Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Christopher Dean Hopkins If you've ever listened to karaoke at a bar, you know that drinking can affect how well someone can sing. Christopher Olson and his colleagues at Oregon Health and Science University recently set out to find if the same was true for birds, specifically zebra finches. "We just showed up in the morning and mixed a little bit of juice with 6 percent alcohol, and put it in their water bottles and put it in the cages," Olson told All Things Considered's Arun Rath. "At first we were thinking that they wouldn't drink on their own because, you know, a lot of animals just won't touch the stuff. But they seem to tolerate it pretty well and be somewhat willing to consume it." The finches long have been used as a model to study human vocal learning, or how people learn to communicate using language, Olson said. Obviously, alcohol affects human speech, so Olson and his team checked for similar problems with the birds. The blood alcohol levels achieved — .05 to .08 percent — would be laughed off by many college students, but because birds metabolize alcohol differently it was plenty to produce the effects the scientists were looking for. Listen to the audio, and you'll hear that the finches' song gets a bit quieter and just a little slurred, or as Olson puts it, "a bit less organized in their sound production" — like a roommate calling from a bar to get a ride home. © 2014 NPR
by Andy Coghlan If quitting smoking is one of your New Year's resolutions, we might have just the thing. Cytisine, a plant extract commonly used in eastern Europe to wean people off cigarettes, appears to be much better at the task than nicotine replacement patches and gums. Not to be confused with the DNA building block cytosine, cytisine is an alkaloid extract from the laburnum or golden rain tree (Laburnum anagyroides), which grows all over Europe. It works by blocking nicotine's access to the brain's pleasure receptors. Like nicotine, cytisine is toxic when ingested in large amounts but is safe at low doses. It is produced commercially mainly in Bulgaria and Poland, and has been used as a quitting aid in eastern European countries since the 1960s but is largely unknown elsewhere. Clinical trials carried out in the 60s and 70s did not meet US and European standards so did not lead to wider adoption. Researchers in New Zealand have now carried out a fresh trial of cytisine. They recruited 1310 smokers who intended to quit and gave exactly half of them cytisine as a course of tablets, taken daily in diminishing doses for 25 days. The other half received standard nicotine replacement therapy (NRT) – either as patches, gums or lozenges – for two months. The researchers noted the number of people who managed to abstain from smoking at one week, one month, two months and six months into the trial. Throughout, they found that people taking cytisine were less likely to have smoked than those using NRT. Six months in, 143 of the 655 cytisine recipients were still not smoking compared with 100 in the NRT group. © Copyright Reed Business Information Ltd.
Keyword: Drug Abuse
Link ID: 20434 - Posted: 12.20.2014
By ANDREW POLLACK It is either the most exciting new treatment for depression in years or it is a hallucinogenic club drug that is wrongly being dispensed to desperate patients in a growing number of clinics around the country. It is called ketamine — or Special K, in street parlance. While it has been used as an anesthetic for decades, small studies at prestigious medical centers like Yale, Mount Sinai and the National Institute of Mental Health suggest it can relieve depression in many people who are not helped by widely used conventional antidepressants like Prozac or Lexapro. And the depression seems to melt away within hours, rather than the weeks typically required for a conventional antidepressant. But some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials, and they are alarmed that clinics are springing up to offer ketamine treatments, charging hundreds of dollars for sessions that must be repeated many times. “We don’t know what the long-term side effects of this are,” said Dr. Anthony J. Rothschild, a professor of psychiatry at the University of Massachusetts Medical School. Some psychiatrists say the drug has not been studied enough to be ready for use outside of clinical trials. Credit Sandy Huffaker for The New York Times Pharmaceutical companies hope to solve the problem by developing drugs that work like ketamine but without the side effects, which are often described as out-of-body experiences. © 2014 The New York Times Company
by Viviane Callier It's a fresh problem. People who smoke menthol cigarettes often smoke more frequently and can be less likely to quit – and it could be because fresh-tasting menthol is changing their brains to more sensitive to nicotine. How menthol enhances nicotine addiction has been something of a mystery. Now, Brandon Henderson at the California Institute of Technology in Pasadena and his colleagues have shown that exposing mice to menthol alone causes them to develop more nicotinic receptors, the parts of the brain that are targeted by nicotine. Menthol can be used medically to relieve minor throat irritations, and menthol-flavoured cigarettes were first introduced in the 1920s. But smokers of menthol cigarettes can be less likely to quit. In one study of giving up smoking, 50 per cent of unflavoured-cigarette smokers were able to quit, while menthol smokers showed quitting rates as low as 23 per cent, depending on ethnicity. Over time, smokers of both menthol and unflavoured cigarettes acquire more receptors for nicotine, particularly in neurons involved in the body's neural pathways for reward and motivation. And research last year showed that smokers of menthol cigarettes develop even more of these receptors than smokers of unflavoured cigarettes. To understand how menthol may be altering the brain, Henderson's team exposed mice to either menthol with nicotine, or menthol alone. They found that, even without nicotine, menthol increased the numbers of brain nicotinic receptors. They saw a 78 per cent increase in one particular brain region – the ventral tegmental area – which is involved in the dopamine signalling pathway that mediates in addiction. © Copyright Reed Business Information Ltd.
Keyword: Drug Abuse
Link ID: 20395 - Posted: 12.06.2014
By Sarah C. P. Williams Craving a stiff drink after the holiday weekend? Your desire to consume alcohol, as well as your body’s ability to break down the ethanol that makes you tipsy, dates back about 10 million years, researchers have discovered. The new finding not only helps shed light on the behavior of our primate ancestors, but also might explain why alcoholism—or even the craving for a single drink—exists in the first place. “The fact that they could put together all this evolutionary history was really fascinating,” says Brenda Benefit, an anthropologist at New Mexico State University, Las Cruces, who was not involved in the study. Scientists knew that the human ability to metabolize ethanol—allowing people to consume moderate amounts of alcohol without getting sick—relies on a set of proteins including the alcohol dehydrogenase enzyme ADH4. Although all primates have ADH4, which performs the crucial first step in breaking down ethanol, not all can metabolize alcohol; lemurs and baboons, for instance, have a version of ADH4 that’s less effective than the human one. Researchers didn’t know how long ago people evolved the more active form of the enzyme. Some scientists suspected it didn’t arise until humans started fermenting foods about 9000 years ago. Matthew Carrigan, a biologist at Santa Fe College in Gainesville, Florida, and colleagues sequenced ADH4 proteins from 19 modern primates and then worked backward to determine the sequence of the protein at different points in primate history. Then they created copies of the ancient proteins coded for by the different gene versions to test how efficiently each metabolized ethanol. They showed that the most ancient forms of ADH4—found in primates as far back as 50 million years ago—only broke down small amounts of ethanol very slowly. But about 10 million years ago, the team reports online today in the Proceedings of the National Academy of Sciences, a common ancestor of humans, chimpanzees, and gorillas evolved a version of the protein that was 40 times more efficient at ethanol metabolism. © 2014 American Association for the Advancement of Science.
By EUGENIA BONE I TRIED magic mushrooms out of curiosity and in middle age. I’d been on the amateur mycological circuit for a couple of years, but hallucinogenic species were rarely mentioned at the foraging expeditions and conferences I attended. It’s almost as if they were the black sheep of mycology: embarrassing to serious taxonomy jocks. I read some books on the subject, but most were tripper’s guides that didn’t utilize, um, specific language or current science. Psychoactive mushrooms had been in a kind of scientific ghetto ever since they were criminalized in 1968. But now the drug derived from the mushroom, psilocybin, is finally being re-examined for its medical applications. A study published last month in the Journal of the Royal Society Interface compared M.R.I.s of the brains of subjects injected with psilocybin with scans of their normal brain activity. The brains on psilocybin showed radically different connectivity patterns between cortical regions (the parts thought to play an important role in consciousness). The researchers mapped out these connections, revealing the activity of new neural networks between otherwise disconnected brain regions. The researchers suspect that these unusual connections may be responsible for the synesthetic experience trippers describe, of hearing colors, for example, and seeing sounds. The part of the brain that processes sound may be connecting to the part of the brain that processes sight. The study’s leader, Paul Expert at King’s College London, told me that his team doubted that this psilocybin-induced connectivity lasted. They think they are seeing a temporary modification of the subject’s brain function. © 2014 The New York Times Company
By Tara Parker-Pope Most people who drink to get drunk are not alcoholics, suggesting that more can be done to help heavy drinkers cut back, a new government report concludes. The finding, from a government survey of 138,100 adults, counters the conventional wisdom that every “falling-down drunk” must be addicted to alcohol. Instead, the results from the National Survey on Drug Use and Health show that nine out of 10 people who drink too much are not addicts, and can change their behavior with a little — or perhaps a lot of — prompting. “Many people tend to equate excessive drinking with alcohol dependence,’’ sad Dr. Robert Brewer, who leads the alcohol program at the Centers for Disease Control and Prevention. “We need to think about other strategies to address these people who are drinking too much but who are not addicted to alcohol.” Excessive drinking is viewed as a major public health problem that results in 88,000 deaths a year, from causes that include alcohol poisoning and liver disease, to car accidents and other accidental deaths. Excessive drinking is defined as drinking too much at one time or over the course of a week. For men, it’s having five or more drinks in one sitting or 15 drinks or more during a week. For women, it’s four drinks on one occasion or eight drinks over the course of a week. Underage drinkers and women who drink any amount while pregnant also are defined as “excessive drinkers.” Surprisingly, about 29 percent of the population meets the definition for excessive drinking, but 90 percent of them do not meet the definition of alcoholism. That’s good news because it means excessive drinking may be an easier problem to solve than previously believed. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 20342 - Posted: 11.21.2014
By RONI CARYN RABIN The Food and Drug Administration on Thursday approved a powerful long-acting opioid painkiller, alarming some addiction experts who fear that its widespread use may contribute to the rising tide of prescription drug overdoses. The new drug, Hysingla, and another drug approved earlier this year, Zohydro, contain pure hydrocodone, a narcotic, without the acetaminophen used in other opioids. But Hysingla is to be made available as an “abuse-deterrent” tablet that cannot easily be broken or crushed by addicts looking to snort or inject it. Nearly half of the nation’s overdose deaths involved painkillers like hydrocodone and oxycodone, according to a 2010 study by the Centers for Disease Control and Prevention. More than 12 million people used prescription painkillers for nonmedical reasons that year, according to the study. Prescription opioid abuse kills more adults annually than heroin and cocaine combined, and sends 420,000 Americans to emergency rooms every year, according to the C.D.C. Hysingla, however, will not be not abuse-proof, said officials at the F.D.A. and the drug’s manufacturer, Purdue Pharma. Its extended-release formulation, a pill to be taken once every 24 hours by patients requiring round-the-clock pain relief, will contain as much as 120 milligrams of hydrocodone. The F.D.A. warned that doses of 80 milligrams or more “should not be prescribed to people who have not previously taken an opioid medication,” but officials described the abuse-deterrent formulation as a step forward. © 2014 The New York Times Company
Sara Reardon A technique that makes mouse brains transparent shows how the entire brain responds to cocaine addiction and fear. The findings could uncover new brain circuits involved in drug response. In the technique, known as CLARITY, brains are infused with acrylamide, which forms a matrix in the cells and preserves their structure along with the DNA and proteins inside them. The organs are then treated with a detergent that dissolves opaque lipids, leaving the cells completely clear. To test whether CLARITY could be used to show how brains react to stimuli, neuroscientists Li Ye and Karl Deisseroth of Stanford University in California engineered mice so that their neurons would make a fluorescent protein when they fired. (The system is activated by the injection of a drug.) The researchers then trained four of these mice to expect a painful foot shock when placed in a particular box; another set of mice placed in the box received cocaine, rather than shocks. Once the mice had learned to associate the box with either pain or an addictive reward, the researchers tested how the animals' brains responded to the stimuli. They injected the mice with the drug that activated the fluorescent protein system, placed them in the box and waited for one hour to give their neurons time to fire. The next step was to remove the animals' brains, treat them with CLARITY, and image them using a system that could count each fluorescent cell across the entire brain (see video). A computer combined these images into a model of a three-dimensional brain, which showed the pathways that lit up when mice were afraid or were anticipating cocaine. © 2014 Nature Publishing Group
By Nicholas Bakalar Exposure to secondhand smoke and roadway traffic may be tied to increased body mass index in children and adolescents, a new study suggests. Researchers studied 3,318 children in 12 Southern California communities beginning at an average age of 10, and then followed them through age 18. They used parental questionnaires to establish exposure to smoking, and data on traffic volume and levels of nitrogen dioxide, ozone and particulates to track pollution. The study, in Environmental Health Perspectives, controlled for many other factors: sex, initial B.M.I., asthma, physical activity, insurance status, parental education and income, acres of parks and open space nearby, percentage of people living in poverty in each community. But even after accounting for these issues and more, they found that compared with children exposed to no secondhand smoke or near-roadway air pollution, B.M.I. was 0.80 higher in children exposed to pollution alone, 0.85 higher in those exposed to secondhand smoke alone, and 2.15 higher in those exposed to both. A normal B.M.I. for adults is 18.5 to 24.9. Higher than 25 is considered overweight, and above 30 obese. “It would be interesting to know more about the mechanism,” said the lead author, Dr. Rob McConnell, a professor of preventive medicine at the University of Southern California. “But the finding challenges the view that obesity is due solely to increased caloric intake and reduced physical activity. That’s not the whole story.” © 2014 The New York Times Company
By Tom Shroder After more than 30 years in which psychedelics were considered dangerous remnants of the 1960s, the drugs have begun to make a comeback, this time as potential remedies for a host of tough-to-treat maladies. Pilot studies and clinical trials of LSD, psilocybin, ketamine and MDMA have shown that the drugs, often in combination with talk therapy, can be given safely under medical supervision and may help people dealing with opiate and tobacco addiction, alcoholism, anxiety, depression and post-traumatic stress disorder, or PTSD. That these investigations have shown potential is not surprising to many researchers. A generation of scientists and practitioners had used psychedelics successfully with thousands of patients until the research was banned in 1970, after the drugs were embraced by an exploding counterculture that seemed to threaten the status quo. In the panicked reaction, psychedelics were listed along with heroin in the highest rungs of prohibition. Ironically, this failed to stop recreational use but it shut the science down cold. As one researcher put it, “It was as if psychedelic drugs had become undiscovered.” But a small cadre of psychiatrists and researchers, often risking careers and reputations, pushed to bring psychedelics back to the lab and the clinic. Their persistence paid off. Beginning in the 1990s, the Food and Drug Administration approved the first human clinical studies of psychedelic drugs in a quarter of a century. By 2004, the first FDA-approved trial of the medicinal use of a psychedelic drug, in this case a trial of MDMA-assisted therapy for PTSD involving 24 subjects, was underway. Now such studies are proliferating.
|By Bret Stetka The brain is protected by formidable defenses. In addition to the skull, the cells that make up the blood-brain barrier keep pathogens and toxic substances from reaching the central nervous system. The protection is a boon, except when we need to deliver drugs to treat illnesses. Now researchers are testing a way to penetrate these bastions: sound waves. Kullervo Hynynen, a medical physicist at Sunnybrook Research Institute in Toronto, and a team of physicians are trying out a technique that involves giving patients a drug followed by an injection of microscopic gas-filled bubbles. Next patients don a cap that directs sound waves to specific brain locations, an approach called high-intensity focused ultrasound. The waves cause the bubbles to vibrate, temporarily forcing apart the cells of the blood-brain barrier and allowing the medication to infiltrate the brain. Hynynen and his colleagues are currently testing whether they can use the method to deliver chemotherapy to patients with brain tumors. They and other groups are planning similar trials for patients with other brain disorders, including Alzheimer's disease. Physicians are also considering high-intensity focused ultrasound as an alternative to brain surgery. Patients with movement disorders such as Parkinson's disease and dystonia are increasingly being treated with implanted electrodes, which can interrupt problematic brain activity. A team at the University of Virginia hopes to use focused ultrasound to deliver thermal lesions deep into the brain without having patients go under the knife. © 2014 Scientific American
Details of the role of glutamate, the brain’s excitatory chemical, in a drug reward pathway have been identified for the first time. This discovery in rodents — published today in Nature Communications — shows that stimulation of glutamate neurons in a specific brain region (the dorsal raphe nucleus) leads to activation of dopamine-containing neurons in the brain’s reward circuit (dopamine reward system). Dopamine is a neurotransmitter present in regions of the brain that regulate movement, emotion, motivation, and feelings of pleasure. Glutamate is a neurotransmitter whose receptors are important for neural communication, memory formation, and learning. The research was conducted at the Intramural Research Program (IRP) of the National Institute on Drug Abuse (NIDA), which is part of the National Institutes of Health. The research focused on the dorsal raphe nucleus, which has long been a brain region of interest to drug abuse researchers, since nerve cells in this area connect to part of the dopamine reward system. Many of the pathways are rich in serotonin, a neurotransmitter linked to mood regulation. Even though electrical stimulation of the dorsal raphe nucleus promotes reward-related behaviors, drugs that increase serotonin have low abuse potential. As a result, this region of the brain has always presented a seeming contradiction, since it is involved in drug reward but is also abundant in serotonin - a chemical not known for a role in drug reinforcement. This has led researchers to theorize that another neurotransmitter may be responsible for the role that the dorsal raphe nucleus plays in reward.
Keyword: Drug Abuse
Link ID: 20308 - Posted: 11.13.2014
By Kate Kelland LONDON (Reuters) - British scientists say they have found the best way yet to analyze the effects of smoking on the brain -- by taking functional magnetic resonance imaging (fMRI) scans of people while they puff on e-cigarettes. In a small pilot study, the researchers used electronic cigarettes, or e-cigarettes, to mimic the behavioral aspects of smoking tobacco cigarettes, and say future studies could help scientists understand why smoking is so addictive. E-cigarettes use battery-powered cartridges to produce a nicotine-laced vapor to inhale -- hence the new term "vaping". Their use has rocketed in recent years, but there is fierce debate about the risks and benefits. Some public health experts say they could help millions quit tobacco cigarettes, while others argue they could "normalize" the habit and lure children into smoking. While that argument rages, tobacco kills some 6 million people a year, and the World Health Organization estimates that could rise beyond 8 million by 2030. Matt Wall, an imaging scientist at Imperial College London who led the study using e-cigarettes, said he was not aiming to pass judgment on their rights or wrongs, but to use them to dig deeper into smoking addiction. The fact that other forms of nicotine replacement therapy, such as patches or gum, have had only limited success in getting hardened smokers to quit suggests they are hooked on more than just nicotine, he noted. © 2014 Scientific American
By Jia You Like humans, flies are attracted to alcohol. Fruit flies (Drosophila melanogaster, above) prefer to lay their eggs on rotten food that can contain ethanol in as high as 7% concentration. (That’s 14 proof to you bar hoppers.) And just like people, the insects differ in their ability to hold their drinks. Biologists know that compared with flies from tropical Africa, flies from temperate regions such as Europe survive longer when exposed to ethanol vapors of high concentrations, and they know it has something to do with enzymes on the flies’ second chromosomes, which break down alcohol and are more active in European flies. But now, biologist James Fry of the University of Rochester in New York has pinpointed a missing piece of the story: the role played by the flies’ third chromosomes. After studying flies collected from Vienna and Cameroon, Fry found that the Vienna flies break down alcohol much faster than Cameroon ones, as expected. But when he replaced the third chromosomes in Cameroon flies with those from Vienna, the African flies gained much more resistance, Fry reports online today in The Journal of Experimental Biology. In a specialized population of flies that could not detoxify alcohol, however, the genetic engineering made no difference whatsoever. Fry suggests that’s because the third chromosomes in European flies help them tolerate acetic acid, a byproduct of internal alcohol breakdown that also gives vinegar its sour taste. There’s no telling what the acetic acid does to the flies, but previous studies on mice have found that it may be responsible for hangover headaches, Fry says. © 2014 American Association for the Advancement of Science
By Julia Calderone Antidepressant use among Americans is skyrocketing. Adults in the U.S. consumed four times more antidepressants in the late 2000s than they did in the early 1990s. As the third most frequently taken medication in the U.S., researchers estimate that 8 to 10 percent of the population is taking an antidepressant. But this spike does not necessarily signify a depression epidemic. Through the early 2000s pharmaceutical companies were aggressively testing selective serotonin reuptake inhibitors (SSRIs), the dominant class of depression drug, for a variety of disorders—the timeline below shows the rapid expansion of FDA-approved uses. As the drugs' patents expired, companies stopped funding studies for official approval. Yet doctors have continued to prescribe them for more ailments. One motivating factor is that SSRIs are a fairly safe option for altering brain chemistry. Because we know so little about mental illness, many clinicians reason, we might as well try the pills already on the shelf. Doctors commonly use antidepressants to treat many maladies they are not approved for. In fact, studies show that between 25 and 60 percent of prescribed antidepressants are actually used to treat nonpsychological conditions. The most common and well-supported off-label uses of SSRIs include: Abuse and dependence ADHD (in children and adolescents) Anxiety disorders Autism (in children) Bipolar disorder Eating disorders Fibromyalgia Neuropathic pain Obsessive-compulsive disorder Premenstrual dysphoric disorder © 2014 Scientific American
Link ID: 20300 - Posted: 11.11.2014
By Abby Phillip If you're confused about what marijuana use really does to people who use it, you're not alone. For years, the scientific research on health effects of the drug have been all over the map. Earlier this year, one study suggested that even casual marijuana use could cause changes to the brain. Another found that marijuana use was also associated with poor sperm quality, which could lead to infertility in men. But marijuana advocates point to other research indicating that the drug is far less addictive than other drugs, and some studies have found no relationship between IQ and marijuana use in teens. Researchers at the Center for Brain Health at the University of Texas in Dallas sought to clear up some of the confusion with a study that looked at a relatively large group of marijuana users and evaluated their brains for a slew of different indicators. What they found was complex, but the pattern was clear: The brains of marijuana users were different than those of non-marijuana users. The area of the brain responsible for establishing the reward system that helps us survive and also keeps us motivated was smaller in users than in non-marijuana users. But there was also evidence that the brain compensated for this loss of volume by increasing connectivity and the structural integrity of the brain tissue. Those effects were more pronounced for marijuana users who started young. "The orbitofrontal cortex is one of the primary regions in a network of brain areas called the reward system," explained Francesca Filbey, lead author of the study and an associate professor of the neurogenetics of addictive behavior at the University of Texas in Dallas. "
How Magic Mushrooms Rearrange Your Brain By Brandon Keim A new way of looking at brain activity may give insight into how psychedelic drugs produce their consciousness-altering effects. In recent years, a focus on brain structures and regions has given way to an emphasis on neurological networks: how cells and regions interact, with consciousness shaped not by any given set of brain regions, but by their interplay. Understanding the networks, however, is no easy task, and researchers are developing ever more sophisticated ways of characterizing them. One such approach, described in a new Proceedings of the Royal Society Interface study, involves not simply networks but networks of networks. Perhaps some aspects of consciousness arise from these meta-networks—and to investigate the proposition, the researchers analyzed fMRI scans of 15 people after being injected with psilocybin, the active ingredient in magic mushrooms, and compared them to scans of their brain activity after receiving a placebo. Investigating psychedelia wasn’t the direct purpose of the experiment, said study co-author Giovanni Petri, a mathematician at Italy’s Institute for Scientific Interchange. Rather, psilocybin makes for an ideal test system: It’s a sure-fire way of altering consciousness. “In a normal brain, many things are happening. You don’t know what is going on, or what is responsible for that,” said Petri. “So you try to perturb the state of consciousness a bit, and see what happens.” A representation of that is seen in the image above. Each circle depicts relationships between networks—the dots and colors correspond not to brain regions, but to especially connection-rich networks—with normal-state brains at left, and psilocybin-influenced brains at right. © 2014 Condé Nast.
By Elizabeth Pennisi It’s not such a stretch to think that humans can catch the Ebola virus from monkeys and the flu virus from pigs. After all, they are all mammals with fundamentally similar physiologies. But now researchers have discovered that even a virus found in the lowly algae can make mammals its home. The invader doesn’t make people or mice sick, but it does seem to slow specific brain activities. The virus, called ATCV-1, showed up in human brain tissue several years ago, but at the time researchers could not be sure whether it had entered the tissue before or after the people died. Then, it showed up again in a survey of microbes and viruses in the throats of people with psychiatric disease. Pediatric infectious disease expert Robert Yolken from Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues were trying to see if pathogens play a role in these conditions. At first, they didn't know what ATCV-1 was, but a database search revealed its identity as a virus that typically infects a species of green algae found in lakes and rivers. The researchers wanted to find out if the virus was in healthy people as well as sick people. They checked for it in 92 healthy people participating in a study of cognitive function and found it in 43% of them. What’s more, those infected with the virus performed 10% worse than uninfected people on tests requiring visual processing. They were slower in drawing a line connecting a sequence of numbers randomly placed on a page, for example. And they seemed to have shorter attention spans, the researchers report online today in the Proceedings of the National Academy of Sciences. The effects were modest, but significant. © 2014 American Association for the Advancement of Science
Link ID: 20258 - Posted: 10.29.2014
By ABIGAIL SULLIVAN MOORE The gray matter of the nucleus accumbens, the walnut-shaped pleasure center of the brain, was glowing like a flame, showing a notable increase in density. “It could mean that there’s some sort of drug learning taking place,” speculated Jodi Gilman, at her computer screen at the Massachusetts General Hospital-Harvard Center for Addiction Medicine. Was the brain adapting to marijuana exposure, rewiring the reward system to demand the drug? Dr. Gilman was reviewing a composite scan of the brains of 20 pot smokers, ages 18 to 25. What she and fellow researchers at Harvard and Northwestern University found within those scans surprised them. Even in the seven participants who smoked only once or twice a week, there was evidence of structural differences in two significant regions of the brain. The more the subjects smoked, the greater the differences. Moderate marijuana use by healthy adults seems to pose little risk, and there are potential medical benefits, including easing nausea and pain. But it has long been known that, with the brain developing into the mid-20s, young people who smoke early and often are more likely to have learning and mental health problems. Now researchers suggest existing studies are no longer sufficient. Much of what’s known is based on studies conducted years ago with much less powerful pot. Marijuana samples seized by the federal Drug Enforcement Agency show the concentration of THC, the drug’s psychoactive compound, rising from a mean of 3.75 percent in 1995 to 13 percent in 2013. Potency seesaws depending on the strain and form. Fresh Baked, which sells recreational marijuana in Boulder, Colo., offers “Green Crack,” with a THC content of about 21 percent, and “Phnom Pen,” with about 8 percent. The level in a concentrate called “Bubble Hash” is about 70 percent; cartridges for vaporizers, much like e-cigarettes, range from 15 to 30 percent THC. © 2014 The New York Times Company