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by Sara Reardon, New Orleans, Louisiana Does beer make you shlur your wordsh? You're not alone: drunk zebra finches (Taeniopygia guttata) sing songs that are blurrier and more disordered than those of their sober counterparts. What's more, binge drinking may permanently impair juvenile finches' ability to learn new songs – which could have implications for our understanding of the effect of heavy drinking on adolescents. Having a unique and interesting song is important for zebra finches to mate, and each male develops his own signature tune as he matures, says Christopher Olson of Oregon Health and Science University in Portland. Because zebra finch song is so well studied, Olson and colleagues decided to find out how alcohol would affect it. First, they had to find out whether finches are even interested in alcohol. When they gave a group of adult finches 6 per cent ethanol in their water bottles, the birds drank enough of it that their blood alcohol content sometimes reached 0.8 per cent: the legal limit for drivers in many places. The birds were also happy to sing while drunk. Using audio analysis software, the researchers determined the degree of "white noise", or disorganised sounds, in their songs. The drunk birds' songs were significantly more broken and disorganised. "It's their husky bar voice," says Olson. © Copyright Reed Business Information Ltd.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Language and Our Divided Brain
Link ID: 17383 - Posted: 10.18.2012
Cort Pedersen at the University of North Carolina at Chapel Hill and his team gave 11 alcohol-dependent volunteers two daily doses of an oxytocin nasal spray or a placebo, during the first three days of a detox programme. The volunteers also received lorazepam - a detox drug - when their withdrawal symptoms reached a specific level. The oxytocin group had fewer alcohol cravings and milder withdrawal symptoms than the placebo group, and used just one-fifth of the lorazepam (Alcoholism: Clinical and Experimental Research, doi.org/jgp). "Four [oxytocin] volunteers didn't need any lorazepam at all," says Pedersen. This is good news because lorazepam is highly addictive. While it reduces anxiety and seizures during alcohol withdrawal, users can experience insomnia and cravings when they come off the drug. Although it is unclear how oxytocin - famed for its role in social bondingMovie Camera - helps to aid withdrawal, it has no known side effects. Pedersen hopes that alcoholics who take the hormone will therefore be less likely to experience the unpleasant symptoms that can lead to relapse. © Copyright Reed Business Information Ltd.
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17362 - Posted: 10.13.2012
By NORIMITSU ONISHI LOS ANGELES — One year after federal law enforcement officials began cracking down on California’s medical marijuana industry with a series of high-profile arrests around the state, they finally moved into Los Angeles last month, giving 71 dispensaries until Tuesday to shut down. At the same time, because of a well-organized push by a new coalition of medical marijuana supporters, the City Council last week repealed a ban on the dispensaries that it had passed only a couple of months earlier. Despite years of trying fruitlessly to regulate medical marijuana, California again finds itself in a marijuana-laced chaos over a booming and divisive industry. Nobody even knows how many medical marijuana dispensaries are in Los Angeles. Estimates range from 500 to more than 1,000. The only certainty, supporters and opponents agree, is that they far outnumber Starbucks. “That’s the ongoing, ‘Alice in Wonderland’ circus of L.A.,” said Michael Larsen, president of the Neighborhood Council in Eagle Rock, a middle-class community that has 15 dispensaries within a one-and-a-half-mile radius of the main commercial area, many of them near houses. “People here are desperate, and there’s nothing they can do.” Though the neighborhood’s dispensaries were among those ordered to close by Tuesday, many are still operating. As he looked at a young man who bounded out of the Together for Change dispensary on Thursday morning, Mr. Larsen said, “I’m going to go out on a limb, but that’s not a cancer patient.” In the biggest push against medical marijuana since California legalized it in 1996, the federal authorities have shut at least 600 dispensaries statewide since last October. California’s four United States attorneys said the dispensaries violated not only federal law, which considers all possession and distribution of marijuana to be illegal, but state law, which requires operators to be nonprofit primary caregivers to their patients and to distribute marijuana strictly for medical purposes. © 2012 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17343 - Posted: 10.08.2012
By Ashutosh Jogalekar In a previous post I described the benefits and enduring value of Small Science. I emphasized the fact that in the current economy and funding environment, Small Science is likely to be consistent while Big Science happens in fits and starts. And I talked about how crowdsourcing and crowdfunding could bring great value to both Big and Small Science. Now I want to describe a crowd funded Small Science project that could prove very valuable in understanding the root causes of one of the most pernicious scourges of our time – methamphetamine addiction. Ethan Perlstein at Princeton and David Sulzer at Columbia are interested in dissecting the different ways in which meth acts in and on the brain and they have taken the bold step of pitching this as a crowdfunding project. Their project and others like it could not only help us develop new treatments for meth addition but they could address a more general and key question; how do psychotropic drugs work? It turns out that in spite of the legions of psychiatrists prescribing a record number of antidepressants and other medications every year, we still don’t have a good idea how these compounds work. The same lack of understanding permeates our efforts in tackling the addiction epidemic. From a chemical standpoint the simplicity of psychotropic drugs like meth and PCP is breathtaking. The fact that a few carbon, hydrogen, oxygen and nitrogen atoms arranged in and around a simple ring can cause such profound behavioral changes in human beings continues to beguile and fascinate us. Sadly, our knowledge of the mechanism of action of these molecules as well as legal psychotropic drugs has reached a kind of roadblock. © 2012 Scientific American
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17339 - Posted: 10.06.2012
By LISA SANDERS, M.D. On Thursday, we challenged Well readers to try their hand at solving the case of a comatose young woman dropped off at the emergency room by her friends after attending a concert the previous night. More than 350 people wrote in, and more than 90 of you were able to figure it out. The Correct Diagnosis Is … … Ecstasy-induced hyponatremia. Over the past 20 years there have been many reports of young people, mostly young women, who have had seizures or become unconscious after taking the illegal drug Ecstasy, also known as MDMA. The cause is a dangerously low level of sodium in the bloodstream. The brain is exquisitely sensitive to the exact right balance of sodium and water, and when they are out of whack, nausea, confusion and seizures can follow. It’s a rare but dangerous side effect of the drug. Nearly one in five patients reported to have this complication died. Others had permanent brain damage. When this complication was first observed, it was thought to be because of an overconsumption of water. The drug was used widely at concerts or “raves,” and attendees were told to drink lots of water to replace what was sweated out in the crowded, hot concert and dance floors. Further research revealed that the drug actually alters the way the brain and the kidney work so that the body holds on to water and dumps sodium. This change is exaggerated by the presence of estrogen, so women are far more likely to be affected than men. Why the drug can have this effect on any given individual is not well understood, but it is clear that it is not because of an overdose or a contaminant. It appears to be a response to the drug itself. Copyright 2012 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of Internal States
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 17338 - Posted: 10.06.2012
By PAUL CHRISTOPHER, M.D. “I’m addicted to painkillers,” J., a thickset construction worker, told me on a recent afternoon in the emergency room, his wife at his side. Two years before, after months of pain, stiffness and swelling in his hands and neck, his primary physician had diagnosed rheumatoid arthritis and had prescribed three medications: two to slow the disease and one, oxycodone, for pain. Bolstered by the painkiller, J. had felt more limber and energetic than he had in years. “I could finally keep up with the other guys,” he told me. He worked harder, and his pain worsened. His primary physician increased the oxycodone dose. Soon, J. was looking forward more to the buzz than to the relief the pills brought. He went to see two other physicians who, unaware that he was double-dipping, prescribed similar medications. When a co-worker offered to sell him painkillers directly, J.’s use spiraled out of control. By the time I saw him, he was taking dozens of pills a day, often crushing and snorting them to speed the onset of his high. With remarkable candor, he described how the drugs had marred every facet of his life — from days of missed work to increasing debt, deteriorating health and marital strain. But when I listed the treatment options that might help, J. shook his head, looked from me to his wife, and got up. “I’m all set,” he said, holding up his hands. Then he walked out of the room. Despair fell on his wife’s face. “Please,” she said, grabbing my arm, “you can’t let him leave.” Copyright 2012 The New York Times Company
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17327 - Posted: 10.03.2012
By Laura Sanders A dose of Ritalin makes healthy women more reckless in a gambling game. After taking the stimulant, participants in an experiment shifted their betting strategy and kept playing even when faced with stakes too high for most folks. Though solid numbers are scarce, evidence suggests that many healthy people turn to Ritalin (also known as methylphenidate) and other stimulants to boost mental capacity. Some college students, for instance, rely on these “smart pills” to focus attention in cram sessions before tests. The new results, published in the Sept. 19 Journal of Neuroscience, suggest that the drugs might have unanticipated consequences for these people, says study coauthor Daniel Campbell-Meiklejohn of New York University. Scientists have known that the very same drug has an opposite effect in people with attention deficit hyperactivity disorder and a kind of dementia, normalizing these people’s risky behavior. Scientists can’t yet explain Ritalin’s divergent effects, but they suspect that variations in how the brain handles the chemical messenger dopamine may be involved. Researchers enlisted 40 healthy women to take either Ritalin or a placebo, and later play a gambling game. The game was rigged so that the players would quickly rack up a loss and then have to choose whether to double-down in the hopes of recovering their money. “That’s the sad part of the game,” says Campbell-Meiklejohn, who conducted the study while at Aarhus University in Denmark. “You really can’t win.” © Society for Science & the Public 2000 - 2012
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17275 - Posted: 09.19.2012
2012 by Graham Lawton My usual pick-me-up on a Monday morning is a cup of coffee. Today it's going to be something very different. I've been up since 6 am. I've had a breath test for alcohol, a urine test for drugs and a psychological test for mental health. Then I'm handed a red pill and a glass of water. I swallow it… and I'm told to relax. Which is easier said than done when you don't know if you've just taken vitamin C or 83 milligrams of pure MDMA. Half an hour later I'm inside an fMRI brain scanner, my head clamped in place and a visor over my face. It's noisy and claustrophobic but I'm reassured by the panic button in my hand and a voice from the control room. And then I start to feel it. A tingle of energy, like pins and needles, starts in the pit of my stomach and rises slowly, not unpleasant but not exactly pleasurable either. It builds in intensity, then breaks into a wave of bliss. The placebo effect can be powerful but when it happens again, I'm in no doubt. I'm coming up. I'm taking part in a groundbreaking study on MDMA, the drug commonly known as ecstasy. The research is run by David Nutt of Imperial College London, a former government adviser and one of the few UK researchers licensed to study class-A drugsMovie Camera. His main aim is to discover what MDMA does to the human brain, something that, remarkably, has never been done before. A second goal is to study MDMA as a therapy for post-traumatic stress disorder. © Copyright Reed Business Information Ltd
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 17274 - Posted: 09.19.2012
by Hannah Krakauer The downside to cannabis use has been made clearer. The most detailed study yet of the drug's long-term effects shows that those who start a weed habit as teens enter middle age with an 8-point deficit in IQ compared to non-users. Evidence is growing that cannabis-based drugs can benefit health, but suspicions remain that persistent cannabis use from an early age can have a detrimental effect on cognition. Confirming those suspicions is tricky, though, since cognitive impairment observed later in life could have been present before the drug was first used. To get around the problem Madeline Meier at Duke University in Durham, North Carolina, and her colleagues have taken the long view. They used a detailed health study which followed 1000 people in Dunedin, New Zealand, from birth until age 38. The data allowed them to compare IQ tests taken by the participants at age 13 – before any of them began using cannabis – with the same participants' IQ scores as adults, in some cases after years of cannabis use. The study showed that those who developed the most persistent dependence on the drug showed the greatest subsequent decline in IQ, losing 6 points on average regardless of how early the habit began. Within that group, those who began taking the drug before their 18th birthday saw a subsequent decline in IQ of 8 points, on average. © Copyright Reed Business Information Ltd.
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17209 - Posted: 08.28.2012
By Bruce Bower All too often, high school students have to decide whether to join in on gulping down booze with the cool kids or lighting up a cigarette with parking-lot rebels. A new study suggests that genetics plays a role in the likelihood that some teens will succumb to this kind of peer pressure. Adolescents generally report drinking and smoking a lot in schools with high levels of such behavior, and doing so relatively infrequently in schools with low levels of substance use. These trends were stronger in teens with two copies of a short version of a gene called 5HTT than peers with two long versions, sociologist Jonathan Daw of the University of Colorado Boulder reported August 18 at the American Sociological Association’s annual meeting in Denver. Teens who had inherited one long and one short gene reported rates of alcohol and cigarette use that fell in between those of the other two groups, regardless of how much substance use occurred at their schools, Daw and his colleagues found. The 5HTT gene helps regulate transmission of serotonin, a chemical messenger in the brain. Daw’s team likens teens with the two short versions of the gene to social chameleons, more likely to conform to smoking and drinking styles of students around them than teens with one or no short variants. “Our data suggest that, alongside many other influences on adolescent substance use, genetics partly underlie individuals’ susceptibility to peer smoking and drinking,” Daw says. © Society for Science & the Public 2000 - 2012
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17189 - Posted: 08.22.2012
By Scicurious Or not. I so want to like press releases. But I got this press release: “SCIENTISTS CAN NOW BLOCK HEROIN, MORPHINE ADDICTION” And I got the paper along with it. As I read the paper, my head slowly hit the desk. And hit it again, and again, as I compared the press release to the paper and prepared to write this post. I will have a lovely little round bruise now. But let’s get the big questions out of the way first: 1. Is this paper good? Oh yes! Really neat! Cool new mechanism! 2. Does it “block” heroin addiction? No. This press release hurts us precious. It hurts us. This paper has a lot of GREAT things about it, and there’s a lot of potential for the future with a new mechanism for drug action, especially in the area of pain relief (which sadly got short shrift in the press release). But no one has cured addiction yet. © 2012 Scientific American
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17171 - Posted: 08.16.2012
by Kai Kupferschmidt Tabloid journalists have long known that you can discover dirty secrets by going through people's garbage. Now, researchers have done something similar in the name of science, albeit on a grander—and smellier—scale. They have analyzed the sewage of 19 European cities to find out how much of certain illicit drugs people in those cities consume. "The technique needs further work and validation, but this paper shows that it is a feasible approach for estimating drug use on a large scale," says Fritz Sörgel, head of the Institute for Biomedical and Pharmaceutical Research in Nuremberg, Germany, who was not involved in the work. To put figures on illicit drug use, researchers routinely use surveys, supplemented by data from police and customs. But they have been pushing for more accurate and objective methods to estimate the amounts consumed. One possibility is to sample the sewage of a city and look for chemical traces of the drugs themselves or metabolites created when a drug passes through the human body. "The surveys tell you what people take, but not how much, not how big the market is," says Kevin Thomas, a toxicologist at the Norwegian Institute for Water Research in Oslo and one of the authors of the new paper. "Sewage tells you that." During one week in March 2011, Thomas and colleagues collected daily samples representing 24 hours of sewage flow from 21 sewage treatment plants in 19 cities across Europe—from Antwerp to Zagreb. The samples were analyzed for traces of five different drugs by local labs according to a fixed protocol. © 2010 American Association for the Advancement of Science.
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17104 - Posted: 07.30.2012
By Laura Sanders Light use of the club drug Ecstasy may cause subtle memory deficits. People who popped just three Ecstasy tablets a month over the course of a year saw their memory slip on a laboratory test, scientists report online July 25 in Addiction. The new results offer some of the best evidence yet that the drug can change the brain, says psychiatric neuroscientist Ronald Cowan of Vanderbilt University Medical Center in Nashville. “It’s been very, very difficult to convince people that there’s a causative effect of the drug,” he says. “This adds strong evidence to that.” Scientists debate whether Ecstasy, a drug that brings euphoria, boundless energy and heightened sensory experiences, can actually harm the brain in part by screwing with cells that produce the chemical messenger serotonin. Past studies have been notoriously hard to interpret because brain differences seen between Ecstasy users and nonusers could have existed long before the drug use began. And people who use Ecstasy frequently tend to use other drugs too, making it hard to tease out Ecstasy’s effect. For the study, Daniel Wagner of the University of Cologne in Germany and his colleagues wanted to catch people as they started using Ecstasy. The team recruited 149 people who had used Ecstasy five or fewer times and ran the subjects through a battery of brain tests looking for signs of mental deficits. One year later, the team retested 43 people who had not used Ecstasy since being recruited, and 23 who had used 10 or more Ecstasy pills in that time. These people reported using an average of 33.6 tablets. © Society for Science & the Public 2000 - 2012
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17096 - Posted: 07.28.2012
Most children exposed to high levels of alcohol in the womb do not develop the distinct facial features seen in fetal alcohol syndrome, but instead show signs of abnormal intellectual or behavioral development, according to a study by researchers at the National Institutes of Health and researchers in Chile. These abnormalities of the nervous system involved language delays, hyperactivity, attention deficits or intellectual delays. The researchers used the term s functional neurologic impairment to describe these abnormalities. The study authors documented an abnormality in one of these areas in about 44 percent of children whose mothers drank four or more drinks per day during pregnancy. In contrast, abnormal facial features were present in about 17 percent of alcohol exposed children. Fetal alcohol syndrome refers to a pattern of birth defects found in children of mothers who consumed alcohol during pregnancy. These involve a characteristic pattern of facial abnormalities, growth retardation, and brain damage. Neurological and physical differences seen in children exposed to alcohol prenatally — but who do not have the full pattern of birth defects seen in fetal alcohol syndrome — are classified as fetal alcohol spectrum disorders. “Our concern is that in the absence of the distinctive facial features, health care providers evaluating children with any of these functional neurological impairments might miss their history of fetal alcohol exposure,” said Devon Kuehn, M.D., of the Epidemiology Branch of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH institute involved in the study. “As a result, children might not be referred for appropriate treatment and services.” Their findings appear online in Alcoholism: Clinical and Experimental Research.
Related chapters from BP6e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17082 - Posted: 07.24.2012
By Ruth Williams Until recently, most scientists believed that neurons were the all-important brain cells controlling mental functions and that the surrounding glial cells were little more than neuron supporters and “glue.” Now research published in March in Cell reveals that astrocytes, a type of glia, have a principal role in working memory. And the scientists made the discovery by getting mice stoned. Marijuana impairs working memory—the short-term memory we use to hold on to and process thoughts. Think of the classic stoner who, midsentence, forgets the point he was making. Although such stupor might give recreational users the giggles, people using the drug for medical reasons might prefer to maintain their cognitive capacity. To study how marijuana impairs working memory, Giovanni Marsicano of the University of Bordeaux in France and his colleagues removed cannabinoid receptors—proteins that respond to marijuana's psychoactive ingredient THC—from neurons in mice. These mice, it turned out, were just as forgetful as regular mice when given THC: they were equally poor at memorizing the position of a hidden platform in a water pool. When the receptors were removed from astrocytes, however, the mice could find the platform just fine while on THC. The results suggest that the role of glia in mental activity has been overlooked. Although research in recent years has revealed that glia are implicated in many unconscious processes and diseases, this is one of the first studies to suggest that glia play a key role in conscious thought. “It's very likely that astrocytes have many more functions than we thought,” Marsicano says. “Certainly their role in cognition is now being revealed.” © 2012 Scientific American,
Related chapters from BP6e: Chapter 17: Learning and Memory; Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17039 - Posted: 07.14.2012
Many people who abused the painkiller OxyContin by inhaling or injecting it switched to heroin after the prescription's formula changed, U.S. researchers say. OxyContin was designed to slowly release the opioid drug oxycodone. After people started abusing it by crushing the pills and inhaling the powder or dissolving the pills in water and injecting it to get a rush, the drug maker introduced a new formula in the U.S. in 2010 to make inhaling and injecting more difficult. The new pills are harder to crush and dissolve more slowly. In Wednesday's issue of the New England Journal of Medicine, investigators in the U.S. said use of OxyContin by inhalation and injection has dropped significantly since the abuse-deterrent form went on the market. "In that sense, the new formulation was very successful," said author and principal investigator Theodore Cicero, a professor of neuropharmacology in psychiatry at Washington University School of Medicine in St. Louis, Mo. "The most unexpected, and probably detrimental, effect of the abuse-deterrent formulation was that it contributed to a huge surge in the use of heroin," he added in a release. OxyContin was a popular drug in suburban and urban areas, where drug abusers have now shifted either to more potent opioids if they can find them or to heroin, he said. © CBC 2012
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 17028 - Posted: 07.12.2012
By James Gallagher Health and Science reporter, BBC News, Istanbul Time-lapse photography has shown that embryos of smoking women develop more slowly. French academics in an IVF clinic took regular pictures of an egg from the moment it was fertilised until it was ready to be implanted into the mother. At all stages of development, embryos from smokers were consistently a couple of hours behind, a study showed. The lead researcher, from Nantes University Hospital, said: "You want a baby, quit smoking". Smoking is known to reduce the chances of having a child. It is why some hospitals in the UK ask couples to give up smoking before they are given fertility treatment. As eggs fertilised through IVF initially develop in the laboratory before being implanted, it gave doctors a unique opportunity to film the embryos as they divide into more and more cells. Researchers watched 868 embryos develop - 139 from smokers. In the clinic the embryos of non-smokers reached the five-cell stage after 49 hours. In the smokers it took 50 hours. The eight-cell stage took 62 hours in smokers' embryos, while non-smokers' embryos reached that point after 58 hours. Senior embryologist and lead researcher, Dr Thomas Freour, told the BBC: "Embryos from smoking women, they behave slower, there is a delay in their development. BBC © 2012
Related chapters from BP6e: Chapter 4: The Chemical Bases 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: 17003 - Posted: 07.05.2012
By Ian Chant Psychedelic drugs are making a quiet comeback, as a smattering of recent studies have demonstrated their medicinal potential. The latest finding suggests it is time to revisit LSD as a treatment for addiction. Pål-Ørjan Johansen and Teri Krebs of the Norwegian University of Science and Technology analyzed six clinical trials of LSD from 1966 to 1970 and published their results in March in the Journal of Psychopharmacology. The study subjects were being treated for alcohol abuse at inpatient clinics. They all underwent the standard treatment regimen for addiction, but some of them were also given a single, small dose of LSD during a therapeutic session. The results of the old studies were tepid, but they all hinted that LSD had helped. Pooling the data gave Johansen and Krebs more statistical power. “Instead of six small studies, you have one big study,” Krebs says, and the results of that larger study were much more robust. Of those who had taken LSD, 59 percent decreased their alcohol consumption, as compared with 38 percent of subjects who did not take LSD. Six months after leaving treatment, those who took LSD were 15 percent more likely to be sober. For just one dose of a psychiatric drug to remain effective for months is an impressive feat that researchers attribute to the unique qualities of psychedelics such as LSD. The feelings of openness and well-being brought on by the drug seem to help people see themselves—and their problems—in a different light. In this way, LSD could act as a kind of chemical catalyst for the “moment of clarity” cited by many addicts as a turning point in their treatment. © 2012 Scientific American,
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 16984 - Posted: 06.30.2012
by Sara Reardon Forget patches: gene therapy could suppress cigarette cravings by preventing the brain from receiving nicotine. The treatment is effective in mice, but with gene therapy still not fully tested in people, human trials and treatments are a long way off. For drug users who really can't quit, vaccination might one day be an option, and several groups have attempted to develop such treatments. But nicotine vaccines have mostly flopped. This is because nicotine is a very small molecule, so the immune system has difficulty recognising the drug and making antibodies that bind it. Physicians can inject antibodies directly into a patient, but this treatment quickly becomes expensive because the antibodies don't last long. Ronald Crystal of Weill Cornell Medical College in New York and his team decided to bypass that problem by putting the gene for a nicotine antibody right into the body. They selected the strongest antibody against nicotine from a mouse and isolated the gene that produced it. They then placed this gene into a carrier called adeno-associated virus (AAV), which is widely used for gene therapyMovie Camera. When the researchers injected the virus and its cargo into nicotine-addicted mice, the rodents' livers took up the virus, began making antibodies and pumped them into the bloodstream. The researchers injected two cigarettes' worth of nicotine into AAV-infected mice. The antibodies were able to bind 83 per cent of the drug before it reached the brain. © Copyright Reed Business Information Ltd
Related chapters from BP6e: Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 16980 - Posted: 06.28.2012
By KATIE THOMAS A research director for Pfizer was positively buoyant after reading that an important medical conference had just featured a study claiming that the new arthritis drug Celebrex was safer on the stomach than more established drugs. “They swallowed our story, hook, line and sinker,” he wrote in an e-mail to a colleague. The truth was that Celebrex was no better at protecting the stomach from serious complications than other drugs. It appeared that way only because Pfizer and its partner, Pharmacia, presented the results from the first six months of a yearlong study rather than the whole thing. The companies had a lot riding on the outcome of the study, given that Celebrex’s effect on the stomach was its principal selling point. Earlier studies had shown it was no better at relieving pain than common drugs — like ibuprofen — already on the market. The research chief’s e-mail, sent in 2000, is among thousands of pages of internal documents and depositions unsealed recently by a federal judge in a long-running securities fraud case against Pfizer. While the companies’ handling of the research was revealed a dozen years ago, the documents provide a vivid picture of the calculation made by Pfizer at the time and its efforts ever since to overcome doubts about the drug. The documents suggest that officials made a strategic decision during the early trial to be less than forthcoming about the drug’s safety. They show that executives considered attacking the trial’s design before they even knew the results and disregarded the advice of an employee and an outside consultant who had argued the companies should disclose the fact that they were using incomplete data. © 2012 The New York Times Company
Related chapters from BP6e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemical Bases of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 16962 - Posted: 06.25.2012




