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By THOMAS FULLER SANTA ROSA, Calif. — In the heart of Northern California’s wine country, a civil engineer turned marijuana entrepreneur is adding a new dimension to the art of matching fine wines with gourmet food: cannabis and wine pairing dinners. Sam Edwards, co-founder of the Sonoma Cannabis Company, charges diners $100 to $150 for a meal that experiments with everything from marijuana-leaf pesto sauce to sniffs of cannabis flowers paired with sips of a crisp Russian River chardonnay. “It accentuates the intensity of your palate,” Mr. Edwards, 30, said of the dinners, one of which was held recently at a winery with sweeping views of the Sonoma vineyards. “We are seeing what works and what flavors are coming out.” Sonoma County, known to the world for its wines, is these days a seedbed of cannabis experimentation. The approval of recreational cannabis use by California voters in November has spurred local officials here to embrace the pot industry and the tax income it may bring. “We’re making this happen,” said Julie Combs, a member of the Santa Rosa City Council, who is helping lead an effort to issue permits to cannabis companies. “This is an industry that can really help our region.” Of the many ways in which California is on a collision course with the Trump administration, from immigration to the environment, the state’s enthusiastic embrace of legalized and regulated marijuana may be one of the biggest tests of the federal government’s power. Attorney General Jeff Sessions has equated marijuana with heroin and, on Wednesday, mentioned cannabis in the context of the “scourge of drug abuse.” © 2017 The New York Times Compan

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23379 - Posted: 03.20.2017

Doctors who limit the supply of opioids they prescribe to three days or less may help patients avoid the dangers of dependence and addiction, a new study suggests. Among patients without cancer, a single day's supply of a narcotic painkiller can result in 6 per cent of patients being on an opioid a year later, the researchers said. The odds of long-term opioid use increased most sharply in the first days of therapy, particularly after five days of taking the drugs. The rate of long-term opioid use increased to about 13 per cent for patients who first took the drugs for eight days or more, according to the report. "Awareness among prescribers, pharmacists and persons managing pharmacy benefits that authorization of a second opioid prescription doubles the risk for opioid use one year later might deter overprescribing of opioids," said senior researcher Martin Bradley. He is from the division of pharmaceutical evaluation and policy at the University of Arkansas for Medical Sciences. "The chances of long-term opioid use, use that lasts one year or more, start increasing with each additional day supplied, starting after the third day, and increase substantially after someone is prescribed five or more days, and especially after someone is prescribed one month of opioid therapy," Bradley said. The odds of chronic opioid use also increase when a second prescription is given or refilled, he noted. ©2017 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23373 - Posted: 03.19.2017

By MATT RICHTEL Amid an opioid epidemic, the rise of deadly synthetic drugs and the widening legalization of marijuana, a curious bright spot has emerged in the youth drug culture: American teenagers are growing less likely to try or regularly use drugs, including alcohol. With minor fits and starts, the trend has been building for a decade, with no clear understanding as to why. Some experts theorize that falling cigarette-smoking rates are cutting into a key gateway to drugs, or that antidrug education campaigns, long a largely failed enterprise, have finally taken hold. But researchers are starting to ponder an intriguing question: Are teenagers using drugs less in part because they are constantly stimulated and entertained by their computers and phones? The possibility is worth exploring, they say, because use of smartphones and tablets has exploded over the same period that drug use has declined. This correlation does not mean that one phenomenon is causing the other, but scientists say interactive media appears to play to similar impulses as drug experimentation, including sensation-seeking and the desire for independence. Or it might be that gadgets simply absorb a lot of time that could be used for other pursuits, including partying. Nora Volkow, director of the National Institute on Drug Abuse, says she plans to begin research on the topic in the next few months, and will convene a group of scholars in April to discuss it. The possibility that smartphones were contributing to a decline in drug use by teenagers, Dr. Volkow said, was the first question she asked when she saw the agency’s most recent survey results. The survey, “Monitoring the Future,” an annual government-funded report measuring drug use by teenagers, found that past-year use of illicit drugs other than marijuana was at the lowest level in the 40-year history of the project for eighth, 10th and 12th graders. © 2017 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: 23357 - Posted: 03.15.2017

Ian Sample Science editor Selling high calorie foods in plain packaging could help in the battle against obesity according to a leading researcher who has won a share of the most lucrative prize in neuroscience for his work on the brain’s reward system. The colourful wrapping and attractive advertising of calorie-rich foods encourage people to buy items that put them at risk of overeating and becoming obese in the future, said Wolfram Schultz, a professor of neuroscience at the University of Cambridge. “We should not advertise, propagate or encourage the unnecessary ingestion of calories,” Schultz said at a press conference held on Monday to announce the winners of the 2017 Brain Prize. “There should be some way of regulating the desire to get more calories. We don’t need these calories.” “Colourful wrapping of high energy foods of course makes you buy more of that stuff and once you have it in your fridge, it’s in front of you every time you open the fridge and ultimately you’re going to eat it and eat too much,” he added. Schultz shares the €1m prize from the Lundbeck Foundation in Denmark with professors Peter Dayan, director of the Gatsby Computational Neuroscience Unit at UCL, and Ray Dolan, director of the Max Planck UCL Centre for Computational Psychiatry and Ageing. Together, the scientists unravelled how the brain uses rewards to learn and shape behaviour.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23320 - Posted: 03.06.2017

By Alistair Steele, CBC News The opioid crisis that's claiming lives across the country has taken a particularly sinister turn in the nation's capital. Or so it appears. Much of the public discussion — and a good deal of the news coverage — surrounding the growing number of deaths by opioid overdose in Ottawa has concentrated on the cruel toll the drugs are taking on the city's teenagers, particularly those living in the western suburb of Kanata. The fake prescription pills they take recreationally are cheap and easy to find, but they can also be laced with potentially lethal doses of fentanyl. This tragic trend was given a fresh, young face when Grade 9 student Chloe Kotval, just 14, died from an overdose on Valentine's Day. Police later confirmed pills found near the girl's body contained fentanyl. In a statement released the day of their daughter's funeral, Kotval's parents wrote: "We are concerned about the epidemic nature of the use of high-grade pharmaceuticals amongst young people and their lack of knowledge about them — the consequences of using them are real and terrible." While families have every right to be concerned and to prepare for the worst, there's no evidence showing young people are any more susceptible to opioid overdoses than any other group of drug users in Ottawa. Sean O'Leary, whose own teenage daughter became addicted to counterfeit percocets, told CBC about coming home one night to find a 17-year-old boy who had overdosed in his garage. ©2017 CBC/Radio-Canada.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23312 - Posted: 03.04.2017

Recently, an international team of researchers reported that the cerebellum may play a previously unforeseen role in brain alterations associated with the addictive consumption of drugs. Until now, the cerebellum—which has historically been viewed by most neuroscientists as primarily the seat of fine-tuned motor control and coordination—has gone under the radar of drug addiction specialists. The latest reports linking the cerebellum and drug addiction were based on a broad range of groundbreaking research published over the past two years. These findings were recently compiled and featured in two different journals: Neuroscience & Biobehavioral Reviews and the Journal of Neuroscience. Bringing all of this research together was the brainchild of Marta Miquel, professor in the research group Addiction and Neuroplasticity at the Universitat Jaume I (UJI) in Spain. Miguel spearheaded her own original research as well as the initiative to collect multidisciplinary research from a broad spectrum of international institutions and to present these cerebellar findings cohesively under one umbrella. (Cerebellar is the sister word to cerebral and means “relating to or located in the cerebellum.”) In addition to the UJI team, contributing research for this compilation of studies on the cerebellum and addiction came from the University of Cambridge and University of Leeds (United Kingdom); University of Turin (Italy); Universidad Veracruzana (Mexico); the University of Kentucky, Washington State University, and McLean Hospital Translational Neuroscience Laboratory and Mailman Research Center (USA). Psychology Today © 1991-2017 Sussex Publishers, LLC

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: 23301 - Posted: 03.02.2017

By Jessica Hamzelou Fancy a coffee after that cigarette? Smoking makes you drink more caffeinated drinks, possibly by changing your metabolism so that you break down caffeine quicker, pushing you to drink more to get the same hit. That’s according to Marcus Munafò at the University of Bristol, UK, and his colleagues who have looked into the smoking and drinking habits of about 250,000 people. It’s impossible to do a randomised controlled trial (the most rigorous kind of scientific trial) when it comes to smoking, because it would be unethical to ask a randomly selected group of people to smoke. The next best thing is to study huge biobanks of health data. These biobanks contain information about people’s genes, diets and lifestyles. To explore the relationship between smoking and caffeine, Munafo and his colleagues analysed data from biobanks in the UK, Norway and Denmark. They were particularly interested in people who had inherited a variant of a gene that has already been shown to increase cigarette smoking. The team found that people who had this gene variant also consumed more coffee – but only if they smoked. British people with the same variant also drank more tea, although their Danish and Norwegian counterparts didn’t. This is probably due to cultural differences, says Munafò. “People in Norway and Denmark don’t chain drink tea in the same way that people in the UK do,” he says. © 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: 23287 - Posted: 02.27.2017

Allison Aubrey If you drink more alcohol than you want to or should, you're not alone. A nationwide survey by the National Institutes of Health found that 28 percent of adults in the U.S. are heavy drinkers or drink more than is recommended. Yet, most heavy drinkers don't get the help they need. "The biggest problem we have in the field is that less than 10 percent of individuals with an alcohol use disorder get any treatment whatsoever," says George Koob, director of the National Institute on Alcohol Abuse and Alcoholism. Part of the challenge, researchers say, is that many drinkers don't realize that a medicine long used to help people addicted to opioids quit their drug habit can help alcoholics and other heavy drinkers cut back, too. "I thought my only option was AA," John tells NPR. We've agreed to use only his middle name; disclosing his trouble with alcohol publicly, he says, would jeopardize his business. He's a 47-year-old professional who says he started out as a social drinker — a few beers with his softball team after a game. But he sank into a deep depression after several deaths in his family, and sought "solace the bottle," he says. "I wanted to numb my thoughts," says John. He'd often start with hard liquor in the morning, John says, and it wasn't uncommon to have eight drinks or more before the end of the day. © 2017 npr

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23286 - Posted: 02.27.2017

By Christine Vestal NEW YORK — After a 12-year battle with debilitating abdominal conditions that forced her to stop working, marijuana has helped Lynn Sabulski feel well enough to look for a job. Sabulski is among nearly 14,000 patients in New York state who are certified to use medical marijuana for one of 10 ­conditions, including her ­primary diagnosis, inflammatory bowel disease. Marijuana doesn’t address her underlying disease, but it does relieve her painful symptoms. Nationwide, an estimated 1.4 million patients in 28 states and the District of Columbia use legal medical marijuana for a varying list of conditions. A much smaller number of patients in 16 states use limited extracts of the plant, primarily to treat seizure disorders. In the midst of an opioid crisis, some medical practitioners and researchers say they think that greater use of marijuana for pain relief could result in fewer people using the highly addictive prescription painkillers that led to the epidemic. A 2016 study by researchers at Johns Hopkins Bloomberg School of Public Health found that states with medical marijuana laws had 25 percent fewer opioid overdose deaths than states that do not have medical marijuana laws. And another study published in Health Affairs last year found that prescriptions for opioid painkillers such as OxyContin, Vicodin and Percocet paid for by Medicare dropped substantially in states that adopted medical marijuana laws. © 1996-2017 The Washington Post

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23285 - Posted: 02.27.2017

By Alice Klein The proof is in the packaging. Making all cigarette packets look the same reduces the positive feelings smokers associate with specific brands and encourages quitting, Australian research shows. The findings come ahead of the UK and Ireland introducing plain tobacco packaging in May. Australia was the first nation to introduce such legislation in December 2012. Since then, all cigarettes have been sold in plain olive packets with standard fonts and graphic health warnings. The primary goal was to make cigarettes less appealing so that people would not take up smoking in the first place. But an added bonus has been the number of existing smokers who have ditched the habit. Between 2010 and 2013, the proportion of daily smokers in Australia dropped from 15.1 to 12.8 per cent – a record decline. The number of calls to quit helplines also increased by 78 per cent after the policy change. Brand betrayal This drop in smoking popularity can be partly explained by a loss of brand affinity, says Hugh Webb at the Australian National University in Canberra. People derive a sense of belonging and identity from brands, he says. For example, you may see yourself as a “Mac person” or a “PC person” and feel connected to other people who choose that brand. “Marketers are extremely savvy about cultivating these brand identities.” © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 23271 - Posted: 02.24.2017

By WINNIE HU Ruth Brunn finally said yes to marijuana. She is 98. She pops a green pill filled with cannabis oil into her mouth with a sip of vitamin water. Then Ms. Brunn, who has neuropathy, settles back in her wheelchair and waits for the jabbing pain in her shoulders, arms and hands to ebb. “I don’t feel high or stoned,” she said. “All I know is I feel better when I take this.” Ms. Brunn will soon have company. The nursing home in New York City where she lives, the Hebrew Home at Riverdale, is taking the unusual step of helping its residents use medical marijuana under a new program to treat various illnesses with an alternative to prescription drugs. While the staff will not store or administer pot, residents are allowed to buy it from a dispensary, keep it in locked boxes in their rooms and take it on their own. From retirement communities to nursing homes, older Americans are increasingly turning to marijuana for relief from aches and pains. Many have embraced it as an alternative to powerful drugs like morphine, saying that marijuana is less addictive, with fewer side effects. For some people, it is a last resort when nothing else helps. Marijuana, which is banned by federal law, has been approved for medical use in 29 states, including New York, and the District of Columbia. Accumulating scientific evidence has shown its effectiveness in treating certain medical conditions. Among them: neuropathic pain, severe muscle spasms associated with multiple sclerosis, unintentional weight loss, and vomiting and nausea from chemotherapy. There have also been reports that pot has helped people with Alzheimer’s disease and other types of dementia as well as Parkinson’s disease. © 2017 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: 23255 - Posted: 02.20.2017

Jon Hamilton Researchers have created mice that appear impervious to the lure of cocaine. Even after the genetically engineered animals were given the drug repeatedly, they did not appear to crave it the way typical mice do, a team reports in Nature Neuroscience. "They didn't keep going into the room where they received the cocaine and they seemed to be just as happy exploring all around the cage," says Shernaz Bamji, a professor in the Department of Cellular and Physiological Sciences at the University of British Columbia in Vancouver. "Addiction is a form of learning," Bamji says. And somehow, these mice never learned to associate the pleasurable feelings produced by cocaine with the place where they received the drug. The result was startling because the scientists thought these mice would be especially susceptible to addiction. "We repeated the experiment several times to see if we had made a mistake," Bamji says. The reason for the team's surprise had to do with proteins that affect learning. The animals had been genetically engineered to produce high levels of proteins called cadherins in the brain's "reward circuit," which plays an important role in addiction. And genetic studies have suggested that people with high levels of cadherins are more susceptible to drug addiction. Cadherins act a bit like glue, binding cells together. Usually this glue enhances learning by strengthening the connections, or synapses, between brain cells. © 2017 npr

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: 23228 - Posted: 02.14.2017

By Abigail Zuger, M.D. It was in 2011 that the Centers for Disease Control first drew public attention to the ongoing nationwide opioid crisis. Much earnest commentary has explored the roots of this new killer epidemic since then, focusing on the broad highway between heroin and pain pills, and the online pharmacies, pill mills, and bad-apple doctors who fueled the two-way traffic and enabled catastrophe. Forgive me for rolling my eyes. Anyone with a prescription pad and a shred of common sense saw this whole thing coming down the pike decades ago, a speeding 18-wheeler, tires squealing, no brakes. Furthermore, it has long been clear that while the bad medical apples certainly did their share of damage, there is not a health policy guru or medical school dean in the country whose sins of omission and commission are not also partly responsible. Call it an epidemic of unconscious collusion or, as Dr. Anna Lembke bluntly states, a nation’s doctors “trapped in a system gone mad.” In less than 200 pages, this may be the most important medical book of the decade for finally getting the story of the opioid epidemic exactly right. As far as I am concerned, “Drug Dealer, M.D.,” in less than 200 unassuming, readable, and carefully referenced pages, may be the most important medical book of the decade for finally getting the story of this epidemic exactly right. And it’s not the medical bad apples Lembke is talking about in her title — it’s every doctor in the country. Copyright 2017 Undark

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 23218 - Posted: 02.13.2017

By KATHARINE Q. SEELYE and ABBY GOODNOUGH MANCHESTER, N.H. — Chad Diaz began using heroin when he was 12. Now 36 and newly covered by Medicaid under the Affordable Care Act, he is on Suboxone, a substitute opioid that eases withdrawal symptoms and cravings, and he is slowly pulling himself together. “This is the best my life has gone in many, many years,” Mr. Diaz, a big man wearing camouflage, said as he sat in a community health center here. If Congress and President Trump succeed in dismantling the Affordable Care Act, he will have no insurance to pay for his medication or counseling, and he fears he will slide back to heroin. “If this gets taken from me, it’s right back to Square 1,” he said. “And that’s not a good place. I’m scary when I’m using. I don’t care who I hurt.” As the debate over the fate of the health law intensifies, proponents have focused on the lifesaving care it has brought to people with cancer, diabetes and other physical illnesses. But the law has also had a profound, though perhaps less heralded, effect on mental health and addiction treatment, vastly expanding access to those services by designating them as “essential benefits” that must be covered through the A.C.A. marketplaces and expanded Medicaid. The Center on Budget and Policy Priorities, a left-leaning research group, calculates that 2.8 million people with substance use disorders, including 220,000 with opioid disorders, have coverage under the A.C.A. As the opioid epidemic continues to devastate communities nationwide, public health officials say the law has begun to make a critical difference in their ability to treat and rehabilitate people. © 2017 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: 23215 - Posted: 02.11.2017

By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist

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: 23203 - Posted: 02.09.2017

Hannah Devlin Science correspondent It sounds like torment for the smoker attempting to quit: handling packets of cigarettes and watching footage of people smoking, without being allowed to light up. However, scientists believe that lengthy exposure to environmental triggers for cravings could be precisely what smokers need to help them quit. The technique, known as extinction therapy, targets the harmful Pavlovian associations that drive addiction with the aim of rapidly “unlearning” them. The latest study, by scientists at the Medical University of South Carolina, found that after two one-hour sessions people smoked significantly fewer cigarettes one month after treatment compared to a control group. The study was not an unqualified success – many participants still relapsed after treatment – but the authors believe the work could pave the way for new approaches to treating addiction. Michael Saladin, the psychologist who led the work, said: “When I initially saw the results from this study it was pretty eye-opening.” In smokers, environmental triggers have typically been reinforced thousands of times so that the sight of a lighter, for instance, becomes inextricably linked to the rush of nicotine that the brain has learned will shortly follow. After quitting an addictive substance, these associations fade slowly over time, but people often flounder in the first days and weeks when cravings are most powerful. Saladin and others believe it is possible to fast-track this process in carefully designed training sessions, to help people over the initial hurdle. © 2017 Guardian News and Media Limited

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: 23187 - Posted: 02.04.2017

Elizabeth Eaton Electronic cigarettes may increase the risk of heart disease, researchers at UCLA report. The team found that two risk factors for heart disease were elevated in 16 e-cigarette users compared with 18 nonsmokers. “The pattern was spot-on” for what has been seen in heart attack patients and those with heart disease and diabetes, says cardiologist Holly Middlekauff, a coauthor of the study published online February 1 in JAMA Cardiology. But because the study only looked at a small number of people, the results are not definitive — just two or three patients can skew results, John Ambrose, a cardiologist with the University of California, San Francisco cautions. Plus, he says, some of the e-cigarette users in the study used to smoke tobacco, which may have influenced the data. Even so, Ambrose called the study interesting, noting that “the medical community just doesn’t have enough information” to figure out if e-cigarettes are dangerous. E-cigarette smokers in the study had heartbeat patterns that indicated high levels of adrenaline — also known as epinephrine — in the heart, a sign of heart disease risk. Researchers also found signs of increased oxidative stress, an imbalance of certain protective molecules that can cause the hardening and narrowing of arteries. © Society for Science & the Public 2000 - 2017.

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: 23180 - Posted: 02.02.2017

Meghan Rosen New X-ray crystallography images reveal how an LSD molecule gets trapped within a protein that senses serotonin, a key chemical messenger in the brain. The protein, called a serotonin receptor, belongs to a family of proteins involved in everything from perception to mood. The work is the first to decipher the structure of such a receptor bound to LSD, which gets snared in the protein for hours. That could explain why “acid trips” last so long, study coauthor Bryan Roth and colleagues report January 26 in Cell. It’s “the first snapshot of LSD in action,” he says. “Until now, we had no idea how it worked at the molecular level.” But the results might not be that relevant to people, warns Cornell University biophysicist Harel Weinstein. Roth’s group didn’t capture the main target of LSD, a serotonin receptor called 5-HT2A, instead imaging the related receptor 5-HT2B. That receptor is “important in rodents, but not that important in humans,” Weinstein says. Roth’s team has devoted decades to working on 5-HT2A, but the receptor has “thus far been impossible to crystallize,” he says. Predictions of 5-HT2A’s structure, though, are very similar to that of 5-HT2B, he says. LSD, or lysergic acid diethylamide, was first cooked up in a chemist’s lab in 1938. It was popular (and legal) for recreational use in the early 1960s, but the United States later banned the drug (also known as blotter, boomer, Purple Haze and electric Kool-Aid). |© Society for Science & the Public 2000 - 201

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: 23175 - Posted: 02.01.2017

By Roni Jacobson The psychedelic drug ibogaine is known for two things: its reputation in some circles as a panacea for addiction and the visceral hallucinations it induces. Positive anecdotes abound from people who have sought out the illegal drug at underground clinics. Just one dose, they say, brings near-instant relief from cravings and withdrawal symptoms, a veritable miracle for seemingly intractable addictions. But the side effects of this plant-derived substance can be dangerous or even deadly. Now, with encouraging evidence from animal studies, drugs are being developed to replicate ibogaine's impact on addiction without the side effects. A drug that is chemically related to ibogaine but lacks its hallucinogenic properties is set to begin phase II clinical trials in California early this year. If the results continue to be promising, addiction treatment as we know it could change radically. For decades research on ibogaine has been stymied by its classification as a Schedule I drug, the most tightly regulated category. Yet the results of animal studies have been intriguing. In May 2016 a meta-analysis examining 32 such studies, mostly in mice and rats, found that ibogaine reduced self-administration of cocaine, opioids and alcohol. An earlier study from 2015 found that noribogaine, the substance that ibogaine breaks down to when ingested, reduced self-administration of nicotine in addicted rats by 64 percent. Now Savant HWP, a pharmaceutical company in California, has developed a drug called 18-MC, a compound chemically related to ibogaine, which it hopes will produce the antiaddictive properties without triggering hallucinations. They are betting that the “trip” is not a necessary component of the therapy—an idea shared by some academics. © 2017 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: 23170 - Posted: 01.31.2017

By Andrew Joseph, Public health officials on Thursday said they had detected a bizarre cluster of cases in which patients in Massachusetts developed amnesia over the past few years — a highly unusual syndrome that could be connected to opioid use. The officials have identified only 14 cases so far. But officials said it’s possible that clinicians have simply missed other cases. The patients were all relatively young — they ranged in age from 19 to 52. Thirteen of the 14 patients identified had a substance use disorder, and the 14th patient tested positive for opioids and cocaine on a toxicology screen. “What we’re concerned about is maybe a contaminant or something else added to the drug might be triggering this,” said Dr. Alfred DeMaria, the state epidemiologist at the Massachusetts Department of Public Health and an author of the new report. “Traditionally there’s no evidence that the drugs themselves can do this.” The pattern emerged when Dr. Jed Barash, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., reported four of the amnesia cases to the state’s public health department. The department then sent out an alert to specialists, including neurologists and emergency physicians, asking about similar cases, ultimately identifying 10 more from 2012 to 2016 at hospitals in eastern Massachusetts. (The patients included one person who lived in New Hampshire and one person who was visiting Massachusetts from Washington state.) © 2017 Scientific American,

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: 23163 - Posted: 01.28.2017