Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Ian Sample, science correspondent A cup or two of coffee could boost the brain's ability to store long-term memories, researchers in the US claim. People who had a shot of caffeine after looking at a series of pictures were better at distinguishing them from similar images in tests the next day, the scientists found. The task gives a measure of how precisely information is stored in the brain, which helps with a process called pattern separation which can be crucial in everyday situations. If the effect is real, and some scientists are doubtful, then it would add memory enhancement to the growing list of benefits that moderate caffeine consumption seems to provide. Michael Yassa, a neuroscientist who led the study at Johns Hopkins University in Baltimore, said the ability to separate patterns was vital for discriminating between similar scenarios and experiences in life. "If you park in the same parking lot every day, the spot you choose can look the same as many others. But when you go and look for your car, you need to look for where you parked it today, not where you parked it yesterday," he said. Writing in the journal Nature Neuroscience, Yassa described how 44 volunteers who were not heavy caffeine consumers and had abstained for at least a day were shown a rapid sequence of pictures on a computer screen. The pictures included a huge range of items, such as a hammer, a chair, an apple, a seahorse, a rubber duck and a car. © 2014 Guardian News and Media Limited
By NICHOLAS BAKALAR We know that smoking is bad for you — and that it ages you prematurely. Now a study provides photographic evidence for this claim. Scientists gathered health and lifestyle information on 79 pairs of identical adult twins who fit into one of three groups: a pair in which one was a smoker and the other had never smoked; a pair in which both were smokers; or a pair in which both were smokers but with at least a 5-year difference in the duration of their smoking habit. They photographed them and had independent judges rate the pictures side-by-side for wrinkles, crow’s feet, jowls, bags under the eyes, creases around the nose, lines around the lips and other evidence of aging skin. The differences in some other factors that can age skin prematurely — alcohol consumption, sunscreen use and perceived stress at work — were statistically insignificant between twin pairs. But the judges’ decisions on which twin looked older coincided almost perfectly with their smoking histories. “The purpose of this study was to offer scientific evidence that smoking changes not only longevity, but also quality of appearance,” said the senior author, Dr. Bahman Guyuron, chairman of the plastic surgery department at University Hospital, Case Medical Center in Cleveland. “It is harmful any way you look at it.” Copyright 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 19118 - Posted: 01.11.2014
By Ashutosh Jogalekar Often you will hear people talking about why drugs are expensive: it’s the greedy pharmaceutical companies, the patent system, the government, capitalism itself. All these factors contribute to increasing the price of a drug, but one very important factor often gets entirely overlooked: Drugs are expensive because the science of drug discovery is hard. And it’s just getting harder. In fact purely on a scientific level, taking a drug all the way from initial discovery to market is considered harder than putting a man on the moon, and there’s more than a shred of truth to this contention. In this series of posts I will try to highlight some of the purely scientific challenges inherent in the discovery of new medicines. I am hoping that this will make laymen appreciate a little better why the cost of drugs doesn’t have everything to do with profit and power and much to do with scientific ignorance and difficulty; as one leading scientist I know quips, “Drugs are not expensive because we are evil, they are expensive because we are stupid.” I could actually end this post right here by stating one simple, predominant reason why the science of drug discovery is so tortuous: it’s because biology is complex. The second reason is because we are dealing with a classic multiple variable optimization problem, except that the variables to be optimized again pertain to a very poorly understood, complex and unpredictable system. The longer answer will be more interesting. The simple fact is that we still haven’t figured out the workings of biological systems – the human body in this case – to an extent that allows us to rationally and predictably modify, mitigate or cure their ills using small organic molecules. That we have been able to do so to an unusually successful degree is a tribute to both human ingenuity and plain good luck. But there’s still a very long way to go. © 2014 Scientific American
Link ID: 19105 - Posted: 01.07.2014
by Alyssa Botelho Women with breast cancer often enjoy several years in remission, only to then be given the devastating news that they have developed brain tumours. Now we are finally starting to understand how breast cancer cells are able to spread undetected in the brain: they masquerade as neurons and hijack their energy supply. For every tumour that originates in the brain, 10 arrive there from other organ systems. Understanding how tumours spread, or metastasise, and survive in the brain is important because the survival rate of people with brain metastases is poor – only a fifth are still alive a year after being diagnosed. Rahul Jandial, a neurosurgeon at the City of Hope Cancer Center in Duarte, California, wanted to explore how breast cancer cells are able to cross the blood-brain barrier and escape destruction by the immune system. "If, by chance, a malignant breast cancer cell swimming in the bloodstream crossed into the brain, how would it survive in a completely new, foreign habitat?" Jandial says. He and his team wondered if breast cancer cells that could use the resources around them – neurotransmitters and other chemicals in the brain – would be the ones that survived and flourished. To test the idea, they took samples of metastatic breast cancer cells from the brains of several women and grew them in the lab. They compared the expression of proteins involved in detecting and absorbing GABA – a common neurotransmitter that neurons convert into energy – in these cells with what happens in non-metastatic breast cancer cells. © Copyright Reed Business Information Ltd
Link ID: 19102 - Posted: 01.07.2014
by Bethany Brookshire When most people think of the quintessential lab mouse, they think of a little white mouse with red eyes. Soft fur. A timid nature. But scientists think of something very different. This mouse is black, small and fast, with pink ears and a pinkish tail. It’s got black eyes to match. The fur may be soft, but the temper sure isn’t. This is the C57 Black 6 mouse. Each Black 6 mouse should be almost identical to every other Black 6 mouse. They have been bred to their own siblings for hundreds of generations, so there should be very few genetic differences left. But even supposedly identical mouse strains have their differences. These take the form of mutations in single DNA base pairs that accumulate in different populations. Recently, researchers showed that one of these tiny changes in a single gene was enough to produce a huge difference in how two groups of Black 6 mice respond to drugs. And the authors identified a surprising number of other small DNA differences still waiting to be explored. On one level, the new work offers scientists a novel tool for identifying genes that could relate to behaviors. But it also serves as a warning. “Identical” mouse populations aren’t as alike as many scientists had assumed. The Black 6, the most common lab mouse in the United States, is used for everything from drug abuse studies to cancer research. The Black 6 is also the reference strain for the Mouse Genome Sequencing Consortium. Whenever scientists discover a new genetic change in a mouse strain, they compare it first against the Black 6. And it’s the mouse used by the International Knockout Mouse Consortium (now the International Mouse Phenotyping Consortium), which keep a library of mouse embryos with different deleted genes. The Allen Brain Atlas, a database of neuroanatomy and gene activity throughout the mouse brain, relies on the Black 6 as well. © Society for Science & the Public 2000 - 2014
People with severe mental illness such as schizophrenia or bipolar disorder have a higher risk for substance use, especially cigarette smoking, and protective factors usually associated with lower rates of substance use do not exist in severe mental illness, according to a new study funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. Estimates based on past studies suggest that people diagnosed with mood or anxiety disorders are about twice as likely as the general population to also suffer from a substance use disorder. Statistics from the 2012 National Survey on Drug Use and Health indicate close to 8.4 million External Web Site Policy adults in the United States have both a mental and substance use disorder. However, only 7.9 percent of people receive treatment for both conditions, and 53.7 percent receive no treatment at all, the statistics External Web Site Policy indicate. “Drug use impacts many of the same brain circuits that are disrupted in severe mental disorders such as schizophrenia,” said NIDA Director Dr. Nora D. Volkow. “While we cannot always prove a connection or causality, we do know that certain mental disorders are risk factors for subsequent substance use disorders, and vice versa.” In the current study, 9,142 people diagnosed with schizophrenia, schizoaffective disorder, or bipolar disorder with psychotic features, and 10,195 controls matched to participants according to geographic region, were selected using the Genomic Psychiatry Cohort program. Mental disorder diagnoses were confirmed using the Diagnostic Interview for Psychosis and Affective Disorder (DI-PAD), and controls were screened to verify the absence of schizophrenia or bipolar disorder in themselves or close family members. The DI-PAD was also used for all participants to determine substance use rates.
by Paul Heltzel Have you ever looked at your dorsal fin — I mean, really looked at it? Dolphins, nature’s playful jokers, apparently have a little habit they’ve been keeping a secret: They get high. A BBC film crew recently captured some unusual footage of dolphins passing a puffer fish between them. The fish then secretes a toxin — a defense mechanism — which the dolphins appear to enjoy — a lot. As the dolphins nudged the puffer fish back and forth, they fell into a trancelike state, reports the Guardian. “At one point the dolphins are seen floating just underneath the water’s surface, apparently mesmerized by their own reflections,” according to the Guardian. Filmmaker John Downer cleverly disguised underwater cameras as squid, tuna and other dolphins to record the footage. Downer told the BBC the dolphins handled the puffer carefully, so they wouldn’t hurt or kill it. “The dolphins were specifically going for the puffers,” Downer said, “and deliberately handling them with care.” © 2014 Discovery Communications, LLC.
Keyword: Drug Abuse
Link ID: 19088 - Posted: 01.02.2014
For tobacco hornworms, bad breath might be the key to surviving the night. As their name suggests, these desert-dwelling caterpillars (larvae of the Manduca sexta moth) regularly chomp on nicotine-laced tobacco leaves. Scientists observed that caterpillars feeding on genetically modified, nicotine-free tobacco plants were more likely to disappear during the night than those chowing down on regular tobacco, leading them to suspect that the hornworms might be repurposing the toxic chemical to defend themselves against nocturnal predators like wolf spiders (Camptocosa parallela, pictured above feasting on a larva). The researchers investigated a gene called CYP6B46, which is active in the hornworm’s gut. Turning the gene off resulted in higher nicotine levels in the hornworms’ poop, suggesting that the gene helps the larvae avoid excreting the chemical by pumping it out of their guts and into their blood. The caterpillars had to be exuding the toxic nicotine somehow, so the scientists gave them an insect version of a breathalyzer test and discovered that they breathe it out with every exhale, the team reports online today in the Proceedings of the National Academy of Sciences. This “toxic halitosis” repelled wolf spiders, which actually flee from caterpillars with nicotine on their breath, as you can see in this video. Still, bad breath is no guarantee of a long life: It didn’t deter some of the hornworms’ other predators, including big-eyed bugs and antlion larvae. © 2013 American Association for the Advancement of Science
Link ID: 19078 - Posted: 12.31.2013
Imagine this: Every day, you can feel people looking at you warily. They want to hurt you. Even the police are out to get you. You try to rid your mind of all the ill-intentioned people, but you can't ignore the other thing that is gnawing at you. Those bugs on your arm won't leave you alone, no matter how often you gouge at them. Such are the hallucinations and paranoia felt by those with a stimulant drug addiction. Sometimes the substance abuse is so severe it causes neurological damage and psychosis becomes a chronic condition. Combine untreated addiction with homelessness and physical health problems, and you get a health emergency. Vancouver police and the region's health authorities are desperately trying to figure out how to help the most vulnerable of mentally ill drug addicts. The province estimates that roughly 130,000 people in British Columbia suffer from a severe addiction and/or mental health illness. But police and emergency workers are increasingly dealing with a much smaller group of people whose brains have been damaged by their stimulant addiction and who appear to be responsible for random violent acts on Vancouver's streets. Dr. Nader Sharifi, addiction medicine lead with the Fraser Health Authority, said there are few good treatment options for those people. "It's a bit of a challenging question, because what we have available isn't necessarily structured for this patient sub-type. It's either structured for addiction, or structured for mental health illness, but not necessarily the two together." © CBC 2013
By ANAHAD O'CONNOR A new federal report shows that the percentage of American high school students who smoke marijuana is slowly rising, while the use of alcohol and almost every other drug is falling. The report raises concerns that the relaxation of restrictions on marijuana, which can now be sold legally in 20 states and the District of Columbia, has been influencing use of the drug among teenagers. Health officials are concerned by the steady increase and point to what they say is a growing body of evidence that adolescent brains, which are still developing, are susceptible to subtle changes caused by marijuana. “The acceptance of medical marijuana in multiple states leads to the sense that if it’s used for medicinal purposes, then it can’t be harmful,” said Dr. Nora D. Volkow, director of the National Institute on Drug Abuse, which issued the report. “This survey has shown very consistently that the greater the number of kids that perceive marijuana as risky, the less that smoke it.” Starting early next year, recreational marijuana use will also be legal in Colorado and Washington. Experts debate the extent to which heavy marijuana use may cause lasting detriment to the brain. But Dr. Volkow said that one way marijuana might affect cognitive function in adolescents was by disrupting the normal development of white matter through which cells in the brain communicate. According to the latest federal figures, which were part of an annual survey, Monitoring the Future, more than 12 percent of eighth graders and 36 percent of seniors at public and private schools around the country said they had smoked marijuana in the past year. About 60 percent of high school seniors said they did not view regular marijuana use as harmful, up from about 55 percent last year. Copyright 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 19049 - Posted: 12.18.2013
By DANNY HAKIM LONDON — European food regulators said on Tuesday that a class of pesticides linked to the deaths of large numbers of honey bees might also harm human health, and they recommended that the European Commission further restrict their use. The commission, which requested the review, has already taken a tougher stance than regulators in other parts of the world against neonicotinoids, a relatively new nicotine-derived class of pesticide. Earlier this year, some were temporarily banned for use on many flowering crops in Europe that attract honey bees, an action that the pesticides’ makers are opposing in court. Now European Union regulators say the same class of pesticides “may affect the developing human nervous system” of children. They focused on two specific versions of the pesticide, acetamiprid and imidacloprid, saying they were safe to use only in smaller amounts than currently allowed. Imidacloprid was one of the pesticides placed under a two-year ban this year. The review was prompted by a Japanese study that raised similar concerns last year. Imidacloprid is one of the most popular insecticides, and is used in agricultural and consumer products. It was developed by Bayer, the German chemicals giant, and is the active ingredient in products like Bayer Advanced Fruit, Citrus & Vegetable Insect Control, which can be purchased at stores internationally, including Home Depot in the United States. Acetamiprid is sold by Nisso Chemical, a German branch of a Japanese company, though it was developed with Bayer’s help. It is used in consumer products like Ortho Flower, Fruit & Vegetable Insect Killer. The action by European regulators could affect the entire category of neonicotinoid pesticides, however. James Ramsay, a spokesman for the European Food Safety Authority, which conducted the review, said the agency was recommending a mandatory submission of studies related to developmental neurotoxicity “as part of the authorization process in the E.U.” © 2013 The New York Times Company
By ALAN SCHWARZ After more than 50 years leading the fight to legitimize attention deficit hyperactivity disorder, Keith Conners could be celebrating. Severely hyperactive and impulsive children, once shunned as bad seeds, are now recognized as having a real neurological problem. Doctors and parents have largely accepted drugs like Adderall and Concerta to temper the traits of classic A.D.H.D., helping youngsters succeed in school and beyond. But Dr. Conners did not feel triumphant this fall as he addressed a group of fellow A.D.H.D. specialists in Washington. He noted that recent data from the Centers for Disease Control and Prevention show that the diagnosis had been made in 15 percent of high school-age children, and that the number of children on medication for the disorder had soared to 3.5 million from 600,000 in 1990. He questioned the rising rates of diagnosis and called them “a national disaster of dangerous proportions.” “The numbers make it look like an epidemic. Well, it’s not. It’s preposterous,” Dr. Conners, a psychologist and professor emeritus at Duke University, said in a subsequent interview. “This is a concoction to justify the giving out of medication at unprecedented and unjustifiable levels.” The rise of A.D.H.D. diagnoses and prescriptions for stimulants over the years coincided with a remarkably successful two-decade campaign by pharmaceutical companies to publicize the syndrome and promote the pills to doctors, educators and parents. With the children’s market booming, the industry is now employing similar marketing techniques as it focuses on adult A.D.H.D., which could become even more profitable. Few dispute that classic A.D.H.D., historically estimated to affect 5 percent of children, is a legitimate disability that impedes success at school, work and personal life. Medication often assuages the severe impulsiveness and inability to concentrate, allowing a person’s underlying drive and intelligence to emerge. © 2013 The New York Times Company
Smoking tobacco or marijuana, taking prescription painkillers, or using illegal drugs during pregnancy is associated with double or even triple the risk of stillbirth, according to research funded by the National Institutes of Health. Researchers based their findings on measurements of the chemical byproducts of nicotine in maternal blood samples; and cannabis, prescription painkillers and other drugs in umbilical cords. Taking direct measurements provided more precise information than did previous studies of stillbirth and substance use that relied only on women’s self-reporting. The study findings appear in the journal Obstetrics & Gynecology. “Smoking is a known risk factor for stillbirth, but this analysis gives us a much clearer picture of the risks than before,” said senior author Uma M. Reddy, M.D., MPH, of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH institute that supported the study. “Additionally, results from the latest findings also showed that likely exposure to secondhand smoke can elevate the risk of stillbirth.” Dr. Reddy added, “With the legalization of marijuana in some states, it is especially important for pregnant women and health care providers to be aware that cannabis use can increase stillbirth risk.” The study enrolled women between March 2006 and September 2008 in five geographically defined areas delivering at 59 hospitals participating in the Stillbirth Collaborative Research Network External Web Site Policy. Women who experienced a stillbirth and those who gave birth to a live infant participated in the study. The researchers tested blood samples at delivery from the two groups of women and the umbilical cords from their deliveries to measure the exposure to the fetus. They also asked participants to self-report smoking and drug use during pregnancy.
By Ben Thomas 2013’s Nobel prize in Physiology or Medicine honors three researchers in particular – but what it really honors is thirty-plus years of work not only from them, but also from their labs, their graduate students and their collaborators. Winners James Rothman, Randy Schekman and Thomas Südhof all helped assemble our current picture of the cellular machinery that enables neurotransmitter chemicals to travel from one nerve cell to the next. And as all three of these researchers agree, that process of understanding didn’t catalyze until the right lines of research, powered by the right tools, happened to converge at the right time. Long before that convergence, though, these three scientists began by seeking the answers to three different questions – none of which seemed to have anything to do with the others. When James Rothman started out as a researcher at Harvard in 1978, his goal was to find out exactly how vesicle transmission worked. Vesicles – Latin for “little vessels” – are the microscopic capsules that carry neurotransmitter molecules like serotonin and dopamine from one brain cell to another. By the late 1960s, the old-guard biochemist George Palade, along with other researchers, had already deduced that synaptic vesicles are necessary for neurotransmission – but the questions of which proteins guided these tiny vessels on their journey, and how they docked with receiving neurons, remained mysterious. Yale University's James Rothman set out to break down the process of vesicle transmission, chemical-by-chemical, reaction-by-reaction. Courtesy of Yale University. In other words, although researchers had established the existence of this vesicle transmission process, no one knew exactly what made it work, or how. © 2013 Scientific American
Link ID: 19022 - Posted: 12.11.2013
by Bethany Brookshire When neurons throughout the brain and body send messages, they release chemical signals. These chemicals, neurotransmitters, pass into the spaces between neurons, or synapses, binding to receptors to send a signal along. When they are not in use, neurotransmitters are stored within the cell in tiny bubbles called vesicles. During signaling, these vesicles head to the membrane of the neuron, where they dump neurotransmitter into the synapse. And after delivering their cargo, most vesicles disappear. But more vesicles keep forming, filling with neurotransmitters so neurons can keep sending signals. What goes up must come down. When vesicles go out, they must come back. But how fast to the vesicles re-appear? Must faster, it turns out, than we first thought. Neurotransmission happens fast. An electrical signal comes down a neuron in your brain and triggers vesicles to move to the cell membrane. When the vesicles merge into the membrane and release their chemical cargo, the neurotransmitters float across the open synapse to the next neuron. This happens every time the neuron “fires.” This needs to happen very quickly, as neurons often fire at 100 hertz, or 100 times per second. Some neurons perform a “kiss-and-run,” opening up a temporary pore in the membrane, releasing a little bit of neurotransmitter and darting away again. Other vesicles need to merge with the synapse entirely. With the assistance of docking proteins, these vesicles fuse with the membrane of the neuron to release the neurotransmitters, a process called exocytosis. © Society for Science & the Public 2000 - 2013.
Link ID: 19021 - Posted: 12.11.2013
By Sandra Steingard, What does it mean that the man who killed 12 people at the Washington Naval Yard had told people that he was “hearing voices”? I have spent 30 years as a psychiatrist treating people who are psychotic. Almost every day I meet with individuals who hear voices that no one else hears, are sure the TV or radio is talking to them or have such confused thinking that it is hard to understand what they are trying to tell me. Sometimes these patients lead quiet lives. But not uncommonly these voices get them into trouble. I’ve had patients who call the police repeatedly, demanding that they stop bugging their phone. And others who stay up all night talking back at the voices. Some accuse family members of being involved in the torment. In many cases, this is a frightening experience — for the people I see and those who love them. And the labels we use — “schizophrenia,” “bipolar disorder,” “psychosis” — only crudely capture these experiences. About 60 years ago, a group of drugs was discovered that appeared to quiet the voices, improve the clarity of thought and lessen the preoccupation with delusion beliefs. Originally called major tranquilizers and later renamed antipsychotic drugs, these have been considered essential for the treatment of people with schizophrenia. Once it was clear that these drugs were helpful in the short term, questions arose over how long people should remain on them. Studies done in the 1970s and 1980s looked at people who were stabilized after being treated with antipsychotic drugs for several months and then followed them for up to two years. Some continued on the drugs, while others stopped taking them. The relapse rate was much higher in the group that stopped the medications. Based on these studies, treatment guidelines now state that people should stay on anti-psychotics indefinitely. The problem with “indefinitely” is that antipsychotic drugs have many troubling side effects. © 1996-2013 The Washington Post
Link ID: 19011 - Posted: 12.10.2013
by Laura Sanders If you own a television, a computer or a smartphone, you may have seen ads for Lumosity, the brain-training regimen that promises to sharpen your wits and improve your life. Take the bait, and you’ll first create a profile that includes your age, how much sleep you get, the time of day you’re most productive and other minutiae about your life and habits. After this digital debriefing, you can settle in and start playing games designed to train simple cognitive skills like arithmetic, concentration and short-term recall. The 50 million people signed up for Lumosity presumably have done so because they want to improve their brains, and these games promise an easy, fun way to do that. The program also offers metrics, allowing users to chart their progress over weeks, months and years. Written in these personal digital ledgers are clues that might help people optimize their performance. With careful recordkeeping, for example, you might discover that you hit peak brainpower after precisely one-and-a-half cups of medium roast coffee at 10:34 a.m. on Tuesdays. But you’re not the only one who has access to this information. With each click, your performance data will fly by Internet into the eager hands of scientists at Lumos Labs, the San Francisco company that created Lumosity. Giant datasets like this one, created as a by-product of people paying money to learn about and improve themselves, will revolutionize research in human health and behavior, some scientists believe. Lumos Labs researchers hope that their brain-training data in particular could reveal deep truths about how the human mind works. They believe that they have a nimble, customizable and cheap way to discover things about the brain that would otherwise take huge amounts of money and many years to unearth with standard lab-based studies. Other researchers have also taken note, and some have gotten permission to use Lumosity data in their own research. Some of these researchers are hunting for subtle signatures of Alzheimer’s in the data. Others are investigating more fundamental mysteries with cross-cultural studies of how the brain builds emotions and how memory works. © Society for Science & the Public 2000 - 2013.
By David Nutt Imagine being an astronomer in a world where the telescope was banned. This effectively happened in the 1600s when, for over 100 years, the Catholic Church prohibited access to knowledge of the heavens in a vain attempt to stop scientists proving that the earth was not the center of the universe. ‘Surely similar censorship could never happen today,’ I hear you say—but it does in relation to the use of drugs to study the brain. Scientists and doctors are banned from studying many hundreds of drugs because of outdated United Nations charters dating back to the 1960s and 1970s. Some of the banned drugs include cannabis, psychedelics and MDMA (now widely known as ecstasy). The most remarkable example is that of the psychedelic LSD, a drug accidentally discovered by the Swiss chemist Albert Hofmann while he was working for the pharmaceutical company Sandoz to find new treatments for migraine. Once the ability of LSD to alter brain function became apparent, Hofmann and others realized it had enormous potential as a tool to explore and treat the brain. The immediate effects of LSD to alter brain states offered unique insight into states such as consciousness and psychosis; the long-lasting changes in self-awareness it brought on were seen as potentially useful for conditions such as addiction. Pharmaceutical company Sandoz saw LSD as so important that they chose to make it widely available to researchers in the 1950s. Researchers conducted over 1,000 studies at that time, most of which yielded significant results. However, once young Americans started using the drug recreationally—partly in protest against the Vietnam War—it was banned, both there and all over the world. Since then, research into the science behind the drug and its effects on the brain has come to a halt. Yet, we have begun to rectify the situation using the shorter-acting psychedelic psilocybin (also known as magic mushrooms). In just a couple of experiments, scientists have discovered remarkable and unexpected effects on the brain, leading them to start a clinical trial in depression. Other therapeutic targets for psychedelics are cluster headaches, OCD and addiction. © 2013 Scientific American
By Janet Davison, CBC News If headlines in the past few weeks are to be believed, a "Flesh-eating 'zombie' drug" that could devour users "from the inside out" is finding its way onto American streets. Then came reports suggesting that "krokodil," a cheap and highly addictive homemade substitute for heroin that surfaced first in Russia about 10 years ago, had appeared in Ontario's Niagara region. But so far, neither the U.S. Drug Enforcement Agency nor Health Canada has identified krokodil, also known as desomorphine, in any samples they've analyzed since the DEA found two instances of it in 2004. And police in Niagara are now saying the reported cases of the drug — an ugly concoction of codeine mixed with common products such as gasoline, lighter fluid, paint thinner or industrial cleaning oil — haven't been medically confirmed. Krokodil is named for the Russian word for crocodile and its tendency to turn users' skin rough and scaly. The injectable opioid can cause brain damage and severe tissue damage, sometimes leading to gangrene, amputations and even death. It has also been linked to pneumonia, blood poisoning, meningitis, liver and kidney problems, rotting gums and bone infections. The horrific health problems the drug has caused among the well over 100,000 users in Russia and Ukraine have been well documented by researchers in publications such as the International Journal of Drug Policy. But so far there is no solid, official proof that krokodil has reached Canada. The recent news reports about the drug coupled with the lack of hard evidence to back them up underline how difficult it is for health and law enforcement officials to keep up with the evolving mix of street drugs. © CBC 2013
Keyword: Drug Abuse
Link ID: 18967 - Posted: 11.25.2013
Medical marijuana can alleviate pain and nausea, but it can also cause decreased attention span and memory loss. A new study in mice finds that taking an over-the-counter pain medication like ibuprofen may help curb these side effects. "This is what we call a seminal paper," says Giovanni Marsicano, a neuroscientist at the University of Bordeaux in France who was not involved in the work. If the results hold true in humans, they "could broaden the medical use of marijuana," he says. "Many people in clinical trials are dropping out from treatments, because they say, ‘I cannot work anymore. I am stoned all the time.’ ” People have used marijuana for hundreds of years to treat conditions such as chronic pain, multiple sclerosis, and epilepsy. Studies in mice have shown that it can reduce some of the neural damage seen in Alzheimer's disease. The main psychoactive ingredient, tetrahydrocannabinol (THC), is approved by the Food and Drug Administration to treat anorexia in AIDS patients and the nausea triggered by chemotherapy. Although recreational drug users usually smoke marijuana, patients prescribed THC take it as capsules. Many people find the side effects hard to bear, however. The exact cause of these side effects is unclear. In the brain, THC binds to receptors called CB1 and CB2, which are involved in neural development as well as pain perception and appetite. The receptors are normally activated by similar compounds, called endocannabinoids, that are produced by the human body. When one of these compounds binds to CB1, it suppresses the activity of an enzyme called cyclooxygenase-2 (COX-2). The enzyme has many functions. For instance, painkillers such as ibuprofen and aspirin work by blocking COX-2. Researchers have hypothesized that the suppression of COX-2 could be the cause of THC's side effects, such as memory problems. © 2013 American Association for the Advancement of Science