Chapter 15. Emotions, Aggression, and Stress
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by Jessica Hamzelou IF YOU knew you were about to go through a stressful experience, would you pop a pill to protect yourself from its knock-on effects? It's an idea that has been mooted after a drug seemed to make mice immune to the negative impacts of stressful events. But could we rationalise prescribing such a drug? We all experience stress during our lives, whether it be a one-off event, such as a loved one dying, or chronic, low-level stress that results from struggling to make ends meet, for example. While most people find ways to cope, for some a particularly stressful event can trigger depression. What if there was a way to boost our stress resilience and thus shield us from depression? Rebecca Brachman at Columbia University in New York stumbled across the idea while she was giving ketamine to mice with the symptoms of depression. Even though the ketamine-taking mice had been chronically stressed, when they were dropped in a pool of water – a one-off stressful event – they were unperturbed and swam to an exit. Mice not given the drug made no attempt to escape, a classic sign of depression in rodents. There was also no change in the ketamine-taking animals' cognitive abilities or metabolism – both of which are altered in human depression. "It's really remarkable," says Brachman. "They basically look like mice that haven't been stressed." A single dose of ketamine protected mice from developing the symptoms of depression after stressful events for four weeks. But the drug only seemed to stop the symptoms of depression – some of the animals still exhibited anxiety behaviours. "It seems to protect against depression rather than anxiety," says Brachman, who controversially describes it as a depression "vaccine". The work will be published in Biological Psychiatry. © Copyright Reed Business Information Ltd
By Neuroskeptic | Neuroscientists might need to rethink much of what’s known about the amygdala, a small brain region that’s been the focus of a lot of research. That’s according to a new paper just published in Scientific Reports: fMRI measurements of amygdala activation are confounded by stimulus correlated signal fluctuation in nearby veins draining distant brain regions. The amygdala is believed to be involved in emotion, especially negative emotions such as fear. Much of the evidence for this comes from fMRI studies showing that the amygdala activates in response to stimuli such as images of scared faces. However, according to the authors of the new paper, Austrian neuroscientists Roland N. Boubela and colleagues, there’s a flaw in these fMRI studies. The problem, they say, is that the amygdala happens to be located next to a large vein, called the basal vein of Rosenthal (BVR). fMRI works by detecting blood oxygenation, so changes in the oxygen level in the blood within the BVR could produce signal changes that could be mistaken for activation in the amygdala. Because the BVR drains blood from several brain regions, some of which are themselves involved in emotion processing, the BVR could act as a proxy for emotion-related neural activation elsewhere in the brain, which is then projected onto the amygdala. Neuroscientists have long been aware of potential large vein contributions to the fMRI signal, but it hasn’t generally been seen as a serious concern. According to Boubela et al., however, the problem is serious, when it comes to the amygdala.
Michael C. Corbalis In the quest to identify what might be unique to the human mind, one might well ask whether non-human animals have a theory of mind. In fiction, perhaps, they do. Eeyore, the morose donkey in Winnie-the-Pooh, at one point complains: ‘A little consideration, a little thought for others, makes all the difference.’ In real life, some animals do seem to show empathy toward others in distress. The primatologist Frans de Waal photographed a juvenile chimpanzee placing a consoling arm around an adult chimpanzee in distress after losing a fight, but suggests that monkeys do not do this. However, one study shows that monkeys won’t pull a chain to receive food if doing so causes a painful stimulus to be delivered to another monkey, evidently understanding that it will cause distress. Even mice, according to another study, react more intensely to pain if they perceive other mice in pain. It is often claimed that dogs show empathy toward their human owners, whereas cats do not. Cats don’t empathise—they exploit. Understanding what others are thinking, or what they believe, can be complicated, but perceiving emotion in others is much more basic to survival, and no doubt has ancient roots in evolution. Different emotions usually give different outward signs. In Shakespeare’s “Henry V,” the King recognises the signs of rage, urging his troops to . . . imitate the action of the tiger; Stiffen the sinews, summon up the blood, Disguise fair nature with hard-favour’d rage; Then lend the eye a terrible aspect . . . The human enemy will read the emotion of Henry’s troops, just as the antelope will read the emotion of the marauding tiger. Perhaps the best treatise on the outward signs of emotion is Charles Darwin’s “The Expression of the Emotions in Man and Animals,” which details the way fear and anger are expressed in cats and dogs, although he does not neglect the positive emotions: © 2015 Salon Media Group, Inc.
Richard Harris American medicine is heading into new terrain, a place where a year's supply of drugs can come with a price tag that exceeds what an average family earns. Pharmacy benefit manager Express Scripts says last year more than half a million Americans racked up prescription drug bills exceeding $50,000. Barbara Haedtke of Portland, Ore., knows this all too well. When she was diagnosed with multiple sclerosis in 2001 at the age of 35, she was prescribed Avonex, at a cost of around $10,000 a year. Her health insurance paid most of that until she and her husband found themselves without jobs during an economic downturn. "We were in the hole, and so $10,000 was a lot of money," she says. "Under the best circumstances it's a lot of money, but then particularly it was really difficult." Barbara Haedtke says she's grateful for a drug-company program that helps cover copays, but doesn't know how long she'll get that benefit. The drug company gave her the medication at no charge until she once again had a job with insurance, and for that, she says, she's really grateful. But the story doesn't end there. Haedtke used Avonex for about a decade and watched with disbelief as the price more than tripled. She's now taking a new drug, Tecfidera, that's priced even higher — $66,000 a year, according to her pharmacy receipt. The drug is supposed to help reduce the number of episodes that characterize multiple sclerosis, a disease in which nerve fibers gradually degenerate, causing muscle weakness, numbness, loss of balance and even paralysis. © 2015 NPR
Dan Sung A 10-year study has revealed a startling link between high levels of anxiety and an increased risk of death from liver disease. The research, carried out by scientists at the University of Edinburgh, took account for obvious sociological and physiological factors such as alcohol consumption, obesity, diabetes and class, but still the data pointed to a clear relationship between the psychological conditions of stress and depression and the physical health of the hepatic system. There were over 165,000 participants surveyed for mental distress. They were each tracked for over a decade during which time the causes of death for those who passed on were recorded and categorised. What was found was that those who’d scored highly for signs of depression and stress were far more likely to suffer fatal liver disease. “This study provides further evidence for the important links between mind and body, and of the damaging effects psychological distress can have on physical wellbeing,” said Dr Tom Russ of the Centre for Clinical Brain Sciences. The work did not uncover any reasons for direct cause and effect but is the first to identify such a link between mental states and liver damage. Previous research has described how psychological conditions can lead to increased risk of cardiovascular disease which, in turn, may develop into obesity, raised blood pressure and then eventually to liver failure but, with this methodology controlling for such factors, it appears that the link is more direct than was previously thought.
By Will Lippincott In January 2012, two weeks after my discharge from a psychiatric hospital in Connecticut, I made a plan to die. My week in an acute care unit that had me on a suicide watch had not diminished my pain. Back in New York, I stormed out of my therapist’s office and declared I wouldn’t return to the treatment I’d dutifully followed for three decades. Nothing was working, so what was the point? I fit the demographic profile of the American suicide — white, male and entering middle age with a history of depression. Suicide runs in families, research tells us, and it ran in mine. My father killed himself at age 49 in April 1990. A generation before, an aunt of his took her life; before her, there were others. Shame runs in families, too, and no one in mine talked much about mental illness. The first time I was hospitalized for wanting to kill myself, as a teenager, my dad visited me a few days in. I made an effort to greet him with a firm handshake; he shared a few jokes with me. Dad was visibly concerned and told me he loved me. Only after his suicide a few years later did I learn that he, too, had been hospitalized, for depression, when he was in his early 20s. Setting out to start my own life after college, I felt that suicide was a clear and present opportunity, one that glowed more brightly during my depressive episodes. But I had an ambitious plan to beat it. I’d be a performer: work hard, keep my goals in the line of sight at all times, and make as much money as I could. Professional success would be my first line of defense to keep hopelessness at bay. In parallel, I’d find excellent doctors and be a compliant patient, take my meds and show up for talk therapy. And for a long time, through my 20s and 30s, that plan worked. © 2015 The New York Times Company
Link ID: 20949 - Posted: 05.19.2015
by Andy Coghlan When a fly escapes being swatted, what is going on in its head? Is it as terrified as we would be after a close shave with death? Or is buzzing away from assailantsMovie Camera a momentary inconvenience that flies shrug off? It now seems that flies do become rattled. "In humans, fear is something that persists on a longer timescale than a simple escape reflex," says William Gibson of the California Institute of Technology in Pasadena, California. "Our observations suggest flies have a persistent state of defensive arousal, which is not necessarily fear, but which has some similarities to it." This doesn't mean that flies share the same emotional responses to fear as humans, but they do seem to have the same behavioural building blocks of fear as us. Evasive action Gibson and his colleagues exposed fruit flies to overhead shadows resembling aerial predators, such as birds. The more shadows they were exposed to, the more the flies resorted to evasive behaviour, such as hopping, jumping or freezing. When the shadow passed over once per second, by the time the shadow had fallen 10 times, the average running speed of the flies had doubled, for example. Their average number of hops trebled after just two passes. They also offered starved flies food, and part way through the meal threatened them with shadows. The more often the meal was interrupted, the longer the flies took to return to their meal after flying away. © Copyright Reed Business Information Ltd.
By Virginia Morell Hyenas long ago mastered one of the keys to Facebook success: becoming the friend of a friend. The most common large carnivore in Africa, spotted hyenas (Crocuta crocuta), are known for their socially sophisticated behaviors. They live in large, stable clans (as pictured above), which can include as many as 100 individuals. They can tell clan members apart, discriminating among their maternal and paternal kin. They’re also choosy about their pals and form tight bonds only with specific members—the friends of their friends, researchers report in the current issue of Ecology Letters. And it’s this ability to form lasting friendships—or “cohesive clusters,” as the scientists describe a triad of friends—that is most important in maintaining the animals’ social structure. To reach this conclusion, the scientists analyzed more than 50,000 observations of social interactions among spotted hyenas in Kenya’s Maasai Mara National Reserve over 20 years. They found that individual traits, including the hyena’s sex and social rank, as well as environmental factors such as the amount of rainfall and prey abundance, all play a role in the animals’ social dynamics. But the most consistently influential factor was the ability of individual hyenas to form and maintain those tight friendships. The study used a new modeling method, which the researchers say can help other scientists better understand the sociality of other species. And that includes the human animal, who, the scientists note, are also prone to “cohesive clusters,” whether living as hunter-gatherers or as users of social media. © 2015 American Association for the Advancement of Science.
Link ID: 20934 - Posted: 05.16.2015
Robinson Meyer Brett Redding felt like he was out of options. “It started with little things—having trouble making eye contact,” he told me. Soon it got worse. Redding, a 28-year-old salesman in Seattle, found himself freaking out during normal, everyday conversations. He worried any time his boss wanted to talk. He would dread his regular sales calls, and the city’s booming housing market—he works in construction—seemed to make his ever-increasing meetings all the more crushing. He was suffering social anxiety, a common but debilitating mental illness. “I was afraid of losing my job because I couldn’t do it,” he says. His meetings with a therapist weren’t working, and he didn’t “want to mess with antidepressants.” “I’ve always been so social—I’ve never had issues with looking people in the eye and talking with people,” he says. That’s when Redding’s girlfriend saw an ad on Craigslist that promised an online program could help treat Redding’s social anxiety through methods proven by science. “I had nothing to lose,” he says—so he signed up. That service is now called Joyable. I first saw Joyable when an ad for it appeared in Facebook on my phone. “90 percent of our clients see their anxiety decline,” said the ad, next to a sun-glinted, bokeh-heavy photo of a blonde woman. I clicked on. Joyable’s website, full of affable sans serifs and cheery salmon rectangles, looks Pinterest-esque, at least in its design. Except its text didn’t discuss eye glasses or home decor but “evidence-based” methods shown to reduce social anxiety. I knew those phrases: “Evidence-based” is the watchword of cognitive behavioral therapy, or CBT, the treatment now considered most effective for certain anxiety disorders. Joyable dresses a psychologists’s pitch in a Bay Area startup’s clothes. © 2015 by The Atlantic Monthly Group.
Link ID: 20929 - Posted: 05.14.2015
By Emily Underwood We’ve all heard how rats will abandon a sinking ship. But will the rodents attempt to save their companions in the process? A new study shows that rats will, indeed, rescue their distressed pals from the drink—even when they’re offered chocolate instead. They’re also more likely to help when they’ve had an unpleasant swimming experience of their own, adding to growing evidence that the rodents feel empathy. Previous studies have shown that rats will lend distressed companions a helping paw, says Peggy Mason, a neurobiologist at the University of Chicago in Illinois who was not involved in the work. In a 2011 study, for example, Mason and colleagues showed that if a rat is trapped in a narrow plastic tube, its unrestrained cagemate will work on the latch until it figures out how to spring the trap. Skeptics, however, have suggested that the rodents help because they crave companionship—not because their fellow rodents were suffering. The new study, by researchers at the Kwansei Gakuin University in Japan, puts those doubts to rest, Mason says. For their test of altruistic behavior, the team devised an experimental box with two compartments divided by a transparent partition. On one side of the box, a rat was forced to swim in a pool of water, which it strongly disliked. Although not at risk of drowning—the animal could cling to a ledge—it did have to tread water for up to 5 minutes. The only way the rodent could escape its watery predicament was if a second rat—sitting safe and dry on a platform—pushed open a small round door separating the two sides, letting it climb onto dry land. © 2015 American Association for the Advancement of Science
Rob Stein The seasons appear to influence when certain genes are active, with those associated with inflammation being more active in the winter, according to new research released Tuesday. A study involving more than 16,000 people found that the activity of about 4,000 of those genes appears to be affected by the season, researchers reported in the journal Nature Communications. The findings could help explain why certain diseases are more likely than others to strike for the first time during certain seasons, the researchers say. "Certain chronic diseases are very seasonal — like seasonal affective disorder or cardiovascular disease or Type 1 diabetes or multiple sclerosis or rheumatoid arthritis," says John Todd, a geneticist at the University of Cambridge who led the research. "But people have been wondering for decades what the explanation for that is." Todd and his colleagues decided to try to find out. They analyzed the genes in cells from more than 16,000 people in five countries, including the United States and European countries in the Northern Hemisphere, and Australia in the Southern Hemisphere. And they spotted the same trend — in both hemispheres, and among men as well as women. "It's one of those observations where ... the first time you see it, you go, 'Wow, somebody must have seen this before,' " Todd says. Not all young girls avoid dirt. Hannah Rose Akerley, 7, plays in a gigantic lake of mud at the annual Mud Day event in Westland, Mich., last July. © 2015 NPR
By Melissa Mancini, Many veterans are turning to marijuana to ease symptoms of post traumatic stress disorder, despite concerns from the medical community about how effective pot is at treating the condition. There are a "tremendous" number of testimonials from patients with post traumatic stress disorder who say dried cannabis helps them, but there is a lack of randomized, controlled trials, said Dr. Stewart Cameron, a family physician and professor at Dalhousie University's faculty of medicine. In September 2014, the College of Family Physicians of Canada released a document to help doctors decide how to use cannabis in their practices. "They strongly recommended that it not be used for PTSD," said Cameron. "They suggested it should be reserved as a third or fourth line agent in people who suffer certain types of pain." Veterans Affairs paid out $5.2 million for medical marijuana to veterans across Canada last year. Of that, $3.4 million went to veterans in Atlantic Canada. The department could not say which ailments the veterans are treating with marijuana, because Veterans Affairs doesn't track cannabis reimbursement by condition. Medical marijuana advocate Fabian Henry says most of the 500 veterans who visited his company last year were looking for authorization to use marijuana to help with post traumatic stress disorder. Henry's company, Marijuana for Trauma, connects veterans with physicians willing to authorize medical cannabis. The organization has helped hundreds of veterans fill out forms for medical pot reimbursement from Veterans Affairs Canada. Marijuana for Trauma calls cannabis "a natural choice medicine" and says it's "proven to be effective in 85 per cent of those who suffer with PTSD." But Canadian medical authorities are far from assigning such a high efficacy rate to the drug. ©2015 CBC/Radio-Canada.
Jessica Hamzelou Don't be too hard on them. Amoebas that weasel their way into our brains and chow down on our grey matter aren't welcome, but it's how our immune system reacts that's really lethal. Setting the story straight could help us deal with them better. Brain-eating amoebas (Naegleria fowleri) are found in warm freshwater pools around the world, feeding on bacteria. If someone swims in one of these pools and gets water up their nose, the amoeba heads for the brain in search of a meal. Once there, it starts to destroy tissue by ingesting cells and releasing proteins that make other cells disintegrate. The immune system launches a counter-attack by flooding the brain with immune cells, causing inflammation and swelling. It seldom works: of the 132 people known to have been infected in the US since 1962, only three survived. Brain-eating amoeba infections are more common elsewhere. "In Pakistan, we have something like 20 deaths per year," says Abdul Mannan Baig at the Aga Khan University in Karachi. There is no standard treatment. Doctors in the US have recently started trying to kill the amoebas with miltefosine, a drug known to work on the leishmaniasis parasite. Mannan thinks they should take a different approach, because the immune response may be more damaging than the amoeba itself. The problem is that enzymes released by the immune cells can also end up destroying brain tissue. And the swelling triggered by the immune system eventually squashes the brainstem, fatally shutting off communication between the body and the brain. © Copyright Reed Business Information Ltd
Link ID: 20917 - Posted: 05.13.2015
Tina Hesman Saey COLD SPRING HARBOR, N.Y. — Taming animals makes an impression on their DNA. Domesticated animals tend to have genetic variants that affect similar biological processes, such as brain and facial development and fur coloration. Alex Cagan of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, reported the results May 6 at the Biology of Genomes conference. Cagan and colleagues examined DNA in Norway rats (Rattus norvegicus) that had been bred for 70 generations to be either tame or aggressive toward humans. Docility was associated with genetic changes in 1,880 genes in the rats. American minks (Neovison vison) bred for tameness over 15 generations had tameness-associated variants in 525 genes, including 82 that were also changed in the rats. The researchers also compared other domesticated animals, including dogs, cats, pigs and rabbits, with their wild counterparts. The domestic species and the minks had tameness-associated changes in genes for epidermal growth factor and associated proteins that stimulate growth of cells. Those proteins are important for the movement of neural crest cells within an embryo. That finding seems to support a recent hypothesis that changes in neural crest cells could be responsible for domestication syndrome, physical traits, including floppy ears, spotted coats and juvenile faces, which accompany tameness in many domestic animals. © Society for Science & the Public 2000 - 2015.
Patricia Neighmond Terri Bradford has suffered debilitating headache pain all her life. Some days the pain is so bad, she says, "By 11 o'clock in the morning, I'm on the couch in a darkened room with my head packed in ice." Over the years, Bradford, who is 50 years old and lives in Bedford, Mass., has searched desperately for pain relief. She's been to the doctor countless times for countless tests. "Everything I've had, I've had twice," she says. "I've had two spinal taps; I've had so many nerve blocks I've lost count." Bradford is not alone. It's estimated that every year 12 million Americans go to the doctor seeking help for headaches. Nearly one quarter of the population suffers from recurrent severe tension headaches or migraines. People who go to the doctor for headache pain are more likely to be sent for advanced testing and treatment, a study finds. That testing is expensive, it may not be necessary and could even be harmful, says lead researcher Dr. John Mafi of Beth Israel Deaconess Medical Center in Boston. Mafi looked at the rates of advanced imaging like CT scans and MRIs in people with headaches, as well as referrals to other doctors, presumably specialists. He found that from 1999 to 2010, the number of diagnostic tests rose from 6.7 percent of all doctor visits to 13.9 percent. At the same time, referrals to other doctors increased from 6.9 percent to 13.2 percent. So almost double what it was a decade ago. Mafi says this isn't because more people are suffering headaches. The headache rate has remained virtually the same over the past decade. But what has changed is supply and demand. Today there are a lot more advanced diagnostic machines than there were a decade ago, and more patients are asking to be tested. © 2015 NPR
by Bethany Brookshire Certain images conjure up intense emotion: crying children, a bloody face, a snake rearing for a strike. When people take in pictures that hold deep meaning for them, they actually see the images more vividly. For them, emotion gives the world an extra burst of Technicolor and increases the odds that they will remember the scene. But the amount of visual boost — called emotionally enhanced vividness — varies from person to person. Some of this variability is in our genes, a new study finds, suggesting that people really do see the world in different ways. Many of us are familiar with the chemical messenger norepinephrine as a stress chemical. But it doesn’t just dictate whether we fight or flee, says Rebecca Todd, a cognitive neuroscientist at the University of British Columbia in Vancouver. Norepinephrine is also very important for emotional memory. “It’s important in the initial perception of emotional stimuli,” she explains. “It weighs down emotional memories so they burn brighter.” Norepinephrine is produced in an area of the brain called the locus coeruleus. In an ideal system, the cells in this area produce norepinephrine in response to a signal such as stress. The norepinephrine signals pass to other areas of the brain, but some chemical messenger remains, binding to receptors called alpha2b adrenoreceptors on cells in the locus coeruleus. These adrenoreceptors act as a brake, stopping the production of norepinephrine before things get out of hand. The receptors are produced by the gene ADRA2b. But a substantial proportion of Europeans and Africans have a variation on ADRA2b that deletes the alpha2b adrenoreceptor, possibly cutting some of the wires on the norepinephrine brakes. People with this deletion had stronger memories of emotionally charged events, a 2007 study found. Todd and graduate student Mana Ehlers wanted to see if this deletion might affect how people perceived emotional images. © Society for Science & the Public 2000 - 2015.
By Kira Peikoff I draw an uneasy breath as I step into a bright purple office on the 14th floor of Boston’s Prudential Building. I am shown to a small conference table, where I take a seat and await the experiment. A palm-size triangular module is affixed above my right eye. It connects to a single-use strip of electrodes stuck onto my forehead and running down the back of my neck. This is Thync, the latest in transcranial direct current stimulation, or tDCS. The manufacturer says the device, to come out later this year, can alter the user’s mood in minutes via electric current. With a connected smartphone app, the mood-impaired subject chooses one of two settings: “calm vibes” or “energy vibes.” I tap “calm vibes” and wait. Somehow, I am having a hard time picturing myself unwinding at home this way while my husband sips a glass of Merlot. Thync is the latest in a wave of wearable gadgets offering so-called noninvasive brain stimulation. Until recently, it was mostly hobbyists — nine-volt batteries stuck to their heads — who experimented with tDCS as a means of improving concentration, verbal and computation abilities, and creativity. But in the last few years, several companies have introduced slick consumer devices, among them Foc.us, whose headset and controller cost $298, and The Brain Stimulator, whose advanced starter kit costs $150. In January, the journal Brain Stimulation published the largest meta-analysis of tDCS to date. After examining every finding replicated by at least two research groups, leading to 59 analyses, the authors reported that one session of tDCS failed to show any significant benefit for users. © 2015 The New York Times Company
Link ID: 20891 - Posted: 05.05.2015
Paul Oswell “Cool” is a bit of a moving target. Sixty years ago it was James Dean, nonchalantly smoking a cigarette as he sat on a motorbike, glaring down 1950s conformity with brooding disapproval. Five years ago it was Zooey Deschanel holding a cupcake. In a phone interview with Steve Quartz, the co-author of the recently published Cool: How the Brain’s Hidden Quest for Cool Drives Our Economy and Shapes Our World, we skirted around a working definition. Defining cool turns out to be tricky even for someone who has just written an entire book examining the neurological processes behind it. Quartz’s most succinct definition was that cool is “the sweet spot between being innovative and unconventional, but not weird”. Quartz is the director of the Social Cognitive Neuroscience Laboratory at the California Institute of Technology. So when asked to describe what the lab does, he did not deliver a “cool” answer, but rather a precise one: it is, he said, “concerned with all the dimensions of decision making, from simple gambles and risk assessment right up to very complex reasoning and the nature of moral behaviour”. He wrote the book with his colleague Anette Asp, with whom he has long done research on “neuroeconomics” and “neuromarketing”. Those fields use imaging techniques to look at the ways our brains process the emotions and responses we have to brands and products. The results, as Quartz and Asp posit in the book, reflect primal instincts we have around ideas of status. Their technique gives results that are much more accurate about what the kids are into, these days, than traditional marketing focus groups have ever been able to give us. © 2015 Guardian News and Media Limited
Nala Rogers People who are ill often complain of changes in their sense of taste. Now, researchers report that this sensory shift may be caused by a protein that triggers inflammation. Mice that cannot produce the protein, called tumour necrosis factor-α (TNF-α), are less sensitive to bitter flavours than normal mice, according to a study published on 21 April in Brain, Behavior, and Immunity1. People with infections, autoimmune disease or other inflammatory conditions have higher levels of TNF-α than healthy people, and the protein has been shown to reduce food intake2. To investigate the influence of TNF-α on taste, researchers at the Monell Chemical Senses Center in Philadelphia, Pennsylvania, used engineered mice that could not produce the protein. The researchers offered the engineered mice and normal mice water that contained different types and concentrations of flavours. The mice that could not produce TNF-α had normal reactions to sweet, sour, salty and umami flavours, but were less sensitive to bitter ones. “Normal mice will pick up [that taste] at a much lower concentration. They will know this is bitter; they will not like it,” says Hong Wang, a molecular biologist at Monell and an author of the study. “But if the TNF-α gene is not there, then the mice will only start to avoid the bitter solution at higher concentrations.” © 2015 Nature Publishing Group
Neuroscientists have discovered brain circuitry for encoding positive and negative learned associations in mice. After finding that two circuits showed opposite activity following fear and reward learning, the researchers proved that this divergent activity causes either avoidance or reward-driven behaviors. Funded by the National Institutes of Health, they used cutting-edge optical-genetic tools to pinpoint these mechanisms critical to survival, which are also implicated in mental illness. “This study exemplifies the power of new molecular tools that can push and pull on the same circuit to see what drives behavior,” explained Thomas R. Insel, M.D., director of NIH’s National Institute of Mental Health (NIMH). “Improved understanding of how such emotional memory works holds promise for solving mysteries of brain circuit disorders in which these mechanisms are disrupted.” NIMH grantee Kay Tye, Ph.D. External Web Site Policy, Praneeth Namburi and Anna Beyeler, Ph.D., of the Massachusetts Institute of Technology (MIT), Cambridge, and colleagues, report their findings April 29, 2015 in the journal Nature. Prior to the new study, scientists suspected involvement of the circuits ultimately implicated, but were stumped by a seeming paradox. A crossroads of convergent circuits in an emotion hub deep in the brain, thebasolateral amygdala, seem to be involved in both fear and reward learning, but how one brain region could orchestrate such opposing behaviors – approach and avoidance – remained an enigma. How might signals find the appropriate path to follow at this fork in the road?