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Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20592 - Posted: 02.18.2015

By Abigail Zuger, M.D. I had intended to discuss President Obama’s plans for personalized precision medicine with my patient Barbara last week, but she missed her appointment. Or, more accurately, she arrived two hours late, made the usual giant fuss at the reception desk and had to be rescheduled. I was disappointed. Barbara has some insight into the vortex of her own complications, and I thought she might help organize my thoughts. Mr. Obama announced last month that his new budget included $215 million toward the creation of a national databank of medical information, intended to associate specific gene patterns with various diseases and to predict what genetic, lifestyle and environmental factors correlate with successful treatment. Once all those relationships are clarified, the path will open to drugs or other interventions that firm up the good links and interrupt the bad ones. This step up the scientific ladder of medicine has many advocates. Researchers who sequence the genome are enthusiastic, as are those with a financial interest in the technology. Also celebrating are doctors and patients in the cancer community, where genetic data already informs some treatment choices and where the initial thrust of the initiative and much of its funding will be directed. Skeptics point out that genetic medicine, for all its promise, has delivered relatively few clinical benefits. And straightforward analyses of lifestyle and environment effects on health may occasionally lead to clear-cut advice (don’t smoke), but more often sow confusion, as anyone curious about the best way to lose weight or the optimal quantity of dietary salt knows. Without Barbara’s presence, I was left to ponder her medical record, a 20-year saga that might be titled “Genes, Lifestyle and Environment.” and published as a cautionary tale. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 20590 - Posted: 02.18.2015

By Lizzie Wade SAN JOSE, CALIFORNIA—Humans have been using cannabis for more than 5000 years. So why don’t scientists know more about it? Three experts gathered here at the annual meeting of AAAS (which publishes Science) to discuss what scientists and doctors know about the drug and what they still need to learn. “By the end of this session, you’ll know more about cannabis than your physician does,” said Mark Ware, a family physician at the McGill University Health Center in Montreal, Canada, who organized the talk. How does marijuana work? Our brains are primed to respond to marijuana, because “there are chemicals in our own bodies that act like THC [the psychoactive ingredient in pot]” and other compounds in cannabis called cannabinoids, explained Roger Pertwee, a neuropharmacologist at the University of Aberdeen in the United Kingdom who has studied cannabinoids since the 1960s. Cannabinoids produced by our bodies or ingested through marijuana use react with a series of receptors in our brains called the endocannabinoid system, which is involved in appetite, mood, memory, and pain sensation. Scientists have discovered 104 cannabinoids so far, but “the pharmacology of most of them has yet to be investigated,” Pertwee said. What are the known medical uses of marijuana? Marijuana has been used for decades to stimulate appetite and treat nausea and vomiting, especially in patients undergoing chemotherapy. Its success in easing the symptoms of multiple sclerosis patients led to the development of Sativex, a drug manufactured by GW Pharmaceuticals that includes THC and cannabidiol (CBD), a cannabinoid that isn’t psychoactive. © 2015 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 20582 - Posted: 02.16.2015

Smoking potent cannabis was linked to 24% of new psychosis cases analysed in a study by King's College London. The research suggests the risk of psychosis is three times higher for users of potent "skunk-like" cannabis than for non-users. The study of 780 people was carried out by KCL's Institute of Psychiatry, Psychology and Neuroscience. A Home Office spokesman said the report underlines the reasons why cannabis is illegal. Scientists found the risk of psychosis was five times higher for those who use it every day compared with non-users. They also concluded the use of hash, a milder form of the drug, was not associated with increased risk of psychosis. Psychosis refers to delusions or hallucinations that can be present in certain psychiatric conditions such as schizophrenia and bipolar disorder. "Compared with those who had never tried cannabis, users of high potency skunk-like cannabis had a threefold increase in risk of psychosis,' said Dr Marta Di Forti, lead author on the research. She added: "The results show that psychosis risk in cannabis users depends on both the frequency of use and cannabis potency." Dr Di Forti told BBC Radio 4's Today programme that the availability of skunk-like cannabis was becoming more widespread. "In London, it's very difficult to find anything else," she said. "There were lots of reports from police across the UK saying we have become a great producer of skunk. And not only do we use it locally but we export, so this is a Made in England product." Someone suffering from psychosis would often be "extremely paranoid and become very suspicious" about the people around them, she added. She has called for "a clear public message" to cannabis users, comparable to medical advice on alcohol and tobacco. © 2015 BBC

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20581 - Posted: 02.16.2015

By DENISE GRADY However bad you thought smoking was, it’s even worse. A new study adds at least five diseases and 60,000 deaths a year to the toll taken by tobacco in the United States. Before the study, smoking was already blamed for nearly half a million deaths a year in this country from 21 diseases, including 12 types of cancer. The new findings are based on health data from nearly a million people who were followed for 10 years. In addition to the well-known hazards of lung cancer, artery disease, heart attacks, chronic lung disease and stroke, the researchers found that smoking was linked to significantly increased risks of infection, kidney disease, intestinal disease caused by inadequate blood flow, and heart and lung ailments not previously attributed to tobacco. Even though people are already barraged with messages about the dangers of smoking, researchers say it is important to let the public know that there is yet more bad news. “The smoking epidemic is still ongoing, and there is a need to evaluate how smoking is hurting us as a society, to support clinicians and policy making in public health,” said Brian D. Carter, an epidemiologist at the American Cancer Society and the first author of an article about the study, which appears in The New England Journal of Medicine. “It’s not a done story.” In an editorial accompanying the article, Dr. Graham A. Colditz, from Washington University School of Medicine in St. Louis, said the new findings showed that officials in the United States had substantially underestimated the effect smoking has on public health. He said smokers, particularly those who depend on Medicaid, had not been receiving enough help to quit. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20569 - Posted: 02.13.2015

By Michelle Roberts Health editor, BBC News online Women trying for a baby and those in the first three months of pregnancy should not drink any alcohol, updated UK guidelines say. The Royal College of Obstetricians and Gynaecologists (RCOG) had previously said a couple of glasses of wine a week was acceptable. It now says abstinence is the only way to be certain that the baby is not harmed. There is no proven safe amount that women can drink during pregnancy. The updated advice now chimes with guidelines from the National Institute for Health and Care Excellence (NICE). In the US, experts say there is no safe time to drink during pregnancy. But the RCOG highlights around the time of conception and the first three months of pregnancy as the most risky. Drinking alcohol may affect the unborn baby as some will pass through the placenta. Around conception and during the first three months, it may increase the chance of miscarriage, says the RCOG. After this time, women are advised to not drink more than one to two units, more than once or twice a week, it says. Drinking more than this could affect the development of the baby, in particular the way the baby's brain develops and the way the baby grows in the womb, which can lead to foetal growth restriction and increase the risk of stillbirth and premature labour, says the advice. © 2015 BBC

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20568 - Posted: 02.13.2015

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 20506 - Posted: 01.22.2015

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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 20505 - Posted: 01.22.2015

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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20494 - Posted: 01.20.2015

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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20473 - Posted: 01.13.2015

|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,

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 20460 - Posted: 01.08.2015

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Language and Our Divided Brain
Link ID: 20449 - Posted: 01.01.2015

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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20434 - Posted: 12.20.2014

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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20378 - Posted: 12.02.2014

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20342 - Posted: 11.21.2014

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 20337 - Posted: 11.20.2014

Details of the role of glutamate, the brain’s excitatory chemical, in a drug reward pathway have been identified for the first time. This discovery in rodents — published today in Nature Communications — shows that stimulation of glutamate neurons in a specific brain region (the dorsal raphe nucleus) leads to activation of dopamine-containing neurons in the brain’s reward circuit (dopamine reward system). Dopamine is a neurotransmitter present in regions of the brain that regulate movement, emotion, motivation, and feelings of pleasure. Glutamate is a neurotransmitter whose receptors are important for neural communication, memory formation, and learning. The research was conducted at the Intramural Research Program (IRP) of the National Institute on Drug Abuse (NIDA), which is part of the National Institutes of Health. The research focused on the dorsal raphe nucleus, which has long been a brain region of interest to drug abuse researchers, since nerve cells in this area connect to part of the dopamine reward system. Many of the pathways are rich in serotonin, a neurotransmitter linked to mood regulation. Even though electrical stimulation of the dorsal raphe nucleus promotes reward-related behaviors, drugs that increase serotonin have low abuse potential. As a result, this region of the brain has always presented a seeming contradiction, since it is involved in drug reward but is also abundant in serotonin - a chemical not known for a role in drug reinforcement. This has led researchers to theorize that another neurotransmitter may be responsible for the role that the dorsal raphe nucleus plays in reward.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20308 - Posted: 11.13.2014

By Kate Kelland LONDON (Reuters) - British scientists say they have found the best way yet to analyze the effects of smoking on the brain -- by taking functional magnetic resonance imaging (fMRI) scans of people while they puff on e-cigarettes. In a small pilot study, the researchers used electronic cigarettes, or e-cigarettes, to mimic the behavioral aspects of smoking tobacco cigarettes, and say future studies could help scientists understand why smoking is so addictive. E-cigarettes use battery-powered cartridges to produce a nicotine-laced vapor to inhale -- hence the new term "vaping". Their use has rocketed in recent years, but there is fierce debate about the risks and benefits. Some public health experts say they could help millions quit tobacco cigarettes, while others argue they could "normalize" the habit and lure children into smoking. While that argument rages, tobacco kills some 6 million people a year, and the World Health Organization estimates that could rise beyond 8 million by 2030. Matt Wall, an imaging scientist at Imperial College London who led the study using e-cigarettes, said he was not aiming to pass judgment on their rights or wrongs, but to use them to dig deeper into smoking addiction. The fact that other forms of nicotine replacement therapy, such as patches or gum, have had only limited success in getting hardened smokers to quit suggests they are hooked on more than just nicotine, he noted. © 2014 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20307 - Posted: 11.13.2014