Salk Institute and the University of California at San Diego and Hugues Berry of the Université de Lyon in France, has developed the first computer model that incorporates the influence of glia cells on synaptic information transfer. Detailed in the journal PLoS Computational Biology, the model can also be implemented in technologies based on brain networks such as microchips and computer software, Prof. Ben-Jacob says, and aid in research on brain disorders such as Alzheimer's disease and epilepsy.

Regulating the brain's "social network"

The brain is constituted of two main types of cells: neurons and glia. Neurons fire off signals that dictate how we think and behave, using synapses to pass along the message from one neuron to another, explains De Pittà. Scientists theorize that memory and learning are dictated by synaptic activity because they are "plastic," with the ability to adapt to different stimuli. But Ben-Jacob and colleagues suspected that glia cells were even more central to how the brain works. Glia cells are abundant in the brain's hippocampus and the cortex, the two parts of the brain that have the most control over the brain's ability to process information, learn and memorize. In fact, for every neuron cell, there are two to five glia cells. Taking into account previous experimental data, the researchers were able to build a model that could resolve the puzzle.

The brain is like a social network, says Prof. Ben-Jacob. Messages may originate with the neurons, which use the synapses as their delivery system, but the glia serve as an overall moderator, regulating which messages are sent on and when. These cells can either prompt the transfer of information, or slow activity if the synapses are becoming overactive. This makes the glia cells the guardians of our learning and memory processes, he notes, orchestrating the transmission of information for optimal brain function.

New brain-inspired technologies and therapies

The team's findings could have important implications for a number of brain disorders. Almost all neurodegenerative diseases are glia-related pathologies, Prof. Ben-Jacob notes. In epileptic seizures, for example, the neurons' activity at one brain location propagates and overtakes the normal activity at other locations. This can happen when the glia cells fail to properly regulate synaptic transmission. Alternatively, when brain activity is low, glia cells boost transmissions of information, keeping the connections between neurons "alive."

The model provides a "new view" of how the brain functions. While the study was in press, two experimental works appeared that supported the model's predictions. "A growing number of scientists are starting to recognize the fact that you need the glia to perform tasks that neurons alone can't accomplish in an efficient way," says De Pittà. The model will provide a new tool to begin revising the theories of computational neuroscience and lead to more realistic brain-inspired algorithms and microchips, which are designed to mimic neuronal networks.

When children have been exposed to family violence, their brains become increasingly "tuned" for processing possible sources of threat, a new study reports. The findings, reported in the December 6th issue of Current Biology, a Cell Press publication, reveal the same pattern of brain activity in these children as seen previously in soldiers exposed to combat. The study is the first to apply functional brain imaging to explore the impact of physical abuse or domestic violence on the emotional development of children, according to the researchers.

"Enhanced reactivity to a biologically salient threat cue such as anger may represent an adaptive response for these children in the short term, helping keep them out of danger," said Eamon McCrory of University College London. "However, it may also constitute an underlying neurobiological risk factor increasing their vulnerability to later mental health problems, and particularly anxiety." Maltreatment is known to be one of the most potent environmental risk factors associated with anxiety and depression. Still, McCrory said, "relatively little is known how such adversity 'gets under the skin' and increases a child's later vulnerability, even into adulthood."

The new study shows that children with documented exposure to violence in the home differ in their brain response to angry versus sad faces. When presented with angry faces, children with a history of abuse show heightened activity in the brain's anterior insula and amygdala, regions involved in detecting threat and anticipating pain. McCrory says the changes don't reflect damage to the brain. Rather, the patterns represent the brain's way of adapting to a challenging or dangerous environment. Still, those shifts may come at the cost of increased vulnerability to later stress.

Although the results may not have immediate practical implications, they are nonetheless critical given that a significant minority of children are exposed to family violence, McCrory says. "This underlines the importance of taking seriously the impact for a child of living in a family characterized by violence. Even if such a child is not showing overt signs of anxiety or depression, these experiences still appear to have a measurable effect at the neural level."

Human minds have hit an evolutionary "sweet spot" and - unlike computers - cannot continually get smarter without trade-offs elsewhere, according to research by the University of Warwick. Researchers asked the question why we are not more intelligent than we are given the adaptive evolutionary process. Their conclusions show that you can have too much of a good thing when it comes to mental performance. The evidence suggests that for every gain in cognitive functions, for example better memory, increased attention or improved intelligence, there is a price to pay elsewhere - meaning a highly-evolved "supermind" is the stuff of science fiction.

University of Warwick psychology researcher Thomas Hills and Ralph Hertwig of the University of Basel looked at a range of studies, including research into the use of drugs like Ritalan which help with attention, studies of people with autism as well as a study of the Ashkenazi Jewish population. For instance, among individuals with enhanced cognitive abilities- such as savants, people with photographic memories, and even genetically segregated populations of individuals with above average IQ, these individuals often suffer from related disorders, such as autism, debilitating synaesthesia and neural disorders linked with enhanced brain growth.

Similarly, drugs like Ritalan only help people with lower attention spans whereas people who don't have trouble focusing can actually perform worse when they take attention-enhancing drugs. Dr Hills said: "These kinds of studies suggest there is an upper limit to how much people can or should improve their mental functions like attention, memory or intelligence. Take a complex task like driving, where the mind needs to be dynamically focused, attending to the right things such as the road ahead and other road users – which are changing all the time. If you enhance your ability to focus too much, and end up over-focusing on specific details, like the driver trying to hide in your blind spot, then you may fail to see another driver suddenly veering into your lane from the other direction. Or if you drink coffee to make yourself more alert, the trade-off is that it is likely to increase your anxiety levels and lose your fine motor control. There are always trade-offs. In other words, there is a 'sweet spot' in terms of enhancing our mental abilities – if you go beyond that spot - just like in the fairy-tales - you have to pay the price."

Amphetamine use in adolescence can cause neurobiological imbalances and increase risk-taking behavior, and these effects can persist into adulthood, even when subjects are drug free. These are the conclusions of a new study using animal models conducted by McGill University Health Centre (MUHC) researcher Dr. Gabriella Gobbi and her colleagues. The study, published in The International Journal of Neuropsychopharmacology, is one of the first to shed light on how long-term amphetamine use in adolescence affects brain chemistry and behavior. "We looked at the effects of long-term amphetamine use on important neurotransmitters and on risk-taking behavior in adolescent rats," says Dr. Gobbi, a researcher in Mental Illness and Addiction from the Research Institute of the MUHC and associate professor at the Faculty of Medicine at McGill University. "The brain chemistry of these rodents is very similar to that of humans, so this model provided us with very useful insights into amphetamine use in a human population."

Amphetamine is a psychostimulant drug which produces increased wakefulness and focus, in association with decreased fatigue and appetite. This drug, commonly known as "speed", is also used recreationally and as a performance enhancer. According to the United Nations Office on Drugs and Crime (UNODOC) report (2011), more than 10 per cent of adolescents in the U.S. have used amphetamines. In Europe, between two and seven per cent of adolescents have tried amphetamines, and in Canada the number is estimated at just over five per cent.

Study subjects were given one of three dosing regimens of amphetamine during adolescence. When they reached adulthood, drugs were withdrawn and their neurophysiological activity and risk-taking behavior were studied. "We focused on the key neurotransmitters serotonin, dopamine and norepinephrine," Dr. Gobbi explains. "We found abnormalities in brain activity associated with all three of these neurochemicals, called "monoamines". Imbalances of monoamines are associated with emotional disturbances and mental diseases such as depression or addiction." Researchers also noted behavioral changes in all dosing groups. Hyperactivity was observed in rodents exposed to a moderate dose of amphetamine during adolescence, while risk-taking behavior increased in every dosage group. "Obviously we have to be very cautious about applying these results to a human population," says Dr. Gobbi. "However, given the basic similarities between human and rodent brains, these results are cause for concern. They suggest that the effects of amphetamine use can persist into adulthood, even if the subject is no longer taking drugs, and that these effects include a tendency toward risk-taking behavior."

A cognitive map enables orientation

The cerebellum is far more intensively involved in helping us navigate than previously thought. To move and learn effectively in spatial environments our brain, and particularly our hippocampus, creates a "cognitive" map of the environment. The cerebellum contributes to the creation of this map through altering the chemical communication between its neurones. If this ability is inactivated, the brain is no longer able to to create an effective spatial representation and thus navigation in an environment becomes impaired. The details of these observations were recently published in Science by the Ruhr University neuroscientist, Marion André who is a student of the International Graduate School of Neuroscience( IGSN), along with her colleagues in France.

A cognitive map in the hippocampus
In order to navigate efficiently in an environment, we need to create and maintain a reliable internal representation of the external world. A key region enabling such representation is the hippocampus which contains specialized pyramidal neurons named place cells. Each place cell is activated at specific location of the environment and gives dynamic information about self-location relative to the external world. These neurons thus generate a cognitive map in the hippocampal system through the integration of multi sensory inputs combining external information (such as visual, auditory, olfactory and tactile cues) and inputs generated by self-motion (i.e. optic flow, proprioceptive and vestibular information).

Decisive: synaptic plasticity
Our ability to navigate also relies on the potential to use this cognitive map to form an optimal trajectory toward a goal. The cerebellum, a foliate region based at the back of the brain, has been recently shown to participate in the formation of the optimal trajectory. This structure contains neurons that are able to increase or decrease their chemical communication, a mechanism called synaptic plasticity. A decrease in the synaptic transmission of the cerebellar neurons, named long-term depression (LTD) participates in the optimization of the path toward a goal.

No orientation without LTD
Using transgenic mice that had a mutation impairing exclusively LTD of the cerebellar neurons, the neuroscientists were able to show that the cerebellum participates also in the formation of the hippocampal cognitive map. Indeed mice lacking this form of cerebellar plasticity were unable to build a reliable cognitive representation of the environment when they had to use self-motion information. Consequently, they were unable to navigate efficiently towards a goal in the absence of external information (for instance in the dark). This work highlights for the first time an unsuspected function of the cerebellum in shaping the representation of our body in space.

Distinct neural pathways are important for different aspects of language processing, researchers have discovered, studying patients with language impairments caused by neurodegenerative diseases

While it has long been recognized that certain areas in the brain's left hemisphere enable us to understand and produce language, scientists are still figuring out exactly how those areas divvy up the highly complex processes necessary to comprehend and produce language. Advances in brain imaging made within the last 10 years have revealed that highly complex cognitive tasks such as language processing rely not only on particular regions of the cerebral cortex, but also on the white matter fiber pathways that connect them. "With this new technology, scientists started to realize that in the language network, there are a lot more connecting pathways than we originally thought," said Stephen Wilson, who recently joined the University of Arizona's department of speech, language and hearing sciences as an assistant professor. "They are likely to have different functions because the brain is not just a homogeneous conglomerate of cells, but there hasn't been a lot of evidence as to what kind of information is carried on the different pathways."

Working in collaboration with his colleagues at the UA, the department of neurology at the University of California, San Francisco and the Scientific Institute and University Hospital San Raffaele in Milan, Italy, Wilson discovered that not only are the connecting pathways important for language processing, but they specialize in different tasks. Two brain areas called Broca's region and Wernicke's region serve as the main computing hubs underlying language processing, with dense bundles of nerve fibers linking the two, much like fiber optic cables connecting computer servers. But while it was known that Broca's and Wernicke's region are connected by upper and a lower white matter pathways, most research had focused on the nerve cells clustered inside the two language-processing regions themselves.

Working with patients suffering from language impairments because of a variety of neurodegenerative diseases, Wilsons' team used brain imaging and language tests to disentangle the roles played by the two pathways. Their findings are published in a recent issue of the scientific journal Neuron. "If you have damage to the lower pathway, you have damage to the lexicon and semantics," Wilson said. "You forget the name of things, you forget the meaning of words. But surprisingly, you're extremely good at constructing sentences. With damage to the upper pathway, the opposite is true; patients name things quite well, they know the words, they can understand them, they can remember them, but when it comes to figuring out the meaning of a complex sentence, they are going to fail."

The study marks the first time it has been shown that upper and lower tracts play distinct functional roles in language processing, the authors write. Only the upper pathway plays a critical role in syntactic processing.

Wilson collected the data while he was a postdoctoral fellow working with patients with neurodegenerative diseases of varying severity, recruited through the Memory and Aging Center at UCSF. The study included 15 men and 12 women around the age of 66. Unlike many other studies investigating acquired language disorders, which are called aphasias and usually caused by damage to the brain, Wilson's team had a unique opportunity to study patients with very specific and variable degrees of brain damage. "Most aphasias are caused by strokes, and most of the strokes that affect language regions probably would affect both pathways," Wilson said. "In contrast, the patients with progressive aphasias who we worked with had very rare and very specific neurodegenerative diseases that selectively target different brain regions, allowing us to tease apart the contributions of the two pathways."

To find out which of the two nerve fiber bundles does what in language processing, the team combined magnetic resonance brain imaging technology to visualize damaged areas and language assessment tasks testing the participants' ability to comprehend and produce sentences. "We would give the study participants a brief scenario and ask them to complete it with what comes naturally," Wilson said. "For example, if I said to you, 'A man was walking along the railway tracks. He didn't hear the train coming. What happened to the man?' Usually, you would say, 'He was hit by the train,' or something along those lines. But a patient with damage to the upper pathway might say something like 'train, man, hit.' We found that the lower pathway has a completely different function, which is in the meaning of single words."

To test for comprehension of the meaning of a sentence, the researchers presented the patient with a sentence like, "The girl who is pushing the boy is green," and then ask which of the two pictures depicted that scenario accurately. "One picture would show a green girl pushing a boy, and the other would show a girl pushing a green boy," Wilson said. "The colors will be the same, the agents will be the same, and the action is the same. The only difference is, which actor does the color apply to? Those who have only lower pathway damage do really well on this, which shows that damage to that pathway doesn't interfere with your ability to use the little function words or the functional endings on words to figure out the relationships between the words in a sentence."

Wilson said that most previous studies linking neurodegeneration of specific regions with cognitive deficits have focused on damage to gray matter, rather than the white matter that connects regions to one another. "Our study shows that the deficits in the ability to process sentences are above and beyond anything that could be explained by gray matter loss alone," Wilson added. "It is the first study to show that damage to one major pathway more than then other major pathway is associated with a specific deficit in one aspect of language."

Research provides new insight into why some individuals may be more aggressive than others

Fluctuations of serotonin levels in the brain, which often occur when someone hasn't eaten or is stressed, affects brain regions that enable people to regulate anger, new research from the University of Cambridge has shown. Although reduced serotonin levels have previously been implicated in aggression, this is the first study which has shown how this chemical helps regulate behavior in the brain as well as why some individuals may be more prone to aggression. The research findings were published 15 September in the journal Biological Psychiatry.

For the study, healthy volunteers' serotonin levels were altered by manipulating their diet. On the serotonin depletion day, they were given a mixture of amino acids that lacked tryptophan, the building block for serotonin. On the placebo day, they were given the same mixture but with a normal amount of tryptophan. The researchers then scanned the volunteers' brains using functional magnetic resonance imaging (fMRI) as they viewed faces with angry, sad, and neutral expressions. Using the fMRI, they were able to measure how different brain regions reacted and communicated with one another when the volunteers viewed angry faces, as opposed to sad or neutral faces.

The research revealed that low brain serotonin made communications between specific brain regions of the emotional limbic system of the brain (a structure called the amygdala) and the frontal lobes weaker compared to those present under normal levels of serotonin. The findings suggest that when serotonin levels are low, it may be more difficult for the prefrontal cortex to control emotional responses to anger that are generated within the amygdala.

Using a personality questionnaire, they also determined which individuals have a natural tendency to behave aggressively. In these individuals, the communications between the amygdala and the prefrontal cortex was even weaker following serotonin depletion. 'Weak' communications means that it is more difficult for the prefrontal cortex to control the feelings of anger that are generated within the amygdala when the levels of serotonin are low. As a result, those individuals who might be predisposed to aggression were the most sensitive to changes in serotonin depletion.

Dr Molly Crockett, co-first author who worked on the research while a PhD student at Cambridge's Behavioural and Clinical Neuroscience Institute (and currently based at the University of Zurich) said: "We've known for decades that serotonin plays a key role in aggression, but it's only very recently that we've had the technology to look into the brain and examine just how serotonin helps us regulate our emotional impulses. By combining a long tradition in behavioral research with new technology, we were finally able to uncover a mechanism for how serotonin might influence aggression."

Dr Luca Passamonti, co-first author who worked on the research while a visiting scientist at the Cognition and Brain Sciences Unit of the Medical Research Council in Cambridge (and currently based at the Consiglio Nazionale delle Ricerche (CNR), Unità di Ricerca Neuroimmagini, Catanzaro), said: "Although these results came from healthy volunteers, they are also relevant for a broad range of psychiatric disorders in which violence is a common problem. For example, these results may help to explain the brain mechanisms of a psychiatric disorder known as intermittent explosive disorder (IED). Individuals with IED typically show intense, extreme and uncontrollable outbursts of violence which may be triggered by cues of provocation such as a facial expression of anger. "We are hopeful that our research will lead to improved diagnostics as well as better treatments for this and other conditions."

In a study performed on rats, the researchers found that marijuana does not erase the traumatic experience, but only the development of post-trauma symptoms

Cannabinoids (marijuana) administration after experiencing a traumatic event blocks the development of post-traumatic stress disorder (PTSD)-like symptoms in rats, according to a new study conducted at the University of Haifa and published in the journal Neuropsychopharmacology. "We found that there is a 'window of opportunity' during which administering synthetic marijuana helps deal with symptoms simulating PTSD in rats," said Dr. Irit Akirav of the University of Haifa's Department of Psychology, who led the study.

In the study, which Dr. Akirav conducted with research student Eti Ganon-Elazar, the researchers set out to examine how administering cannabinoids (synthetic marijuana) affects the development of PTSD-like symptoms in rats, whose physiological reactions to traumatic and stressful events is similar to human reactions.

In the first part of the study, the researchers exposed a group of rats to extreme stress, and observed that the rats did indeed display symptoms resembling PTSD in humans, such as an enhanced startle reflex, impaired extinction learning, and disruption of the negative feedback cycle of the stress-influenced HPA axis. The rats were then divided into four groups. One was given no marijuana at all; the second was given a marijuana injection two hours after being exposed to a traumatic event; the third group after 24 hours and the fourth group after 48 hours.

A week later, the researchers examined the rats and found that the group that had not been administered marijuana and the group that got the injection 48 hours after experiencing trauma continued to display PTSD symptoms as well as a high level of anxiety. By contrast, the PTSD symptoms disappeared in the rats that were given marijuana 2 or 24 hours after experiencing trauma, even though these rats had also developed a high level of anxiety. "This indicates that the marijuana did not erase the experience of the trauma, but that it specifically prevented the development of post-trauma symptoms in the rat model," said Dr. Akirav, who added that the results suggest there is a particular window of time during which administering marijuana is effective. Because the human life span is significantly longer than that of rats, Dr. Akirav explained, one could assume that this window of time would be longer for humans.

The second stage of the study sought to understand the brain mechanism that is put into operation during the administering of marijuana. To do this, they repeated stage one of the experiment, but after the trauma they injected the synthetic marijuana directly into the amygdala area of the brain, the area known to be responsible for response to trauma. The researchers found that the marijuana blocked development of PTSD symptoms in these cases as well. From this the researchers were able to conclude that the effect of the marijuana is mediated by a CB1 receptor in the amygdala.

Some people feel compelled to pet every furry animal they see on the street, while others jump at the mere sight of a shark or snake on the television screen. No matter what your response is to animals, it may be thanks to a specific part of your brain that is hardwired to rapidly detect creatures of the nonhuman kind. In fact, researchers from the California Institute of Technology (Caltech) and UCLA report that neurons throughout the amygdala—a center in the brain known for processing emotional reactions—respond preferentially to images of animals. Their findings were described in a study published online in the journal Nature Neuroscience.

The collaborative research team was responsible for recruiting 41 epilepsy patients at the Ronald Reagan UCLA Medical Center; these patients were already being monitored for brain activity related to seizures. Using electrodes already in place, the team recorded single-neuron responses in the amygdala as study participants viewed images of people, animals, landmarks, or objects. The amygdalae are two almond-shaped clusters of neurons—cells that are core components of the nervous system—located deep in the medial temporal lobe of the brain.  

"Our study shows that neurons in the human amygdala respond preferentially to pictures of animals, meaning that we saw the most amount of activity in cells when the patients looked at cats or snakes versus buildings or people," says Florian Mormann, lead author on the paper and a former postdoctoral scholar in the Division of Biology at Caltech. "This preference extends to cute as well as ugly or dangerous animals and appears to be independent of the emotional contents of the pictures. Remarkably, we find this response behavior only in the right and not in the left amygdala."

Mormann says this striking hemispheric asymmetry helps strengthen previous findings supporting the idea that, early on in vertebrate evolution, the right hemisphere became specialized in dealing with unexpected and biologically relevant stimuli, or with changes in the environment. "In terms of brain evolution, the amygdala is a very old structure, and throughout our biological history, animals—which could represent either predators or prey—were a highly relevant class of stimuli," he says.

"This is a pretty novel finding, since most amygdala research in the past was usually about faces of people and emotions related to fear rather than pictures of animals," adds Ralph Adolphs, a coauthor on the paper and Bren Professor of Psychology and Neuroscience and Professor of Biology at Caltech. "Nobody would have guessed that cells in the amygdala respond more to animals than they do to human faces, and in particular that they respond to all kinds of animals, not just dangerous ones. I think this will stimulate more research and has the potential to help us better understand phobias of animals."

The study is also a clear illustration of how scientists doing basic research can benefit from working with collaborators in a clinical setting and vice versa. “This is a good example of how special situations in neurosurgery—in this case, patients who are treated in order to cure their epilepsy—can provide a unique window into the workings of the human mind,” says Itzhak Fried, a UCLA neurosurgeon and a coauthor of the study.

"A category-specific response to animals in the right human amygdala" was featured online on August 28 as an advance online publication of Nature Neuroscience. The Caltech team was led by Christof Koch, Troendle Professor of Cognitive and Behavioral Biology, and included Julien Dubois, Simon Kornblith, Milica Milosavljevic, Moran Cerf, Naotsugu Tsuchiya, and Alexander Kraskov. Rodrigo Quian Quiroga and Matias Ison from the University of Leicester also contributed to the study.

For a hormone, oxytocin is pretty famous. It's the "cuddle chemical"—the hormone that helps mothers bond with their babies. Salespeople can buy oxytocin spray on the internet, to make their clients trust them. It's known for promoting positive feelings, but more recent research has found that oxytocin can promote negative emotions, too. The authors of a new review article in Current Directions in Psychological Science, a journal of the Association for Psychological Science, takes a look at what oxytocin is really doing.

Oxytocin's positive effects are well known. Experiments have found that, in games in which you can choose to cooperate or not, people who are given more oxytocin trust their fellow players more. Clinical trials have found that oxytocin can help people with autism, who have trouble in social situations. Studies have also found that oxytocin can increase altruism, generosity, and other behaviors that are good for social life.

But the warm fuzzy side of oxytocin isn't the whole story. "Quite a number of studies have shown it's actually not that simple," says Andrew Kemp of the University of Sydney, who cowrote the paper with his colleague Adam Guastella. Recent studies have found that people who were given oxytocin, then played a game of chance with a fake opponent, had more envy and gloating. These are also both social emotions, but they're negative. "It kind of rocked the research world a little bit," Kemp says. That led some researchers to think that oxytocin promotes social emotions in general, both negative and positive.

But Kemp and Guastella think oxytocin's role is slightly different. Rather than supporting all social emotions, they think it plays a role in promoting what psychologists call approach-related emotions. These are emotions that have to do with wanting something, as opposed to shrinking away. "If you look at the Oxford English Dictionary for envy, it says that the definition of envy is to wish oneself on a level with another, in happiness or with the possession of something desirable," Kemp says. "It's an approach-related emotion: I want what you have." Gloating is also about approach, he says; people who are gloating are happy—a positive, approach-related emotion—about having more than their opponent and about that person's misfortune.

If Kemp and Guastella are right, that could mean that oxytocin could also increase anger and other negative approach-related emotions. That could have important implications for people who are studying how to use oxytocin as a psychiatric treatment. "If you were to take a convicted criminal with a tendency towards aggression and give him oxytocin to make him more social, and if that were to enhance anger as opposed to suppressing anger, then that has very substantial implications," Kemp says.

Further research will show more about what emotions are promoted by oxytocin, Kemp says. "This research is really important because we don't want to go ahead and attempt to treat a range and variety of psychiatric disorders with oxytocin without fully understanding the impact this may have on emotion and mood."

New study sheds light on OBEs in healthy and psychologically normal individuals

Although out-of-body experiences (OBEs) are typically associated with migraine, epilepsy and psychopathology, they are quite common in healthy and psychologically normal individuals as well. However, they are poorly understood. A new study, published in the July 2011 issue of Elsevier's Cortex, has linked these experiences to neural instabilities in the brain's temporal lobes and to errors in the body's sense of itself – even in non clinical populations.

Dr Jason Braithwaite from the Behavioural Brain Sciences Centre, School of Psychology, University of Birmingham, has been investigating the underlying factors associated with the propensity for normal healthy individuals to have an OBE. As well as informing the scientific theories for how such hallucinations can occur, studying these unusual phenomena can also help us to understand how normal "in-the-body" mental processes work and why, when they break down, they produce such striking experiences.

Dr Braithwaite tested a group of individuals, including some "OBEers", for their predisposition to unusual perceptual experiences, and found that the OBEers reported significantly more of a particular type of experience: those known to be associated with neuroelectrical anomalies in the temporal lobes of the brain, as well as those associated with distortions in the processing of body-based information. The OBEers were also less skilled at a task which required them to adopt the perspective of a figure shown on the computer screen. These findings suggest that, even in healthy people, striking hallucinations can and do occur and that these may reflect anomalies in neuroelectrical activity of the temporal lobes, as well as biases in "body representation" in the brain.

New research in the FASEB Journal suggests that activation of nicotinic receptors within the prefrontal region of the mouse brain helps establish appropriate ranking between competing motivations

If you think nicotine receptors are only important to smokers trying to kick the tobacco habit, think again. New research published in the FASEB Journal (http://www.fasebj.org) suggests that these receptors also play an important role in social interaction and the ability to choose between competing motivations. Specifically, scientists from France show that the nicotinic receptors in the prefrontal cortex are essential for social interaction in mice and that this area of the brain is necessary for adapted and balanced social interactions to occur. This new knowledge could one day lead to novel treatments for ADHD, schizophrenia, and depression, among other illnesses.

"One of the main aims would be to understand and help people to make good decisions for themselves (and for others) and to maintain, during old age, such abilities in the social domain as well as in other aspects of our lives," said Sylvie Granon, a researcher involved in the work from the Université Paris Sud XI and CNRS UMR 8620, Centre de Neurosciences Paris-Sud, Orsay, France.

To make this discovery, Granon and colleagues introduced mice into an open space and tested their will to interact with other mice of the same sex or to explore a novel place. The respective times spent for either social contact or novelty exploration were measured and quantitatively evaluated. Researchers then removed the prefrontal cortex in otherwise normal mice, which resulted in mice with significant social deficits. Those genetically modified to lack the nicotinic receptor gene for a widespread subunit called beta2 subtype, seemed to favor social contact rather than the investigation of a novel environment. When the beta2 nicotinic receptor in the brain was re-expressed, a normal balance between social contact and novelty seeking was restored.

"This research can be summed up by saying that it's the real-life equivalent of Chatty Cathy marrying the Marlboro Man," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. "Who could have guessed that there may be a biological explanation for 'social butterflies.' The explanation was found in an area of the brain that for decades has been considered a locus for nicotine addiction."

Study highlights the importance of cognitive skills in exercising control over addictive drugs

A study, completed by researchers from Trinity College and the Research Institute for a Tobacco Free Society, Dublin, Ireland, compares former smokers to current smokers, and obtains insight into how to quit smoking might be discovered by studying the brains of those who have successfully managed to do so.

Functional MRI images were obtained while current smokers, former smokers and never smokers performed tasks designed to assess specific cognitive skills that were reasoned to be important for smoking abstinence. These included a response inhibition task to assess impulse control and the ability to monitor one's behavior and an attention task which assessed the ability to avoid distraction from smoking-related images, which tend to elicit an automatic attention response in smokers.

The investigators found that when doing these tasks, the current smokers compared to the never-smokers showed reduced functioning in prefrontal regions that are related to controlling behavior. In addition, the current smokers showed elevated activity in sub-cortical regions such as the nucleus accumbens that respond to the reward value or salience of the nicotine stimuli. However, in marked contrast, the former smokers did not show this sub-cortical activity, but instead showed increased activity in the frontal lobes – the areas that are critically involved in controlling behavior. Moreover, the former smokers were "super-normal", showing greater levels of activity in these prefrontal regions than the never-smokers.

The implication is that the brain regions responsible for what might be considered "willpower" show more activity in those who have quit smoking. This type of willpower can be measured, can be related to specific brain regions, and would appear to be related to being able to quit cigarettes. These results reinforce the value of smoking cessation therapies that stress the importance of, or that help to train, the cognitive skills involved in exercising control over drug desires.

An individual's personality can have a big effect on their life. Some people are outgoing and gregarious while others find novel situations stressful which can be detrimental to their health and well-being. Increasingly, scientists are discovering that animals are no different.

A new study led by Dr Kathryn Arnold, of the Environment Department at the University of York has added important experimental evidence showing that animal personalities are reflected in their oxidative stress profiles. The research is published in the Journal of Experimental Biology.

Dr Arnold teamed up with graduate student Katherine Herborn, at the Institute of Biodiversity, Animal Health and Comparative Medicine at the University of Glasgow, to classify the personalities of 22 greenfinches. They tested each bird's reactions to a novel situation by adding a brightly coloured cookie-cutter to each greenfinch's food bowl, and timing how long it took for the birds to pluck up courage to approach the food. The researchers found that the boldest birds took only a few seconds to overcome their fear while more timid birds took up to 30 minutes to approach their meal.

Dr Arnold and Katherine Herborn also measured the greenfinches' motivation to explore by attaching an intriguing object to the birds' perches and timing how long it took them to land next to it. However, there was no correlation between the birds' courage and curiosity.

The researchers then measured the birds' damaging reactive oxygen metabolite levels and their defenses against them. Comparing the bird's blood oxidative profiles with their personalities, the team found that the most timid birds had the highest levels of damaging oxygen toxins and the weakest defenses, so they suffered more oxidative stress than braver individuals. Also, the scientists found that the most curious birds (those that approached objects fastest) had better defenses against oxidative damage than less curious greenfinches.

Dr Arnold wants to extend the work to establish how personality traits affects birds in the wild. She says, "Neophobic birds – those that are afraid of new things -- may suffer high costs of oxidative stress and die early because they paid these physiological costs, but they might also be less likely to be eaten by a predator because they are more wary than bolder birds ."

Abstract: High-fructose corn syrup (HFCS) accounts for as much as 40% of caloric sweeteners used in the United States. Some studies have shown that short-term access to HFCS can cause increased body weight, but the findings are mixed. The current study examined both short- and long-term effects of HFCS on body weight, body fat, and circulating triglycerides. In Experiment 1, male Sprague–Dawley rats were maintained for short term (8 weeks) on (1) 12 h/day of 8% HFCS, (2) 12 h/day 10% sucrose, (3) 24 h/day HFCS, all with ad libitum rodent chow, or (4) ad libitum chow alone. Rats with 12-h access to HFCS gained significantly more body weight than animals given equal access to 10% sucrose, even though they consumed the same number of total calories, but fewer calories from HFCS than sucrose. In Experiment 2, the long-term effects of HFCS on body weight and obesogenic parameters, as well as gender differences, were explored. Over the course of 6 or 7 months, both male and female rats with access to HFCS gained significantly more body weight than control groups. This increase in body weight with HFCS was accompanied by an increase in adipose fat, notably in the abdominal region, and elevated circulating triglyceride levels. Translated to humans, these results suggest that excessive consumption of HFCS may contribute to the incidence of obesity.

Bocarsly ME, et al. (2010). High-fructose corn syrup causes characteristics of obesity in rats: Increased body weight, body fat and triglyceride levels. Pharmacol Biochem Behav, doi:10.1016/j.pbb.2010.02.012

Neurons are complicated, but the basic functional concept is that synapses transmit electrical signals to the dendrites and cell body (input), and axons carry signals away (output). In one of many surprise findings, Northwestern University scientists have discovered that axons can operate in reverse: they can send signals to the cell body, too.

It also turns out axons can talk to each other. Before sending signals in reverse, axons can perform their own neural computations without any involvement from the cell body or dendrites. This is contrary to typical neuronal communication where an axon of one neuron is in contact with another neuron's dendrite or cell body, not its axon. And, unlike the computations performed in dendrites, the computations occurring in axons are thousands of times slower, potentially creating a means for neurons to compute fast things in dendrites and slow things in axons.

A deeper understanding of how a normal neuron works is critical to scientists who study neurological diseases, such as epilepsy, autism, Alzheimer's disease and schizophrenia.

The findings are published in the February issue of the journal Nature Neuroscience.

"We have discovered a number of things fundamental to how neurons work that are contrary to the information you find in neuroscience textbooks," said Nelson Spruston, senior author of the paper and professor of neurobiology and physiology in the Weinberg College of Arts and Sciences. "Signals can travel from the end of the axon toward the cell body, when it typically is the other way around. We were amazed to see this."

He and his colleagues first discovered individual nerve cells can fire off signals even in the absence of electrical stimulations in the cell body or dendrites. It's not always stimulus in, immediate action potential out. (Action potentials are the fundamental electrical signaling elements used by neurons; they are very brief changes in the membrane voltage of the neuron.)

Similar to our working memory when we memorize a telephone number for later use, the nerve cell can store and integrate stimuli over a long period of time, from tens of seconds to minutes. (That's a very long time for neurons.) Then, when the neuron reaches a threshold, it fires off a long series of signals, or action potentials, even in the absence of stimuli. The researchers call this persistent firing, and it all seems to be happening in the axon.

Spruston and his team stimulated a neuron for one to two minutes, providing a stimulus every 10 seconds. The neuron fired during this time but, when the stimulation was stopped, the neuron continued to fire for a minute.

"It's very unusual to think that a neuron could fire continually without stimuli," Spruston said. "This is something new -- that a neuron can integrate information over a long time period, longer than the typical operational speed of neurons, which is milliseconds to a second."

This unique neuronal function might be relevant to normal process, such as memory, but it also could be relevant to disease. The persistent firing of these inhibitory neurons might counteract hyperactive states in the brain, such as preventing the runaway excitation that happens during epileptic seizures.

Spruston credits the discovery of the persistent firing in normal individual neurons to the astute observation of Mark Sheffield, a graduate student in his lab. Sheffield is first author of the paper.

The researchers think that others have seen this persistent firing behavior in neurons but dismissed it as something wrong with the signal recording. When Sheffield saw the firing in the neurons he was studying, he waited until it stopped. Then he stimulated the neuron over a period of time, stopped the stimulation and then watched as the neuron fired later.

"This cellular memory is a novelty," Spruston said. "The neuron is responding to the history of what happened to it in the minute or so before."

Spruston and Sheffield found that the cellular memory is stored in the axon and the action potential is generated farther down the axon than they would have expected. Instead of being near the cell body it occurs toward the end of the axon.

Their studies of individual neurons (from the hippocampus and neocortex of mice) led to experiments with multiple neurons, which resulted in perhaps the biggest surprise of all. The researchers found that one axon can talk to another. They stimulated one neuron, and detected the persistent firing in the other unstimulated neuron. No dendrites or cell bodies were involved in this communication.

"The axons are talking to each other, but it's a complete mystery as to how it works," Spruston said. "The next big question is: how widespread is this behavior? Is this an oddity or does in happen in lots of neurons? We don't think it's rare, so it's important for us to understand under what conditions it occurs and how this happens."

Mass. General-led study shows changes over time in areas associated with awareness, empathy, stress

Participating in an 8-week mindfulness meditation program appears to make measurable changes in brain regions associated with memory, sense of self, empathy and stress. In a study that will appear in the January 30 issue of Psychiatry Research: Neuroimaging, a team led by Massachusetts General Hospital (MGH) researchers report the results of their study, the first to document meditation-produced changes over time in the brain's grey matter.

"Although the practice of meditation is associated with a sense of peacefulness and physical relaxation, practitioners have long claimed that meditation also provides cognitive and psychological benefits that persist throughout the day," says Sara Lazar, PhD, of the MGH Psychiatric Neuroimaging Research Program, the study's senior author. "This study demonstrates that changes in brain structure may underlie some of these reported improvements and that people are not just feeling better because they are spending time relaxing."

Previous studies from Lazar's group and others found structural differences between the brains of experienced mediation practitioners and individuals with no history of meditation, observing thickening of the cerebral cortex in areas associated with attention and emotional integration. But those investigations could not document that those differences were actually produced by meditation.

For the current study, MR images were take of the brain structure of 16 study participants two weeks before and after they took part in the 8-week Mindfulness-Based Stress Reduction (MBSR) Program at the University of Massachusetts Center for Mindfulness. In addition to weekly meetings that included practice of mindfulness meditation – which focuses on nonjudgmental awareness of sensations, feelings and state of mind – participants received audio recordings for guided meditation practice and were asked to keep track of how much time they practiced each day. A set of MR brain images were also taken of a control group of non-meditators over a similar time interval.

Meditation group participants reported spending an average of 27 minutes each day practicing mindfulness exercises, and their responses to a mindfulness questionnaire indicated significant improvements compared with pre-participation responses. The analysis of MR images, which focused on areas where meditation-associated differences were seen in earlier studies, found increased grey-matter density in the hippocampus, known to be important for learning and memory, and in structures associated with self-awareness, compassion and introspection. Participant-reported reductions in stress also were correlated with decreased grey-matter density in the amygdala, which is known to play an important role in anxiety and stress. Although no change was seen in a self-awareness-associated structure called the insula, which had been identified in earlier studies, the authors suggest that longer-term meditation practice might be needed to produce changes in that area. None of these changes were seen in the control group, indicating that they had not resulted merely from the passage of time.

"It is fascinating to see the brain's plasticity and that, by practicing meditation, we can play an active role in changing the brain and can increase our well-being and quality of life." says Britta Hölzel, PhD, first author of the paper and a research fellow at MGH and Giessen University in Germany. "Other studies in different patient populations have shown that meditation can make significant improvements in a variety of symptoms, and we are now investigating the underlying mechanisms in the brain that facilitate this change."

Amishi Jha, PhD, a University of Miami neuroscientist who investigates mindfulness-training's effects on individuals in high-stress situations, says, "These results shed light on the mechanisms of action of mindfulness-based training. They demonstrate that the first-person experience of stress can not only be reduced with an 8-week mindfulness training program but that this experiential change corresponds with structural changes in the amydala, a finding that opens doors to many possibilities for further research on MBSR's potential to protect against stress-related disorders, such as post-traumatic stress disorder." Jha was not one of the study investigators.

A cold dose of fear lends an edge to the here-and-now — say, when things go bump in the night.

"That edge sounds good. It sounds adaptive. It sounds like perception is enhanced and that it can keep you safe in the face of danger," says Alexander Shackman, a researcher at the University of Wisconsin-Madison. But it sounds like there's also a catch, one that Shackman and his coauthors — including Richard Davidson, UW-Madison psychology and psychiatry professor — described in the Jan. 19 Journal of Neuroscience. "It makes us more sensitive to our external surroundings as a way of learning where or what a threat may be, but interferes with our ability to do more complex thinking," Davidson says.

Faced with the possibility of receiving an unpleasant electric shock, the study's subjects showed enhanced activity in brain circuits responsible for taking in visual information, but a muted signal in circuitry responsible for evaluating that information. Remove the threat of shock (and thus the stress and anxiety) and the effect is reversed: less power for vigilance, more power for strategic decision-making.

The shift in electrical activity in the brain, captured by a dense mesh of sensors placed on the scalp, may be the first biological description of a paradox in experimental psychology.

It has long been known that imminent danger can enhance the ability to detect faint stimuli in the environment, such as the crackle of a leaf signaling the approach of a predator. But it is equally clear that the stress and anxiety aroused by a threat can profoundly disrupt the ability to think clearly and perform more complex "executive" tasks. "In the last few years, theorists have hypothesized that this paradox might reflect several systems working in conjunction: one responsible for the rapid detection of external stimuli, the other responsible for the slower, more reflective evaluation of that incoming information," Shackman says. "Stress upsets the balance of those systems."

In fact, as the senses go into overdrive, they are probably confounding the rest of the brain all the more. "Your ability to do more complex tasks is disrupted just as the amount of information you're receiving through your eyes and ears is enhanced," Shackman says. "You're having trouble focusing on the information coming in, but your brain is taking in more and more potentially irrelevant information. You can have a viscous feedback loop, a sort of double-whammy effect."

The resulting confusion favors quick, reflexive actions, the "survival instincts" often mentioned by trauma survivors — Noise? RUN! — in a way that was likely adaptive in the dangerous environments in which the ancestors to modern humans evolved. "In our evolutionary past, the dangers we faced were really survival-threatening," Davidson says. "That's not so much the case now. Because of the nature of our brains, we can use our neural capacity to create our own internal danger. We can worry about the future and ruminate about the past."

Either one is likely to present a real hurdle to effective decision-making under stress. "This is part of a growing body of evidence showing that stress does have important consequences for the brain, not just something that arouses the body — tension in your muscles or butterflies in the stomach," says Davidson, who studies the effects of meditation as director of UW-Madison's Center for Investigating Healthy minds. "One of the things we would expect is that if we use an antidote like systematic meditation training to learn to control stress it would not just calm the body, but improve our ability to engage in complex analytical activity," he says.

Even during a recession, pharma is still the nation's third most profitable sector. Here are some of the dirty tricks it employs to stay on top. Read the AlterNet article here.

Sleeping brain "calculates" what to remember and what to forget, study says.

Read the article from National Geographic here.

Scientists of the Charite Berlin and of PTB confirm: Smokers have a thinner cerebral cortex

Is there a relation between the structure of specific regions of the brain and nicotine dependence? This is the question researchers of the Charité – Universitätsmedizin Berlin and of the Physikalisch-Technische Bundesanstalt (PTB) Berlin have been investigating lately. The results of these investigations extend and specify those of preceding studies: A specific region of the cerebral cortex of smokers is thinner than that of people who have never smoked in their lives. This region is decisive for reward, impulse control, and the making of decisions. The questions of whether smoking leads to this cerebral region becoming thinner - or whether people who have a thinner cortex region by nature are more frequently inclined to become smokers - can only be clarified by further investigations.

To investigate the relation between cortical thickness and nicotine dependence, the brains of 22 smokers and 21 people who have never smoked in their lives were investigated with the aid of a magnetic resonance tomograph. The measurements were carried out at PTB in Berlin and furnished high-resolution three-dimensional images of the brain structure. On the basis of these data, the individual thickness of the cortex could be determined at the Charité by means of a special evaluation procedure. A comparison of the two groups showed that in the case of smokers, the thickness of the medial orbito-frontal cortex is, on average, smaller than in the case of people who have never smoked. The thickness of this region decreased in relation to the increase in the daily consumption of cigarettes, and depending on how long in their lives the participants in the study had been smokers.

Cause and effect are, however, still not clear. Although it is known from animal experiments that nicotine changes the development of the brain and leads to a damaging of neurocytes, it cannot be ruled out that the reduced thickness of the frontal cortex region found in the case of the participants in the study already existed before they started smoking. Possibly, it is a genetically conditioned predisposition for nicotine dependence. Scientists want to find out in future studies whether the brain structure of smokers can become normal again after they have given up smoking.

Original publication: Kühn, S.; Schubert, F.; Gallinat, J.: Reduced thickness in medial orbitofrontal cortex in smokers. Biological Psychiatry, 2010 Sept 25

The National Institutes of Health Blueprint for Neuroscience Research is launching a $30 million project that will use cutting-edge brain imaging technologies to map the circuitry of the healthy adult human brain. By systematically collecting brain imaging data from hundreds of subjects, the Human Connectome Project (HCP) will yield insight into how brain connections underlie brain function, and will open up new lines of inquiry for human neuroscience. [read more of NIH press release]

Is that cupcake an innocent indulgence? Or your next hit? We're finding that a sweet tooth makes you just as much an addict as snorting cocaine [read article]

Trivedi, Bijal (2010). Junkie food: Tastes your brain can't resist. New Scientist, 2776. Retrieved from http://www.newscientist.com/article/mg20727761.700-junkie-food-tastes-your-brain-cant-resist.html

New insights spur effort to boost treatment's impact significantly

Scientists have taken another important step toward understanding just how sticking needles into the body can ease pain. In a paper published online May 30 in Nature Neuroscience, a team at the University of Rochester Medical Center identifies the molecule adenosine as a central player in parlaying some of the effects of acupuncture in the body. Building on that knowledge, scientists were able to triple the beneficial effects of acupuncture in mice by adding a medication approved to treat leukemia in people. The research focuses on adenosine, a natural compound known for its role in regulating sleep, for its effects on the heart, and for its anti-inflammatory properties. But adenosine also acts as a natural painkiller, becoming active in the skin after an injury to inhibit nerve signals and ease pain in a way similar to lidocaine.

In the current study, scientists found that the chemical is also very active in deeper tissues affected by acupuncture. The Rochester researchers looked at the effects of acupuncture on the peripheral nervous system – the nerves in our body that aren't part of the brain and spinal cord. The research complements a rich, established body of work showing that in the central nervous system, acupuncture creates signals that cause the brain to churn out natural pain-killing endorphins.

The new findings add to the scientific heft underlying acupuncture, said neuroscientist Maiken Nedergaard, M.D., D.M.Sc., who led the research. Her team is presenting the work this week at a scientific meeting, Purines 2010, in Barcelona, Spain. "Acupuncture has been a mainstay of medical treatment in certain parts of the world for 4,000 years, but because it has not been understood completely, many people have remained skeptical," said Nedergaard, co-director of the University's Center for Translational Neuromedicine, where the research was conducted. "In this work, we provide information about one physical mechanism through which acupuncture reduces pain in the body," she added.

To do the experiment, the team performed acupuncture treatments on mice that had discomfort in one paw. The mice each received a 30-minute acupuncture treatment at a well known acupuncture point near the knee, with very fine needles rotated gently every five minutes, much as is done in standard acupuncture treatments with people.

The team made a number of observations regarding adenosine:

• In mice with normal functioning levels of adenosine, acupuncture reduced discomfort by two-thirds.
• In special "adenosine receptor knock-out mice" not equipped with the adenosine receptor, acupuncture had no effect.
• When adenosine was turned on in the tissues, discomfort was reduced even without acupuncture.
• During and immediately after an acupuncture treatment, the level of adenosine in the tissues near the needles was 24 times greater than before the treatment.

Once scientists recognized adenosine's role, the team explored the effects of a cancer drug called deoxycoformycin, which makes it harder for the tissue to remove adenosine. The compound boosted the effects of acupuncture treatment dramatically, nearly tripling the accumulation of adenosine in the muscles and more than tripling the length of time the treatment was effective. "It's clear that acupuncture may activate a number of different mechanisms," said Josephine P. Briggs, M.D., director of the National Center for Complementary and Alternative Medicine at the National Institutes of Health. "This carefully performed study identifies adenosine as a new player in the process. It's an interesting contribution to our growing understanding of the complex intervention which is acupuncture," added Briggs, who is the spouse of co-author Jurgen Schnermann.

Results could have worldwide implications and prove that all lab mice are not equal

Researchers at the University of Colorado’s Anschutz Medical Campus have found the brains of mice used in laboratories worldwide can be profoundly affected by the type of cage they are kept in, a breakthrough that may require scientists to reevaluate the way they conduct future experiments.

“We assume that mice used in laboratories are all the same, but they are not,” said Diego Restrepo, director of the Neuroscience Program and professor of cell and developmental biology whose paper on the subject was published Tuesday, June 29. “When you change the cages you change the brains and that affects the outcomes of research.”

Mice are the chief research mammals in the world today with some of the most promising cancer, genetic and neuroscience breakthroughs riding on the rodents. Researchers from different universities rely on careful comparison of experimental results for their discoveries; but Restrepo has found that some of these comparisons may not be trustworthy.

He discovered that the brains of mice are extremely sensitive to their environment and can physically change when moved from an enclosure where air circulates freely to one where it doesn’t. Specifically, the portion of the mouse’s brain responsible for its keen sense of smell, the olfactory bulb, is altered.  Restrepo also found profound changes in the levels of aggression when mice are moved from one type of cage to another.

The results, he says, can greatly affect the accuracy of the research. Two labs doing the same experiments may get totally different results and never know why.

“This could explain some of the failures to replicate findings in different laboratories and why contradictory data are published by different laboratories even when genetically identical mice are used as subjects,” said Restrepo.

The consequences could mean good science derailed or promising research abandoned simply due to the design of a mouse cage – something largely overlooked until now.

Restrepo’s findings were just published in PLoS One, the Public Library of Science, a major peer-reviewed scientific journal, and are gaining and increasingly wide audience.

He hopes scientists will work to uncover the depth of the problem and find ways to overcome it.

"We need to ensure that laboratory findings are truly indicative of natural processes and not simply the result of environmental factors within each lab,” he said.

New study published in the journal Brain Injury

The ability to taste and smell can be lost or impaired after a head injury, according to a new study by scientists from the Université de Montréal, the Lucie Bruneau Rehabilitation Centre, as well as the Center for Interdisciplinary Research in Rehabilitation of Greater Montreal. Published in the journal Brain Injury, the investigation established that mild to severe traumatic brain injury could cause olfactory loss.

"The study clearly demonstrates that olfactory deficits can occur in mild traumatic brain injury patients as well as in moderate and severe TBI patients," says study co-author and neuropsychologist Maurice Ptito, a professor at the Université de Montréal School of Optometry. "We also found that patients with a frontal lesion were more likely to show olfactory dysfunctions."

The research team recruited 49 people with TBI (73 percent male with a median age of 43) who completed a questionnaire and underwent two smell tests to measure their olfactory loss. The result: 55 percent of subjects had an impaired sense of smell, while 41 percent of participants were unaware of their olfactory deficit.

"Both tests indicated the same results: patients with frontal injury are more likely to suffer olfactory loss," says lead author Audrey Fortin, a professor at the Université de Montréal School of Optometry and researcher at the Lucie Bruneau Rehabilitation Centre.

Smell plays a vital role in our lives, says Dr. Fortin, since olfaction influences what we eat, can help us detect gas leaks or fires. Smell also has a huge impact on interpersonal relationships, since olfactory disorders have been associated with poor quality of life, depression, mood swings, worries about personal hygiene, loss of appetite and cooking difficulties.

"Olfactory dysfunctions have a negative impact on daily life, health and safety," says Dr. Fortin. "It is important to pay attention to this symptom once a patient's condition has been stabilized following a traumatic brain injury."

What a difference culture makes.

Religious people tend to use their own beliefs as a guide in thinking about what God believes, but are less constrained when reasoning about other people's beliefs, according to new study published in the Nov. 30 early edition of the Proceedings of the National Academy of Sciences.

Nicholas Epley, professor of behavioral science at the University of Chicago's Booth School of Business, led the research, which included a series of survey and neuroimaging studies to examine the extent to which people's own beliefs guide their predictions about God's beliefs. The findings of Epley and his co-authors at Australia's Monash University and UChicago extend existing work in psychology showing that people are often egocentric when they infer other people's beliefs.

The PNAS paper reports the results of seven separate studies. The first four include surveys of Boston rail commuters, UChicago undergraduate students and a nationally representative database of online respondents in the United States. In these surveys, participants reported their own belief about an issue, their estimated God's belief, along with a variety of others, including Microsoft founder Bill Gates, Major League Baseball's Barry Bonds, President George W. Bush, and an average American.

Two other studies directly manipulated people's own beliefs and found that inferences about God's beliefs tracked their own beliefs. Study participants were asked, for example, to write and deliver a speech that supported or opposed the death penalty in front of a video camera. Their beliefs were surveyed both before and after the speech.

The final study involved functional magnetic resonance imaging to measure the neural activity of test subjects as they reasoned about their own beliefs versus those of God or another person. The data demonstrated that reasoning about God's beliefs activated many of the same regions that become active when people reasoned about their own beliefs.

The researchers noted that people often set their moral compasses according to what they presume to be God's standards. "The central feature of a compass, however, is that it points north no matter what direction a person is facing," they conclude. "This research suggests that, unlike an actual compass, inferences about God's beliefs may instead point people further in whatever direction they are already facing."

But the research in no way denies the possibility that God's presumed beliefs also may provide guidance in situations where people are uncertain of their own beliefs, the co-authors noted.

Where the Desire for Change Resides
Scientists have found an area of the brain that becomes highly active when we finally decide to explore the unknown.

60-Second Psych from Scientific American podcasts
9 November 2009

Seizure Makes Woman Mistake Herself For a Man (LiveScience.com)
By Charles Q. Choi
03 September 2009

For the first time, scientists report an instance of a brain seizure making someone believe they underwent a sex transformation.

Are you a "morning person" or a "night owl?"

Scientists at the University of Alberta have found that there are significant differences in the way our brains function depending on whether we're early risers or night owls. Neuroscientists in the Faculty of Physical Education and Recreation looked at two groups of people: those who wake up early and feel most productive in the morning, and those who were identified as evening people, those who typically felt livelier at night. Study participants were initially grouped after completing a standardized questionnaire about their habits.

Using magnetic resonance imaging-guided brain stimulation, scientists tested muscle torque and the excitability of pathways through the spinal cord and brain. They found that morning people's brains were most excitable at 9 a.m. This slowly decreased through the day. It was the polar opposite for evening people, whose brains were most excitable at 9 p.m.

Other major findings:
    * Evening people became physically stronger throughout the day, but the maximum amount of force morning people could produce remained the same.
    * The excitability of reflex pathways that travel through the spinal cord increased over the day for both groups.

These findings show that nervous-system functions are different and have implications for maximizing human performance.

To Get Good Grades, Get Good Sleep.

You’d think that college students would be experts at sleeping.  But odd hours, parties, cramming for tests, personal problems, self-medication with drugs or alcohol and general  can wreck a student’s sleep habits. Which can be bad for the body and the mind.

60-Second Psych from Scientific American podcasts
8 December 2008

A neural link between intelligence and self-control

If you had a choice between receiving $1,000 right now or $4,000 ten years from now, which would you pick? Psychologists use the term "delay discounting" to describe our inability to resist the temptation of a smaller immediate reward in lieu of receiving a larger reward at a later date. Discounting future rewards too much is a form of impulsivity, and an important way in which we can neglect to exert self-control.

Previous research suggests that higher intelligence is related to better self-control, but the reasons for this link are unknown. Psychologists Noah A. Shamosh and Jeremy R. Gray, from Yale University, and their colleagues, were interested in testing the idea that certain brain regions supporting short-term memory play a critical role in this relationship. "It has been known for some time that intelligence and self-control are related, but we didn't know why. Our study implicates the function of a specific brain structure, the anterior prefrontal cortex, which is one of the last brain structures to fully mature," said Dr. Shamosh.

In this study, 103 healthy adults were presented with a delay discounting task to assess self-control: a series of hypothetical choices where they had to choose between two financial rewards, a smaller one which they would receive immediately or another, larger reward which would be received at a later time. The participants then underwent a variety of tests of intelligence and short term memory. On another day, subjects' brain activity was measured using fMRI, while they performed additional short-term memory tasks.

The results show that participants with the greatest activation in the brain region known as the anterior prefrontal cortex also scored the highest on intelligence tests and exhibited the best self-control during the financial reward test. This was the only brain region to show this relation. The results appear in the September issue of Psychological Science, a journal of the Association for Psychological Science.

Previous studies have shown that the anterior prefrontal cortex plays a role in integrating a variety of information. The authors suggest that greater activity in the anterior prefrontal cortex helps people not only to manage complex problems, resulting in higher intelligence, but also aids in dealing with simultaneous goals, leading to better self-control.

Knowledge of the neural mechanisms underlying the relationship between short term memory, intelligence and delay discounting may result in improved techniques of increasing self-control. This is particularly applicable in regulating behavior related to gambling and substance abuse. "Understanding the factors that support better self-control is relevant to a host of important behaviors, ranging from saving for retirement to maintaining physical and mental health," the authors conclude.