Links for Keyword: Drug Abuse

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 1442

By Greg Miller In the mid-19th century, some European doctors became fascinated with a plant-derived drug recently imported from India. Cannabis had been used as medicine for millennia in Asia, and physicians were keen to try it with their patients. No less an authority than Sir John Russell Reynolds, the house physician to Queen Victoria and later president of the Royal College of Physicians in London, extolled the medical virtues of cannabis in The Lancet in 1890. “In almost all painful maladies I have found Indian hemp by far the most useful of drugs,” Reynolds wrote. Like other doctors of his day, Reynolds thought cannabis might help reduce the need for opium-based painkillers, with their potential for abuse and overdose. “The bane of many opiates and sedatives is this, that the relief of the moment, the hour, or the day, is purchased at the expense of to-morrow’s misery,” he wrote. “In no one case to which I have administered Indian hemp, have I witnessed any such results.” More than 125 years later, the misery caused by opioids is clearer than ever, and there are new hints that cannabis could be a viable alternative. Some clinical studies suggest that the plant may have medical value, especially for difficult-to-treat pain conditions. The liberalization of marijuana laws in the United States has also allowed researchers to compare overdoses from painkiller prescriptions and opioids in states that permit medical marijuana versus those that don’t. Yet following up on those hints isn’t easy. Clinical studies face additional hurdles because the plant is listed on Schedule I, the U.S. Drug Enforcement Administration’s (DEA’s) list of the most dangerous drugs. © 2016 American Association for the Advancement of Science.

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: 22832 - Posted: 11.04.2016

Ian Sample Science editor The devastating impact of cigarette smoke on the body’s DNA has been laid bare by the first comprehensive study into the damage tobacco inflicts on human cells. People who smoke a pack of cigarettes each day for a year develop on average 150 extra mutations in every lung cell, and nearly 100 more mutations than usual in each cell of the voice box, researchers found. More still build up in the mouth, bladder, liver and other organs. While chemicals in tobacco smoke have long been known to raise the risk of at least 17 forms of cancer, the precise molecular mechanisms through which they mutate DNA and give rise to tumours in different tissues have never been clear. “This is about running down the root cause of cancers,” said David Phillips, a professor of environmental carcinogenesis at King’s College London and a co-author on the study. “By identifying the root causes, we gain the sort of knowledge we need to think more seriously about cancer prevention.” More than 70 of the 7,000 chemicals found in tobacco smoke are known to cause cancer. Some damage DNA directly, but others ramp up mutations in more subtle ways, often by disrupting the way cells function. The more mutations a cell acquires, the more likely it is to turn cancerous. © 2016 Guardian News and Media Limited

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: 22828 - Posted: 11.04.2016

By SABRINA TAVERNISE WASHINGTON — A decade after electronic cigarettes were introduced in the United States, use has flattened, sales have slowed and, this fall, NJoy, once one of the country’s biggest e-cigarette manufacturers, filed for bankruptcy. It is quite a reversal for an invention once billed as the biggest chance to end smoking as we know it and take aim at the country’s largest cause of preventable death. Use of the devices is slumping because they are not as good as cigarettes at giving a hit of nicotine. Dealing another strike against them, the country’s top public health authorities have sent an unwavering message: Vaping is dangerous. The warning is meant to stop people who have never smoked — particularly children — from starting to vape. But a growing number of scientists and policy makers say the relentless portrayal of e-cigarettes as a public health menace, however well intentioned, is a profound disservice to the 40 million American smokers who could benefit from the devices. Smoking kills more than 480,000 Americans a year. “We may well have missed, or are missing, the greatest opportunity in a century,” said David B. Abrams, senior scientist at the Truth Initiative, an antismoking group. “The unintended consequence is more lives are going to be lost.” American public health experts, led by the Centers for Disease Control and Prevention, have long been suspicious of e-cigarettes. The possible risks of vaping are vast, officials warn, including the potential to open a dangerous new door to addiction for youth. Scientists will not know the full effect for years, so for now, they caution, be wary. But mounting evidence suggests vaping is far less dangerous than smoking, a fact that is rarely pointed out to the American public. Britain, a country with about the same share of smokers, has come to the opposite conclusion from the United States. This year, a prestigious doctors’ organization told the public that e-cigarettes were 95 percent less harmful than cigarettes. British health officials are encouraging smokers to switch. © 2016 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: 22826 - Posted: 11.03.2016

By Laura Wright, Researchers have the clearest-ever picture of the receptor that gives humans the 'high' from marijuana, which could lead to a better understanding of how the drug affects humans. Scientists have long known that molecules from THC, the psychoactive component of marijuana, bind to and activate the receptor known as CB1. But now they know that it has a three-dimensional crystal structure. The authors of the paper, which was published Thursday in the journal Cell, say this information is crucial to improve our understanding of this receptor as marijuana use becomes widespread and, in many places, legalized. Now that they know the shape of the receptor, they can get a better idea of how different molecules bind to it, which is what causes reactions in humans. "What is important is to understand how different molecules bind to the receptor, how they control the receptor function, and how this can affect different people," said Raymond Stevens, co-author of the study. Dr. Mark Ware, the executive director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research at the Alan Edwards pain management unit at the McGill University Health Centre, called the discovery a "breakthrough." "Suddenly we've been given the design of the building," he explained. "We can work out ways to get in the building, we know where the windows and doors and stairs are, and we know kind of how the building is structured now." They both said that knowing the receptor's design can lead to better drug design. K2 synthetic pot It's also a key step to understanding the differences between natural cannabinoids, found in the marijuana plant, and synthetic cannabinoids, made in labs. ©2016 CBC/Radio-Canada.

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: 22776 - Posted: 10.22.2016

By DONNA DE LA CRUZ Some of the most troubling images of the opioid crisis involve parents buying or using drugs with their children in tow. Now new research offers a glimpse into the addicted brain, finding that the drugs appear to blunt a person’s natural parenting instincts. Researchers at the Perelman School of Medicine at the University of Pennsylvania scanned the brains of 47 men and women before and after they underwent treatment for opioid dependence. While in the scanner, the study subjects looked at various images of babies, and the researchers measured the brain’s response. The brain scans were compared with the responses of 25 healthy people. What the study subjects didn’t know was that the photos had been manipulated to adjust the “baby schema,” the term used to describe the set of facial and other features like round faces and big eyes that make our brains register babies as irresistible, kicking in our instinct to care for them. Sometimes the babies’ features were exaggerated to make them even more adorable; in others, the chubby cheeks and big eyes were reduced, making the faces less appealing. Studies show that a higher baby schema activates the part of the brain called the ventral striatum, a key component of the brain reward pathway. Compared with the brains of healthy people, the brains of people with opioid dependence didn’t produce strong responses to the cute baby pictures. But once the opioid-dependent people received a drug called naltrexone, which blocks the effects of opioids, their brains produced a more normal response. “When the participants were given an opioid blocker, their baby schema became more similar to that of healthy people,” said Dr. Daniel D. Langleben, one of the researchers. “The data also raised in question whether opioid medications may affect social cognition in general.” © 2016 The New York Times Company

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: 22760 - Posted: 10.15.2016

Lauren Silverman It's been a wild ride for kratom lately. Since Aug. 31, when the Drug Enforcement Administration announced its intention to classify the plant as a Schedule I substance, a group of kratom vendors filed a lawsuit against the government to block the move, angry advocates took to social media in protest and scientists questioned whether they would be able to continue kratom research. Now, the DEA is withdrawing its notice of intent to put kratom in the most restrictive category of controlled substances, with drugs like LSD and heroin. The DEA says it will instead open an official public comment period — to last until Dec. 1, 2016 — for people to share their experiences using kratom as a medical treatment. It has also requested that the Food and Drug Administration expedite scientific research. DEA spokesman Russ Baer says the DEA received more than 2,000 phone calls since August, mostly in opposition to the plan to classify kratom as Schedule I. "So in a spirit of transparency, and to open this up to public dialogue, we withdrew our notice to temporarily schedule kratom," Baer says. "We will then give full consideration to those comments before we move forward with any action." Kratom is derived from the leaves of a tree native to Southeast Asia. It is a relative of the coffee plant. According to David Kroll, a pharmacologist and medical writer, farmers and indigenous people have used it for hundreds of years as both a stimulant to increase work output and also as a way to relax. © 2016 npr

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: 22752 - Posted: 10.13.2016

By MIKE IVES HONG KONG — President Rodrigo Duterte of the Philippines was elected in May after pledging to kill 100,000 criminals in his first six months in office, vowing that fish in Manila, the capital, would grow fat from eating the bodies of drug dealers and other “do nothings.” In Mr. Duterte’s first three months as president, his bloody campaign led to the killing of about 1,400 drug suspects by the police and hundreds of others by extrajudicial means, according to official estimates. He has also publicly accused thousands of government officials of being involved in the drug trade, in some cases offering no evidence. The campaign has taken particular aim at people who use or sell shabu, a cheap form of methamphetamine that has caused grave health and social problems across the country. Mr. Duterte has likened shabu addicts to zombies and claimed — absent evidence — that many are “no longer viable for rehabilitation” because abusing the drug shrinks their brains. What is methamphetamine? Methamphetamine is an addictive stimulant that can be made from ephedrine and other readily available chemicals. It typically comes in either tablets, called yaba in parts of Asia, or crystalline form. The first variety is common in mainland Southeast Asia, and the second — known as shabu, ice or crystal meth, among other names — is more popular in the Philippines and many other countries. It also tends to be more potent and more deeply intertwined with international drug manufacturing and smuggling networks, according to a report by the United Nations Office on Drugs and Crime. How does the drug affect people who use it? Smoking, snorting, ingesting or injecting methamphetamine can cause aggression, memory loss and a range of other health complications, including heart attack or sudden death. Links between methamphetamine abuse and crime, disease transmission and other social problems have also been documented. A study by the RAND Corporation found that the effects of methamphetamine abuse, including the burden of addiction and treatment, cost the United States $23.4 billion in 2005. © 2016 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: 22751 - Posted: 10.13.2016

Ben Allen Louis Casanova is playing cards with a friend on the back deck of a recovery house in Philadelphia's northern suburbs. He's warm and open as he talks about his past few years. The guy everyone calls Louie started using drugs like Xanax and Valium during his freshman year of high school. At age 18, Casanova turned to heroin. About two years later, the rehab shuffle began. "I relapsed and then I was just getting high. And then I went to treatment again in February of 2015," he says. "Then I relapsed again and went back to treatment." He's 23 now. He's hurt people close to him and his criminal record, fueled by his drug addiction, is long. By Louie's count, he has been through eight inpatient rehabs. Louis says his stays have ranged from about 18 to 45 days. "I did 30 days, and after that I came here," he concludes, talking about his latest visit. A month's stay can be pretty typical among people who go to an inpatient facility. But why? "As far as I know, there's nothing magical about 28 days," says Kimberly Johnson, director of the Center for Substance Abuse Treatment at SAMHSA, the federal agency that studies treatment services. Anne Fletcher, author of the book Inside Rehab, agrees. "It certainly is not scientifically based," she says. "I live in Minnesota where the model was developed and a lot of treatment across the country really stemmed from that." She says the late Daniel Anderson was one of the primary architects of the "Minnesota model," which became the prevailing treatment protocol for addiction specialists. At a state hospital in Minnesota in the 1950s, Anderson saw alcoholics living in locked wards, leaving only to be put to work on a farm. © 2016 npr

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: 22719 - Posted: 10.02.2016

By MAIA SZALAVITZ Drug education is the only part of the middle school curriculum I remember — perhaps because it backfired so spectacularly. Before reaching today’s legal drinking age, I was shooting cocaine and heroin. I’ve since recovered from my addiction, and researchers now are trying to develop innovative prevention programs to help children at risk take a different road than I did. Developing a public antidrug program that really works has not been easy. Many of us grew up with antidrug programs like D.A.R.E. or the Nancy Reagan-inspired antidrug campaign “Just Say No.” But research shows those programs and others like them that depend on education and scare tactics were largely ineffective and did little to curb drug use by children at highest risk. But now a new antidrug program tested in Europe, Australia and Canada is showing promise. Called Preventure, the program, developed by Patricia Conrod, a professor of psychiatry at the University of Montreal, recognizes how a child’s temperament drives his or her risk for drug use — and that different traits create different pathways to addiction. Early trials show that personality testing can identify 90 percent of the highest risk children, targeting risky traits before they cause problems. Recognizing that most teenagers who try alcohol, cocaine, opioids or methamphetamine do not become addicted, they focus on what’s different about the minority who do. © 2016 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: 22715 - Posted: 09.30.2016

By Carl Hart In early August the Drug Enforcement Administration declined to reclassify marijuana under the federal Controlled Substances Act. The drug is currently listed on Schedule I, meaning that it is viewed as having “no currently accepted medical use in treatment” and is therefore technically banned by federal law. The proposed change would have moved it to Schedule II, where it would join morphine, opium and codeine. That would make marijuana potentially available by prescription nationwide. Such a change would have been good for patients and scientists, and it would have represented a big step toward resolving the hypocritical mess that characterizes current law. Despite many people's assumptions to the contrary, the existing law does not ban scientific investigation into the harms and benefits of the drug. It's true that scientists studying marijuana must jump through multiple bureaucratic and regulatory hoops, and one of these just became a bit easier to navigate. Currently researchers who want to study the drug must get it from the University of Mississippi, which is the only university now permitted to grow marijuana plants for research purposes. When the DEA announced in August that it would not reschedule marijuana, it did say that it would let other institutions apply for permission to start growing the plants as well. That was a step in the right direction—but it's not enough. Despite the regulatory barriers, dozens of scientists—myself included—have been engaged in research on the harms and benefits of marijuana for decades, and the evidence shows that the drug has many helpful therapeutic uses. For example, it stimulates appetite in HIV-positive patients, which could be a lifesaver for someone suffering from AIDS wasting syndrome. It is also useful in the treatment of neuropathic pain, chronic pain, and spasticity caused by multiple sclerosis. © 2016 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: 22710 - Posted: 09.30.2016

By Nick Purdon, Leonardo Palleja, CBC News If you met Lisa James, chances are you'd never guess she injects herself with heroin twice a day. She's a devoted mom to her daughter Tia, 24, who has a rare neurological disorder that causes tumours to grow on her spine and brain. She comforts Tia when she's overcome with nausea. She's by her side when she visits doctors. "My relationship with my daughter is better than it's ever been," says James, 48. But James says it wasn't so long ago, her days were spent doing absolutely anything to score heroin. She used to steal hundreds of dollars' worth of meat from grocery stores and sell it on the streets. She even stole from Tia. "I took $500 out of her account and because of the lovely girl that she is, she never wanted to make me feel bad," James says. "If someone had told me I would do something so despicable — I never would have believed it." She says that all changed when she was accepted to the Providence Crosstown Clinic in Vancouver's Downtown Eastside, where she's buzzed in every morning at 9 a.m. She sits down in a sterile room and injects a syringe full of free heroin into her arm. ©2016 CBC/Radio-Canada.

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: 22702 - Posted: 09.28.2016

Emma Yasinski Two often-overlooked medications might help millions of Americans who abuse alcohol to quit drinking or cut back. Public health officials, building on a push to treat people who abuse opioids with medications, want physicians to consider using medications to treat alcohol addiction. The drugs can be used in addition to or sometimes in place of peer-support programs, they say. "We want people to understand we think AA is wonderful, but there are other options," says George Koob, director of the National Institute of Alcohol Abuse and Alcoholism, a part of the federal National Institutes of Health. It is still rare for a person struggling with alcohol to hear that medication therapy exists. This partly reflects the tradition of treating addiction through 12-step programs. It's also a byproduct of limited promotion by the drugs' manufacturers and confusion among doctors about how to use them. A key study funded by the federal government reported last year that only 20 percent people who abuse alcohol will ever receive any form of treatment, which ranges from seeing a counselor or doctor to entering a specialized treatment program. The same is true for opioid addiction — about 80 percent of people dependent on opioids will never receive treatment. © 2016 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: 22698 - Posted: 09.27.2016

By NICHOLAS BAKALAR Ants, like people and rats, can become addicted to morphine. Scientists divided 90 ants into three groups. The first received a solution containing morphine and sugar, which was gradually reduced until the ants were receiving pure morphine. The second group of ants got a sugar solution gradually reduced to pure water, and the third ate just sugar. Then the researchers offered all three groups the choice of sugar or morphine. The ants that had been gradually deprived of sugar and those never exposed to morphine went right back to sugar. But about two-thirds of the ants given morphine chose it over sugar. Ants are the first nonmammal to display drug-seeking behavior, the researchers said. © 2016 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: 22697 - Posted: 09.27.2016

By Mallory Locklear Men and women show different patterns of drug abuse, with women becoming addicted to some substances much more quickly. Now a study in rats has found that sex hormones can reduce opioid abuse. From studies of other drugs, such as cocaine and alcohol, we know that women are less likely to use these substances than men, but become addicted faster when they do. “There are a lot of data to indicate that women transition from that initial use to having a substance-use disorder much more rapidly,” says Mark Smith, a psychologist at Davidson College, North Carolina. Once addicted, women also seem to have stronger drug cravings. Tracking drug use throughout women’s menstrual cycles suggests that both these differences could be shaped by hormones – with more intense cravings and greater euphoria at particular times in the cycle, says Smith. Craving crash Now Smith’s team has investigated the effects of hormones on opioid addiction in rats. Their findings suggest that hormones such as oestrogen and progesterone may help women to kick the habit. The researchers allowed female rats to self-administer heroin, and measured how much they chose to take at different times in their oestrous cycle – a regular sequence of hormone fluctuations similar to those seen in the menstrual cycle in women. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 22685 - Posted: 09.23.2016

By Andy Coghlan You made a choice and it didn’t turn out too well. How will your brain ensure you do better next time? It seems there’s a hub in the brain that doles out rewards and punishments to reinforce vital survival skills. “Imagine you go to a restaurant hoping to have a good dinner,” says Bo Li of Cold Spring Harbor Laboratory in New York. “If the food exceeds your expectations, you will likely come back again, whereas you will avoid it in future if the food disappoints.” Li’s team has discovered that a part of the brain’s basal ganglia area, called the habenula-projecting globus pallidus (GPh), plays a crucial role in this process. They trained mice to associate specific sound cues either with a reward of a drink of water or a punishment of a puff of air in the face, and then surprised them by switching them around. When mice expecting a drink were instead punished with a puff of air, GPh neurons became particularly active. But when the mice were unexpectedly rewarded, the activity of these neurons was inhibited. Further experiments revealed that once activated GPh neurons enforce punishment in the brain, reducing levels of the reward chemical dopamine in regions of the brain that plan actions. © 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: 22681 - Posted: 09.22.2016

Martha Bebinger Five states are voting this fall on whether marijuana should be legal, like alcohol, for recreational use. That has sparked questions about what we know – and don't know – about marijuana's effect on the brain. Research is scarce. The U.S. Drug Enforcement Agency classifies marijuana as a Schedule I drug. That classification puts up barriers to conducting research on it, including a cumbersome DEA approval application and a requirement that scientists procure very specific marijuana plants. One long-term study in New Zealand compared the IQs of people at age 13 and then through adolescence and adulthood to age 38. Those who used pot heavily from adolescence onward showed an average 8 percent drop in IQ. People who never smoked, by contrast, showed slightly increased IQ. Critics pounced on the study, which was published in 2012, because it didn't adjust for many other things that affect IQ such as home life or family income. And there's no proof the IQ differences are due to pot. One of those critics, Nicholas Jackson, now a senior statistician at the University of California, Los Angeles, wondered what would happen if he could rule out some of those elements by comparing twins. "Individuals that share the same genes, grew up in the same household, where the difference between them was that one of the twins was using marijuana and one was not," Jackson says. © 2016 npr

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: 22648 - Posted: 09.13.2016

By Bob Grant Lab rats that compulsively drink are cured of their addiction by a drug that silences neural networks that strengthened as they became dependent on alcohol.FLICKR, SARAH LAVAL Alcohol dependence involves neural reward networks that are strengthened by the regular consumption of alcohol. Using rat models of compulsive drinking, researchers at The Scripps Research Institute (TSRI) have now shown that they can interfere with those specific networks to curb the behavior. They reported their findings last week (September 7) in The Journal of Neuroscience. “We can completely reverse alcohol dependence by targeting a network of neurons,” coauthor Olivier George, a TSRI neuroscientist, said in a statement. “It is very challenging to target such a small population of neurons in the brain, but this study helps to increase our knowledge of a part of the brain that is still a mystery,” added coauthor and TSRI postdoc Giordano de Guglielmo. The researchers used a drug called Daun02 to shut down a specific group of neurons in the amygdalas of rats that drank compulsively. The treated rats stopped imbibing as much, and this behavioral change lasted for several days. “With classic pharmacology we usually observe a 20-40 percent decrease in drinking because the individuals are highly dependent (we model heavy alcoholism),” George told Medical News Today. “Instead, here, the drinking went all the way back down to normal drinking, and without noticeable side effects; very unusual. And, usually, to have long lasting effects like that, you need daily treatment, not a single one; it shows that we might have found alcoholism's Achilles' heel.” © 1986-2016 The Scientist

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: 22647 - Posted: 09.13.2016

By JACK HEALY CINCINNATI — On the day he almost died, John Hatmaker bought a packet of Oreos and some ruby-red Swedish Fish at the corner store for his 5-year-old son. He was walking home when he spotted a man who used to sell him heroin. Mr. Hatmaker, 29, had overdosed seven times in the four years he had been addicted to pain pills and heroin. But he hoped he was past all that. He had planned to spend that Saturday afternoon, Aug. 27, showing his son the motorcycles and enjoying the music at a prayer rally for Hope Over Heroin in this region stricken by soaring rates of drug overdoses and opioid deaths. But first, he decided as he palmed a sample folded into a square of paper, he would snort this. As he crumpled to the sidewalk, Mr. Hatmaker became one of more than 200 people to overdose in the Cincinnati area in the past two weeks, leaving three people dead in what the officials here called an unprecedented spike. Similar increases in overdoses have rippled recently through Indiana, Kentucky and West Virginia, overwhelming ambulance crews and emergency rooms and stunning some antidrug advocates. Addiction specialists said the sharp increases in overdoses were a grim symptom of America’s heroin epidemic, and of the growing prevalence of powerful synthetic opiates like fentanyl. The synthetics are often mixed into batches of heroin, or sprinkled into mixtures of caffeine, antihistamines and other fillers. In Cincinnati, some medical and law enforcement officials said they believed the overdoses were largely caused by a synthetic drug called carfentanil, an animal tranquilizer used on livestock and elephants with no practical uses for humans. Fentanyl can be 50 times stronger than heroin, and carfentanil is as much as 100 times more potent than fentanyl. Experts said an amount smaller than a snowflake could kill a person. © 2016 The New York Times Company

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: 22637 - Posted: 09.07.2016

By Laurie McGinley The Food and Drug Administration, alarmed that increasing numbers of Americans are combining opioid painkillers and benzodiazepines, said Wednesday that it will require tough new warnings on the product labels that spell out the serious dangers of mixing the drugs. The agency said it will require “boxed warnings” — its strongest category — on 389 separate products and will mandate the warning on opioid-containing cough medications. The new language will list the hazards of using the medications in tandem, which include extreme sleepiness, respiratory depression, coma and even death. The agency noted that the misuse of opioids, powerful pain medications such as prescription oxycodone, hydrocodone and morphine, has “increased significantly” in the United States over the past two decades. Benzodiazepines are used to treat anxiety, insomnia and seizure disorders. Both classes of drugs depress the central nervous system and together can raise the risk of adverse outcomes. FDA officials said the number of patients prescribed both an opioid and a benzodiazepine increased by 41 percent — about 2.5 million people — between 2002 and 2014. From 2004 to 2011, the rate of emergency-department visits involving the non-medical use of both drug classes increased significantly and overdose deaths nearly tripled, the FDA said.

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: The Biology of Behavioral Disorders
Link ID: 22620 - Posted: 09.01.2016

Neuroscience News Researchers have identified a brain mechanism that could be a drug target to help prevent tolerance and addiction to opioid pain medication, such as morphine, according to a study by Georgia State University and Emory University. The findings, published in the Nature journal Neuropsychopharmacology in August, show for the first time that morphine tolerance is due to an inflammatory response produced in the brain. This brain inflammation is caused by the release of cytokines, chemical messengers in the body that trigger an immune response, similar to a viral infection. Researchers’ results show blocking a particular cytokine eliminated morphine tolerance, and they were able to reduce the dose of morphine required to alleviate pain by half. “These results have important clinical implications for the treatment of pain and also addiction,” said Lori Eidson, lead author and a graduate student in the laboratory of Dr. Anne Murphy in the Neuroscience Institute of Georgia State. “Until now, the precise underlying mechanism for opioid tolerance and its prevention have remained unknown.” Over 67 percent of the United States population will experience chronic pain at some point in their lives. Morphine is the primary drug used to manage severe and chronic pain, with 3 to 4 percent of adults in the U.S. receiving long-term opioid therapy. However, tolerance to morphine, defined as a decrease in pain relief over time, significantly impedes treatment for about 60 percent of patients. Long-term treatment with opioids is associated with increased risk of abuse, dependence and fatal overdoses.

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: 22596 - Posted: 08.24.2016