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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

Laura Sanders For some people, fentanyl can be a life-saver, easing profound pain. But outside of a doctor’s office, the powerful opioid drug is also a covert killer. In the last several years, clandestine drugmakers have begun experimenting with this ingredient, baking it into drugs sold on the streets, most notably heroin. Fentanyl and closely related compounds have “literally invaded the entire heroin supply,” says medical toxicologist Lewis Nelson of New York University Langone Medical Center. Fentanyl is showing up in other drugs, too. In San Francisco’s Bay Area in March, high doses of fentanyl were laced into counterfeit versions of the pain pill Norco. In January, fentanyl was found in illegal pills sold as oxycodone in New Jersey. And in late 2015, fentanyl turned up in fake Xanax pills in California. This ubiquitous recipe-tinkering makes it impossible for users to know whether they’re about to take drugs mixed with fentanyl. And that uncertainty has proved deadly. Fentanyl-related deaths are rising sharply in multiple areas. National numbers are hard to come by, but in many regions around the United States, fentanyl-related fatalities have soared in recent years. Maryland is one of the hardest-hit states. From 2007 to 2012, the number of fentanyl-related deaths hovered around 30 per year. By 2015, that number had grown to 340. A similar rise is obvious in Connecticut, where in 2012, there were 14 fentanyl-related deaths. In 2015, that number was 188. |© Society for Science & the Public 2000 - 2016.

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: 22581 - Posted: 08.22.2016

By Robin Wylie Scientists have been searching for a genetic explanation for athletic ability for decades. So far their efforts have focused largely on genes related to physical attributes, such as muscular function and aerobic efficiency. But geneticists have also started to investigate the neurologicalbasis behind what makes someone excel in sports—and new findings implicate dopamine, a neurotransmitter responsible for the feelings of reward and pleasure. Dopamine is also involved in a host of other mental functions, including the ability to deal with stress and endure pain. Consequently, the new research supports the idea that the mental—not just the physical—is what sets elite athletes above the rest. In an effort to piece together what makes a great athlete great, researchers at the University of Parma in Italy collected DNA from 50 elite athletes (ones who had achieved top scores at an Olympic Games or other international competition) and 100 nonprofessional athletes (ones who played sports regularly, but below competitive level). They then compared four genes across the two groups that had previously been suggested as linked to athletic ability: one related to muscle development, one involved with transporting dopamine in the brain, another that regulates levels of cerebral serotonin and one involved in breaking down neurotransmitters. The researchers found a significant genetic difference between the two groups in only one of the genes: the one involved in transporting dopamine. Two particular variants of this gene (called the dopamine active transporter, or DAT) were significantly more common among the elite athletes than in the control group. One variant was almost five times more prevalent in the elite group (occurring in 24 percent of the elites versus 5 percent of the rest); the other variant was approximately 1.7 times more prevalent (51 percent versus 30 percent). The results were published in Journal of Biosciences. © 2016 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 22566 - Posted: 08.17.2016

Ramin Skibba Scientists and medical researchers in the United States have been studying the health benefits and risks of marijuana for decades. But despite the increasing availability of legal marijuana, scientists have been forced to obtain the drug from a single source — the University of Mississippi in Oxford, which grows pot for research on a campus farm under a contract with the National Institute on Drug Abuse (NIDA). Now, the university’s monopoly is coming to an end. In an unexpected move, the US Drug Enforcement Administration (DEA) announced on 11 August that it will allow any institution to apply for permission to grow marijuana for research. Nature explains how the policy could transform the study of marijuana. Why do researchers want to study pot — and how do they get it? Researchers have been extracting cannabinoids — chemical compounds found in cannabis — and developing strains of varying strength to test whether they could alleviate chronic pain and treat or mitigate the effects of ailments such as seizures and other neurological disorders. Approved medical-marijuana consumers may buy pot from dispensaries in more than half the country, and recreational marijuana use is permitted in a few states. But researchers are limited to the handful of strains grown by the University of Mississippi farm. © 2016 Macmillan Publishers 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: 22554 - Posted: 08.13.2016

By THE EDITORIAL BOARD Supporters of a saner marijuana policy scored a small victory this week when the Obama administration said it would authorize more institutions to grow marijuana for medical research. But the government passed up an opportunity to make a more significant change. The Drug Enforcement Administration on Thursday turned down two petitions — one from the governors of Rhode Island and Washington and the other from a resident of New Mexico — requesting that marijuana be removed from Schedule 1 of the Controlled Substances Act. Drugs on that list, which include heroin and LSD, are deemed to have no medical use; possession is illegal under federal law, and researchers have to jump through many hoops to obtain permission to study them and obtain samples to study. Having marijuana on that list is deeply misguided since many scientists and President Obama have said that it is no more dangerous than alcohol. Over the years, Congress and attorneys general have deferred to the expertise of the D.E.A., which is the part of the Justice Department that enforces the nation’s drug laws. So the D.E.A. has amassed extensive control over drug policy making. It determines who gets to grow marijuana for research and which scholars are allowed to study it, for example. It has strongly resisted efforts by scientists, state officials and federal lawmakers to reclassify marijuana by rejecting or refusing to acknowledge evidence that marijuana is not nearly as harmful as federal law treats it. Since 1968, the University of Mississippi has been the only institution allowed to grow the plant for research. This has severely limited availability. The D.E.A. now says that because researchers are increasingly interested in studying marijuana, it will permit more universities to grow the cannabis plant and supply it to researchers who have been approved to conduct studies on it. This should make it easier for researchers to obtain varieties of marijuana with varying concentrations of different compounds. © 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: 22553 - Posted: 08.13.2016

By CATHERINE SAINT LOUIS and MATT APUZZO The Obama administration is planning to remove a major roadblock to marijuana research, officials said Wednesday, potentially spurring broad scientific study of a drug that is being used to treat dozens of diseases in states across the nation despite little rigorous evidence of its effectiveness. The new policy is expected to sharply increase the supply of marijuana available to researchers. And in taking this step, the Obama administration is further relaxing the nation’s stance on marijuana. President Obama has said he views it as no more dangerous than alcohol, and the Justice Department has not stood in the way of states that have legalized the drug. For years, the University of Mississippi has been the only institution authorized to grow the drug for use in medical studies. This restriction has so limited the supply of marijuana federally approved for research purposes that scientists said it could often take years to obtain it and in some cases it was impossible to get. But soon the Drug Enforcement Administration will allow other universities to apply to grow marijuana, three government officials said. While 25 states have approved the medical use of marijuana for a growing list of conditions, including Parkinson’s, Crohn’s disease, Tourette’s syndrome, Alzheimer’s, lupus and rheumatoid arthritis, the research to back up many of those treatments is thin. The new policy could begin to change that. “It will create a supply of research-grade marijuana that is diverse, but more importantly, it will be competitive and you will have growers motivated to meet the demand of researchers,” said John Hudak, a senior fellow at the Brookings Institution. The new policy will be published as soon as Thursday in the federal register, according to the three officials, who have seen the policy but spoke on condition of anonymity because they were not authorized to discuss it. © 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: 22539 - Posted: 08.11.2016

By MARTHA C. WHITE A graphic 30-year-old drug education campaign from Partnership for a Drug-Free America is being updated. For a generation of commercial-watching adolescents, it was an indelible image: an egg, sizzling in a frying pan, representing “your brain on drugs.” It was a straightforward message, and the ad’s final line — “Any questions?” — asked as the egg white clouded and cooked, was strictly rhetorical. Three decades later, the Partnership for Drug-Free Kids (the group formerly known as the Partnership for a Drug-Free America) is bringing the frying pan out of retirement and firing up the stove again. But this time questions are the point. The group hopes it can tap into the nostalgia parents may have for the old frying egg ad while also letting them know their children do indeed want answers about drugs. “‘Any questions’ was the end. Now it’s the beginning,” said Scott Seymour, chief creative officer at BFG Communications, which created print and digital banner ads for the new campaign. “The landscape of drugs has really gotten a lot more complex, so we took this idea of having a succession of questions delivered by kids,” he said. The group drew on real inquiries from parents to develop the questions featured in the ads, which cover topics like prescription drugs and marijuana legalization. Children today feel empowered and entitled to ask questions about drugs, and parents are more willing to entertain those questions, observers say. “Because of parenting styles today, parents are engaged with their kids in a different way,” said Kristi Rowe, chief marketing officer at the Partnership for Drug-Free Kids. “They’re really stumped by the questions. They don’t know how to answer them.” © 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: 22524 - Posted: 08.08.2016

Tina Hesman Saey Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests. Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics. Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation. It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats. For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines. |© Society for Science & the Public 2000 - 2016.

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: 22521 - Posted: 08.06.2016

Janet Raloff Over the last three years, growing evidence has shown that electronic cigarettes are not the harmless alternative to smoking that many proponents have argued. Now, a new study traces a large share of e-cigs’ toxic gases to a heat-triggered breakdown of the liquids used to create the vapors. And the hotter an e-cig gets — and the more it’s used — the more toxic compounds it emits, the study shows. “There is this image that e-cigarettes are a lot better than regular cigarettes, if not harmless,” says Hugo Destaillats, a chemist at Lawrence Berkeley National Laboratory in California. But after his team’s new analyses, published July 27 in Environmental Science & Technology, “we are now definitely convinced that they are far from harmless.” Electronic cigarettes draw liquids over one or more hot metal coils to transform them into vapors. Those liquids — polyethylene glycol, glycerin or a mix of the two — are food-grade solvents laced with flavorings and usually nicotine. The Berkeley team used two current models of e-cigs and three different commercially available e-liquids. The experimental setup mechanically drew air through the devices to create the vapors that a user would normally inhale. Heating up The higher an e-cigarette’s voltage, the more toxic aldehydes it produces in each puff of vapor. Once a certain threshold is hit, each voltage increase produces a disproportionate increase (see last bar) in acrolein, acetaldehyde and formaldehyde, three of the most harmful compounds in the vapor. |© Society for Science & the Public 2000 - 2016

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: 22490 - Posted: 07.28.2016

By KATHARINE Q. SEELYE PORTLAND, Me. — A woman in her 30s was sitting in a car in a parking lot here last month, shooting up heroin, when she overdosed. Even after the men she was with injected her with naloxone, the drug that reverses opioid overdoses, she remained unconscious. They called 911. Firefighters arrived and administered oxygen to improve her breathing, but her skin had grown gray and her lips had turned blue. As she lay on the asphalt, the paramedics slipped a needle into her arm and injected another dose of naloxone. In a moment, her eyes popped open. Her pupils were pinpricks. She was woozy and disoriented, but eventually got her bearings as paramedics put her on a stretcher and whisked her to a hospital. Every day across the country, hundreds, if not thousands, of people who overdose on opioids are being brought back to life with naloxone. Hailed as a miracle drug by many, it carries no health risk; it cannot be abused and, if given mistakenly to someone who has not overdosed on opioids, does no harm. More likely, it saves a life. As a virulent opioid epidemic continues to ravage the country, with 78 people in the United States dying of overdoses every day, naloxone’s use has increasingly moved out of medical settings, where it has been available since the 1970s, and into the homes and hands of the general public. But naloxone, also known by the brand name Narcan, has also had unintended consequences. Critics say that it gives drug users a safety net, allowing them to take more risks as they seek higher highs. Indeed, many users overdose more than once, some multiple times, and each time, naloxone brings them back. © 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: 22481 - Posted: 07.27.2016

Ian Sample Science editor They were once considered merely lazy and adorable. But new research into the antics of the slow loris has revealed a wilder side to the docile creatures. Given the chance the innocent-eyed beasts will neck the most alcoholic drinks they can lay their paws on. The ability of the slow loris to seek out the most potent brew in reach was discovered by researchers in the US who wanted to know whether the animals favoured highly-fermented nectar over the less alcoholic forms secreted by plants in their natural habitats. As sugary nectar ferments in the wild, its calorie content rises, making it a potentially more valuable source of energy. In a series of tests with Dharma, an adult female slow loris, biologists at Dartmouth College in New Hampshire found that when presented with a choice of sugary solutions laced with different amounts of alcohol, the loris speedily settled on the most intoxicating. But while the animal was quickly drawn to the nectar substitutes, which contained between 1% and 4% alcohol, the slow loris displayed what the researchers describe as “a relative aversion to tap water”, which was used as a control. Dharma was not alone in her taste for drink. The scientists ran the same series of experiments with two nocturnal aye aye lemurs, a male called Merlin and a female called Morticia. Once again, the primates homed in on the most alcoholic of sugary solutions the researchers knocked up to mimic fermented nectar. © 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: 22460 - Posted: 07.20.2016

By Maia Szalavitz When a family member, spouse or other loved one develops an opioid addiction — whether to pain relievers like Vicodin or to heroin — few people know what to do. Faced with someone who appears to be driving heedlessly into the abyss, families often fight, freeze or flee, unable to figure out how to help. Families are sometimes overwhelmed with conflicting advice about what should come next. Much of the advice given by treatment groups and programs ignores what the data says in a similar way that anti-vaccination or climate skeptic websites ignore science. The addictions field is neither adequately regulated nor effectively overseen. There are no federal standards for counseling practices or rehab programs. In many states, becoming an addiction counselor doesn’t require a high school degree or any standardized training. “There’s nothing professional about it, and it’s not evidence-based,” said Dr. Mark Willenbring, the former director of treatment research at the National Institute on Alcohol Abuse and Alcoholism, who now runs a clinic that treats addictions. Consequently, families are often given guidance that bears no resemblance to what the research evidence shows — and patients are commonly subjected to treatment that is known to do harm. People who are treated as experts firmly proclaim that they know what they are doing, but often turn out to base their care entirely on their own personal and clinical experience, not data. “Celebrity Rehab with Dr. Drew,” which many people see as an example of the best care available, for instance, used an approach that is not known to be effective for opioid addiction. More than 13 percent of its participants died after treatment,1 mainly of overdoses that could potentially have been prevented with evidence-based care. Unethical practices such as taking kickbacks for patient referrals are also rampant.

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: 22458 - Posted: 07.20.2016

By SARAH MASLIN NIR Almost as soon as the young man crouching on a trash-strewed street in Brooklyn pulled out a crumpled dollar bill from his pocket and emptied its contents of dried leaves into a wrapper, he had company. A half-dozen disheveled men and women walked swiftly to where the young man was rolling a cigarette of a synthetic drug known as K2 to wait for a chance to share. The drug has been the source of an alarming and sudden surge in overdoses — over three days this week, 130 people across New York City were treated in hospital emergency rooms after overdosing on K2, almost equaling the total for the entire month of June, according to the city’s health department. About one-fourth of the overdoses, 33, took place on Tuesday along the border of Bedford-Stuyvesant and Bushwick, the same Brooklyn neighborhoods where, despite a heightened presence of police officers, people were again openly smoking the drug on Thursday. In response to the overdoses, the city is sending a health alert to emergency rooms and other health care providers warning about the drug. The outbreak comes after officials this spring lauded what they described as a successful campaign to severely curb the prevalence of K2. On Thursday, Gov. Andrew M. Cuomo announced that the State Police would step up enforcement against the drug and aggressively go after merchants who illegally sell it. The same day, just steps from where people were using the drug, clusters of police officers patrolled beneath the elevated subway tracks along a stretch where, the day before, five bodegas had been raided. K2 is typically sold by convenience stores, though the raids did not turn up any. © 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: 22448 - Posted: 07.16.2016

Suzi Gage Ketamine hydrochloride is a synthetic dissociative anaesthetic. It was first synthesized in the 1960s for medical use, and was first used medicinally during the Vietnam war. Recreationally, it is usually consumed by snorting a white crystalline powder, and at lower doses than when it’s used as an anaesthetic. However it can also be injected, or smoked. It is used in a club setting, but also as a psychedelic. Short term effects When ketamine is snorted, it gets in to the blood stream quickly, and intoxication effects occur soon after it’s taken. Although it’s an anaesthetic, at low doses it raises heart rate. It’s also associated with cognitive impairment during intoxication, including to speech and executive function. It can also induce mild psychedelic effects such as perceptual changes and psychotic-like experiences, which are appealing to some users, but can also be distressing. At slightly higher doses, users can experience a dissociative state, where their mind feels separated from their body. This can also manifest as a feeling of depersonalization. At higher doses, the anaesthetic quality of ketamine becomes more pronounced. People may find it difficult to move and may feel numb, and can experience more vivid hallucinations. This is sometimes called the ‘k-hole’ by users. Amnesia can occur at this level of use. This is a particular danger of using ketamine recreationally: users are vulnerable to assault from others in this state, or can put themselves in danger by not being aware of their surroundings (for example being unaware they are outside and it is cold can lead to hypothermia, or being unaware of surroundings could lead to walking in to traffic). © 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: 22436 - Posted: 07.14.2016