Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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By Gary Stix Everyone knows that ALS is a very bad disease, an awareness underscored by the recent Ice Bucket Challenge. The death of neurons that results in paralysis can be caused by specific genetic mutations. But in most cases, single genes are not the culprit. So researchers have looked for other risk factors that might play a role. Studies have tagged cigarette smoking as a definite danger. Alcohol, another plausible suspect, has yielded equivocal results in previous investigations. To get a better read on ethanol (some earlier studies were small), researchers from Sweden’s Lund University looked at giant medical registries from that country, compiled at various times between 1973 and 2010. They found that individuals who were classified as problem drinkers were a little more than half as likely to be diagnosed with ALS as those who didn’t have “alcohol use disorder.” More than 420,000 problem drinkers were registered during the period surveyed—and there were 7965 patients who received an ALS diagnosis. The study, just reported in The European Journal of Neurology, controlled for gender, education and place of birth, among other factors. But it was unable to tell why drinking might help. It did lead, though, to a number of intriguing speculations. The researchers cited studies in rats, done by other groups, that indicated that ingestion of alcohol decreased the number of brain cells called astrocytes that bore high levels of a certain protein linked to the pathology of ALS. © 2015 Scientific American
|By Simon Makin People with depression process emotional information more negatively than healthy people. They show increased sensitivity to sad faces, for instance, or a weaker response to happy faces. What has been missing is a biological explanation for these biases. Now a study reveals a mechanism: an unusual balance of chemicals in a brain area crucial for the feeling of disappointment. A team led by Roberto Malinow of the University of California, San Diego, studied the lateral habenula, a evolutionarily ancient region deep in the brain [see diagram on bottom]. Neurons in this region are activated by unexpected negative events, such as a punishment out of the blue or the absence of an anticipated reward. For example, studies have shown that primates trained to expect a reward, such as juice, after a visual cue show heightened activity in the lateral habenula if the reward is withheld. Such findings have led to the idea that this area is a key part of a “disappointment circuit.” Past studies have also shown that hyperactivity in the lateral habenula is linked with depressionlike behavior in rodents. In people with depression, low levels of serotonin, the brain chemical targeted by antidepressants, are linked with a rise in lateral habenula activity. The region is unusual because it lacks the standard equipment the brain uses to reduce overactivity: opposing sets of neurons that either increase activity by secreting the chemical glutamate or decrease activity by secreting the chemical GABA. The lateral habenula has very few neurons that decrease activity, so Malinow and his colleagues set out to discover how the brain tamps down activity there. © 2015 Scientific American
Link ID: 20508 - Posted: 01.22.2015
Research suggests that only 20–30% of drug users actually descend into addiction — defined as the persistent seeking and taking of drugs even in the face of dire personal consequences. Why are some people who use drugs able to do so without turning into addicts, while others continue to abuse, even when the repercussions range from jail time to serious health problems? In a comprehensive review in the European Journal of Neuroscience, Barry Everitt outlines the neural correlates and learning-based processes associated with the transition from drug use, to abuse, to addiction. Drug seeking begins as a goal-directed behavior, with an action (finding and taking drugs) leading to a particular outcome (the drug high). This type of associative learning is mediated by the dorsomedial region of the striatum, the area of the brain that is associated with reward processing, which functions primarily through the neurotransmitter dopamine. In this kind of learning, devaluing the outcome (by decreasing the potency of the drug, for example) tends to decrease the pursuit of the action. When the high is not what it used to be, the motivation to continue seeking it out decreases. However, in long-term abusers, this devalued outcome does not reduce the action — indeed, researchers have found that in cases of chronic drug use, a parallel associative learning process eventually comes to the fore. This process is one of stimulus–response; the conditioned stimuli in this case are the various environmental cues — the sight of the powdery white stuff, the smell of burning aluminum foil — that users associate with getting high and that compel them to seek out drugs. © Association for Psychological Science
It is now one hundred years since drugs were first banned - and all through this long century of waging war on drugs, we have been told a story about addiction, by our teachers, and by our governments. This story is so deeply ingrained in our minds that we take it for granted. It seems obvious. It seems manifestly true. Until I set off three and a half years ago on a 30,000-mile journey for my book 'Chasing The Scream - The First And Last Days of the War on Drugs' to figure out what is really driving the drug war, I believed it too. But what I learned on the road is that almost everything we have been told about addiction is wrong - and there is a very different story waiting for us, if only we are ready to hear it. If we truly absorb this new story, we will have to change a lot more than the drug war. We will have to change ourselves. I learned it from an extraordinary mixture of people I met on my travels. From the surviving friends of Billie Holiday, who helped me to learn how the founder of the war on drugs stalked and helped to kill her. From a Jewish doctor who was smuggled out of the Budapest ghetto as a baby, only to unlock the secrets of addiction as a grown man. From a transsexual crack dealer in Brooklyn who was conceived when his mother, a crack-addict, was raped by his father, an NYPD officer. From a man who was kept at the bottom of a well for two years by a torturing dictatorship, only to emerge to be elected President of Uruguay and to begin the last days of the war on drugs. ©2015 TheHuffingtonPost.com, Inc.
By David Shultz The most venomous animal on the planet isn’t a snake, a spider, or a scorpion; it’s a snail—a cone snail, to be precise. The Conus genus boasts a large variety of marine snails that have adopted an equally diverse assortment of venoms. Online today in the Proceedings of the National Academy of Sciences, researchers report an especially interesting addition to the animals’ arsenal: insulin. According to the paper, this marks the first time insulin has been discovered as a component of venom. Not all cone snails incorporate insulin into their venom cocktail, wonderfully known as nirvana cabal; the hormone was found only in a subset of the animals that hunt with a netting strategy that relies on snaring fish in their large, gaping mouthparts. Unlike the feeding tactics of some cone snails that hunt using speedy venom-tipped “harpoons,” the mouth-netting strategy is a rather slow process. For it to work, the fish either needs to be very unaware of its surroundings or chemically sedated. Scientists speculate that it’s the insulin that provides such sedation. Snails like Conus geographus (seen above) actually produce multiple variants of the hormone, some of which, like one called Con-Ins G1, are more similar to fish insulin than snail varieties. Con-Ins G1 isn’t an exact match of fish insulin though; it’s a stripped-down version that the team suspects may be missing bits that would let fish detect the overdose and respond. If they’re correct, the snail’s venom may yield insight into the nuances of how insulin is regulated that may extend to humans. © 2015 American Association for the Advancement of Science
By Consumer Reports The headlines about coffee’s impact on your health seem to change as quickly as the time it takes to drink a cup. Should you savor every drop or try to cut down? Here’s what we know right now: It may lengthen your life. True, coffee drinkers are more likely than nondrinkers to smoke, eat red meat, skimp on exercise and have other life-shortening habits, according to a large 2012 study published in the New England Journal of Medicine. But even after adjusting for such factors, they found that people age 50 to 71 who drank at least one cup of coffee per day had a lower risk than nondrinkers of dying from diabetes, heart disease or other health problems when followed for more than a decade. That may be due to beneficial compounds in coffee such as antioxidants — which might ward off disease — and not caffeine. Decaf drinkers had the same results. It may make you happier. Coffee is not just a pick-me-up; it also has been linked to a lower risk of depression. In a study led by the Harvard School of Public Health that tracked 50,000 women for 10 years, those who drank four or more cups of caffeinated coffee per day were 20 percent less likely to develop depression than nondrinkers. Another study found that adults who drank two to four cups of caffeinated coffee were about half as likely to attempt suicide as decaf drinkers or abstainers. The researchers speculated that long-term coffee drinking may boost the production of “feel good” hormones such as dopamine. It contains many good-for-you chemicals.
By Susan Svrluga Edwin Chapman’s secretary handed him a pile of prescription slips, and the doctor’s pen moved quickly across them: “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” “Buprenorphine/naloxone.” His waiting room was full of heroin-addicted patients there to refill their generic prescriptions for Suboxone, a drug that helps keep their relentless cravings at bay and now outpaces methadone as a treatment. Chapman is an internist, a cardiologist. This drug has transformed his D.C. medical practice — now more than half of his patients are there to seek it, addicts edging out elderly ladies with arthritis and diabetes. And the drug, he believes, has transformed lives. He wishes more people could get it. Yet even as heroin use surges in the United States, destroying neighborhoods and families — drug overdoses kill more people than any other kind of accident — both addicts and doctors say there are barriers that keep some from the treatment they desperately need. “In the past we’ve kind of run away from these patients, put them in methadone clinics, places no one can see them,” said Chapman, who estimates that two-thirds of his heroin-addicted patients tested positive for hepatitis C and more than one in 10 for HIV. “We need to reverse that. Put them in primary care. We need to be taking care of sick folks, not running away from them.
Keyword: Drug Abuse
Link ID: 20480 - Posted: 01.14.2015
By KIRA PEIKOFF At a recent Seahawks football game in Seattle, Shy Sadis, 41, took a drag on a slim vapor pen that looked like a jet black Marlboro. The tip glowed red as he inhaled. But the pen contained no nicotine. Instead, it held 250 milligrams of cannabis oil loaded with THC, the psychoactive ingredient in marijuana. “Nobody noticed,” said Mr. Sadis, who owns several marijuana dispensaries in Washington State. “You pull it out of your pocket, take a hit like a cigarette, put it back, and you’re done. It’s so discreet.” The device, called a JuJu Joint, heralds a union that seems all but inevitable: marijuana and the e-cigarette, together at last in an e-joint. For years, people have been stuffing marijuana in various forms into portable vaporizers and into the cartridges of e-cigarettes. But the JuJu Joint is disposable, requires no charging of batteries or loading of cartridges, and comes filled with 150 hits. You take it out of the package and put it to your lips — that’s it. There is no smoke and no smell. Since their introduction in April, 75,000 JuJu Joints have been sold in Washington State, where marijuana is recreationally and medically legal. The maker says that 500,000 will be sold this year and that there are plans to expand to Colorado and Oregon, where recreational use is legal, and to Nevada, where it is decriminalized. “I wanted to eliminate every hassle that has to do with smoking marijuana,” said Rick Stevens, 62, the inventor and co-founder of JuJu Joints with Marcus Charles, a Seattle entrepreneur. “I wanted it to be discreet and easy for people to handle. There’s no odor, matches or mess.” © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 20473 - Posted: 01.13.2015
Sara Reardon Ketamine, a psychoactive ‘party drug’ better known as Special K, has pharmaceutical companies riding high. Used clinically as an anaesthetic in animals and humans, it has proved an extremely effective treatment for depression, bipolar disorder and suicidal behaviour. It also works incredibly fast. Unlike conventional antidepressants, which generally take weeks to start working, ketamine lifts depression in as little as two hours. “It blew the doors off what we thought we knew about depression treatment,” says psychiatrist James Murrough at Mount Sinai Hospital in New York City. Companies are racing to develop patentable forms of the drug, and researchers are battling to understand how it affects the brain. An increasing number of clinicians are prescribing ketamine off-label for their patients, even as some of their colleagues worry that too little is known about its long-term effects. The excitement over ketamine shows how badly new depression drugs are needed, says Thomas Insel, director of the US National Institute of Mental Health (NIMH) in Bethesda, Maryland. Many drug companies have closed their mental-health divisions in the past five years, and there have been no significant advances in medication for depression in decades. Today’s most common antidepressants target the brain’s serotonin or noradrenaline pathways (some target both). Ketamine blocks the signalling molecule NMDA, a component of the glutamate pathway, which is involved in memory and cognition. Before ketamine was studied, no one even knew that the pathway was involved in depression, Murrough says. © 2015 Nature Publishing Group
|By Tori Rodriguez Coffee and tea may do more than just jolt you awake—they could also help keep your brain healthy, according to a slew of recent studies. Researchers have linked these beverages with protection from depression, Alzheimer's disease and Parkinson's disease. One large study investigated the link between depression and the intake of coffee, tea and sweet drinks [see box below]by following more than a quarter of a million older adults for 10 years. Researchers at the National Institutes of Health recorded consumption of each type of beverage in 1995 and 1996 and then compared those figures with participants' self-reported diagnoses of depression after 2000. Results showed that coffee intake was associated with a slightly lower risk for depression, according to a paper published last April in PLOS ONE. The paper found little effect from tea, but other work has shown tea to be protective. A study reported in November 2013 found older Chinese adults who regularly drank any kind of tea had a significantly smaller risk for depression: 21 percent for those who drank tea between one and five days a week and 41 percent for daily drinkers. The researchers also asked about the participants' leisure activities to ensure that the tea, and not teatime socializing, provided the protective effect. Some studies suggest that coffee and tea drinkers have lower rates of cognitive decline, too, but the evidence is mixed. Research in rodents that has focused on specific compounds in coffee and tea supports the idea that some of these chemicals reduce the risk for Alzheimer's and Parkinson's. In one such study, published online last June in Neurobiology of Aging, supplementing rats' diets with a component of coffee called eicosanoyl-5-hydroxytryptamide shielded the animals' brains against the pathological changes typical of Alzheimer's. © 2015 Scientific American,
Christopher Dean Hopkins If you've ever listened to karaoke at a bar, you know that drinking can affect how well someone can sing. Christopher Olson and his colleagues at Oregon Health and Science University recently set out to find if the same was true for birds, specifically zebra finches. "We just showed up in the morning and mixed a little bit of juice with 6 percent alcohol, and put it in their water bottles and put it in the cages," Olson told All Things Considered's Arun Rath. "At first we were thinking that they wouldn't drink on their own because, you know, a lot of animals just won't touch the stuff. But they seem to tolerate it pretty well and be somewhat willing to consume it." The finches long have been used as a model to study human vocal learning, or how people learn to communicate using language, Olson said. Obviously, alcohol affects human speech, so Olson and his team checked for similar problems with the birds. The blood alcohol levels achieved — .05 to .08 percent — would be laughed off by many college students, but because birds metabolize alcohol differently it was plenty to produce the effects the scientists were looking for. Listen to the audio, and you'll hear that the finches' song gets a bit quieter and just a little slurred, or as Olson puts it, "a bit less organized in their sound production" — like a roommate calling from a bar to get a ride home. © 2014 NPR
by Andy Coghlan If quitting smoking is one of your New Year's resolutions, we might have just the thing. Cytisine, a plant extract commonly used in eastern Europe to wean people off cigarettes, appears to be much better at the task than nicotine replacement patches and gums. Not to be confused with the DNA building block cytosine, cytisine is an alkaloid extract from the laburnum or golden rain tree (Laburnum anagyroides), which grows all over Europe. It works by blocking nicotine's access to the brain's pleasure receptors. Like nicotine, cytisine is toxic when ingested in large amounts but is safe at low doses. It is produced commercially mainly in Bulgaria and Poland, and has been used as a quitting aid in eastern European countries since the 1960s but is largely unknown elsewhere. Clinical trials carried out in the 60s and 70s did not meet US and European standards so did not lead to wider adoption. Researchers in New Zealand have now carried out a fresh trial of cytisine. They recruited 1310 smokers who intended to quit and gave exactly half of them cytisine as a course of tablets, taken daily in diminishing doses for 25 days. The other half received standard nicotine replacement therapy (NRT) – either as patches, gums or lozenges – for two months. The researchers noted the number of people who managed to abstain from smoking at one week, one month, two months and six months into the trial. Throughout, they found that people taking cytisine were less likely to have smoked than those using NRT. Six months in, 143 of the 655 cytisine recipients were still not smoking compared with 100 in the NRT group. © Copyright Reed Business Information Ltd.
Keyword: Drug Abuse
Link ID: 20434 - Posted: 12.20.2014
By ANDREW POLLACK It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country. It is called ketamine — or Special K, in street parlance. While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro. And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant. But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times. “We don’t know what the long-term side effects of this are,” said Dr. Anthony J. Rothschild, a professor of psychiatry at the University of Massachusetts Medical School. Some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials. Credit Sandy Huffaker for The New York Times Pharmaceutical companies hope to solve the problem by developing drugs that work like ketamine but without the side effects, which are often described as out-of-body experiences. © 2014 The New York Times Company
by Viviane Callier It's a fresh problem. People who smoke menthol cigarettes often smoke more frequently and can be less likely to quit – and it could be because fresh-tasting menthol is changing their brains to more sensitive to nicotine. How menthol enhances nicotine addiction has been something of a mystery. Now, Brandon Henderson at the California Institute of Technology in Pasadena and his colleagues have shown that exposing mice to menthol alone causes them to develop more nicotinic receptors, the parts of the brain that are targeted by nicotine. Menthol can be used medically to relieve minor throat irritations, and menthol-flavoured cigarettes were first introduced in the 1920s. But smokers of menthol cigarettes can be less likely to quit. In one study of giving up smoking, 50 per cent of unflavoured-cigarette smokers were able to quit, while menthol smokers showed quitting rates as low as 23 per cent, depending on ethnicity. Over time, smokers of both menthol and unflavoured cigarettes acquire more receptors for nicotine, particularly in neurons involved in the body's neural pathways for reward and motivation. And research last year showed that smokers of menthol cigarettes develop even more of these receptors than smokers of unflavoured cigarettes. To understand how menthol may be altering the brain, Henderson's team exposed mice to either menthol with nicotine, or menthol alone. They found that, even without nicotine, menthol increased the numbers of brain nicotinic receptors. They saw a 78 per cent increase in one particular brain region – the ventral tegmental area – which is involved in the dopamine signalling pathway that mediates in addiction. © Copyright Reed Business Information Ltd.
Keyword: Drug Abuse
Link ID: 20395 - Posted: 12.06.2014
By Sarah C. P. Williams Craving a stiff drink after the holiday weekend? Your desire to consume alcohol, as well as your body’s ability to break down the ethanol that makes you tipsy, dates back about 10 million years, researchers have discovered. The new finding not only helps shed light on the behavior of our primate ancestors, but also might explain why alcoholism—or even the craving for a single drink—exists in the first place. “The fact that they could put together all this evolutionary history was really fascinating,” says Brenda Benefit, an anthropologist at New Mexico State University, Las Cruces, who was not involved in the study. Scientists knew that the human ability to metabolize ethanol—allowing people to consume moderate amounts of alcohol without getting sick—relies on a set of proteins including the alcohol dehydrogenase enzyme ADH4. Although all primates have ADH4, which performs the crucial first step in breaking down ethanol, not all can metabolize alcohol; lemurs and baboons, for instance, have a version of ADH4 that’s less effective than the human one. Researchers didn’t know how long ago people evolved the more active form of the enzyme. Some scientists suspected it didn’t arise until humans started fermenting foods about 9000 years ago. Matthew Carrigan, a biologist at Santa Fe College in Gainesville, Florida, and colleagues sequenced ADH4 proteins from 19 modern primates and then worked backward to determine the sequence of the protein at different points in primate history. Then they created copies of the ancient proteins coded for by the different gene versions to test how efficiently each metabolized ethanol. They showed that the most ancient forms of ADH4—found in primates as far back as 50 million years ago—only broke down small amounts of ethanol very slowly. But about 10 million years ago, the team reports online today in the Proceedings of the National Academy of Sciences, a common ancestor of humans, chimpanzees, and gorillas evolved a version of the protein that was 40 times more efficient at ethanol metabolism. © 2014 American Association for the Advancement of Science.
By EUGENIA BONE I TRIED magic mushrooms out of curiosity and in middle age. I’d been on the amateur mycological circuit for a couple of years, but hallucinogenic species were rarely mentioned at the foraging expeditions and conferences I attended. It’s almost as if they were the black sheep of mycology: embarrassing to serious taxonomy jocks. I read some books on the subject, but most were tripper’s guides that didn’t utilize, um, specific language or current science. Psychoactive mushrooms had been in a kind of scientific ghetto ever since they were criminalized in 1968. But now the drug derived from the mushroom, psilocybin, is finally being re-examined for its medical applications. A study published last month in the Journal of the Royal Society Interface compared M.R.I.s of the brains of subjects injected with psilocybin with scans of their normal brain activity. The brains on psilocybin showed radically different connectivity patterns between cortical regions (the parts thought to play an important role in consciousness). The researchers mapped out these connections, revealing the activity of new neural networks between otherwise disconnected brain regions. The researchers suspect that these unusual connections may be responsible for the synesthetic experience trippers describe, of hearing colors, for example, and seeing sounds. The part of the brain that processes sound may be connecting to the part of the brain that processes sight. The study’s leader, Paul Expert at King’s College London, told me that his team doubted that this psilocybin-induced connectivity lasted. They think they are seeing a temporary modification of the subject’s brain function. © 2014 The New York Times Company
By Tara Parker-Pope Most people who drink to get drunk are not alcoholics, suggesting that more can be done to help heavy drinkers cut back, a new government report concludes. The finding, from a government survey of 138,100 adults, counters the conventional wisdom that every “falling-down drunk” must be addicted to alcohol. Instead, the results from the National Survey on Drug Use and Health show that nine out of 10 people who drink too much are not addicts, and can change their behavior with a little — or perhaps a lot of — prompting. “Many people tend to equate excessive drinking with alcohol dependence,’’ sad Dr. Robert Brewer, who leads the alcohol program at the Centers for Disease Control and Prevention. “We need to think about other strategies to address these people who are drinking too much but who are not addicted to alcohol.” Excessive drinking is viewed as a major public health problem that results in 88,000 deaths a year, from causes that include alcohol poisoning and liver disease, to car accidents and other accidental deaths. Excessive drinking is defined as drinking too much at one time or over the course of a week. For men, it’s having five or more drinks in one sitting or 15 drinks or more during a week. For women, it’s four drinks on one occasion or eight drinks over the course of a week. Underage drinkers and women who drink any amount while pregnant also are defined as “excessive drinkers.” Surprisingly, about 29 percent of the population meets the definition for excessive drinking, but 90 percent of them do not meet the definition of alcoholism. That’s good news because it means excessive drinking may be an easier problem to solve than previously believed. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 20342 - Posted: 11.21.2014
By RONI CARYN RABIN The Food and Drug Administration on Thursday approved a powerful long-acting opioid painkiller, alarming some addiction experts who fear that its widespread use may contribute to the rising tide of prescription drug overdoses. The new drug, Hysingla, and another drug approved earlier this year, Zohydro, contain pure hydrocodone, a narcotic, without the acetaminophen used in other opioids. But Hysingla is to be made available as an “abuse-deterrent” tablet that cannot easily be broken or crushed by addicts looking to snort or inject it. Nearly half of the nation’s overdose deaths involved painkillers like hydrocodone and oxycodone, according to a 2010 study by the Centers for Disease Control and Prevention. More than 12 million people used prescription painkillers for nonmedical reasons that year, according to the study. Prescription opioid abuse kills more adults annually than heroin and cocaine combined, and sends 420,000 Americans to emergency rooms every year, according to the C.D.C. Hysingla, however, will not be not abuse-proof, said officials at the F.D.A. and the drug’s manufacturer, Purdue Pharma. Its extended-release formulation, a pill to be taken once every 24 hours by patients requiring round-the-clock pain relief, will contain as much as 120 milligrams of hydrocodone. The F.D.A. warned that doses of 80 milligrams or more “should not be prescribed to people who have not previously taken an opioid medication,” but officials described the abuse-deterrent formulation as a step forward. © 2014 The New York Times Company
Sara Reardon A technique that makes mouse brains transparent shows how the entire brain responds to cocaine addiction and fear. The findings could uncover new brain circuits involved in drug response. In the technique, known as CLARITY, brains are infused with acrylamide, which forms a matrix in the cells and preserves their structure along with the DNA and proteins inside them. The organs are then treated with a detergent that dissolves opaque lipids, leaving the cells completely clear. To test whether CLARITY could be used to show how brains react to stimuli, neuroscientists Li Ye and Karl Deisseroth of Stanford University in California engineered mice so that their neurons would make a fluorescent protein when they fired. (The system is activated by the injection of a drug.) The researchers then trained four of these mice to expect a painful foot shock when placed in a particular box; another set of mice placed in the box received cocaine, rather than shocks. Once the mice had learned to associate the box with either pain or an addictive reward, the researchers tested how the animals' brains responded to the stimuli. They injected the mice with the drug that activated the fluorescent protein system, placed them in the box and waited for one hour to give their neurons time to fire. The next step was to remove the animals' brains, treat them with CLARITY, and image them using a system that could count each fluorescent cell across the entire brain (see video). A computer combined these images into a model of a three-dimensional brain, which showed the pathways that lit up when mice were afraid or were anticipating cocaine. © 2014 Nature Publishing Group
By Nicholas Bakalar Exposure to secondhand smoke and roadway traffic may be tied to increased body mass index in children and adolescents, a new study suggests. Researchers studied 3,318 children in 12 Southern California communities beginning at an average age of 10, and then followed them through age 18. They used parental questionnaires to establish exposure to smoking, and data on traffic volume and levels of nitrogen dioxide, ozone and particulates to track pollution. The study, in Environmental Health Perspectives, controlled for many other factors: sex, initial B.M.I., asthma, physical activity, insurance status, parental education and income, acres of parks and open space nearby, percentage of people living in poverty in each community. But even after accounting for these issues and more, they found that compared with children exposed to no secondhand smoke or near-roadway air pollution, B.M.I. was 0.80 higher in children exposed to pollution alone, 0.85 higher in those exposed to secondhand smoke alone, and 2.15 higher in those exposed to both. A normal B.M.I. for adults is 18.5 to 24.9. Higher than 25 is considered overweight, and above 30 obese. “It would be interesting to know more about the mechanism,” said the lead author, Dr. Rob McConnell, a professor of preventive medicine at the University of Southern California. “But the finding challenges the view that obesity is due solely to increased caloric intake and reduced physical activity. That’s not the whole story.” © 2014 The New York Times Company