Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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


Links 21 - 40 of 2274

Haroon Siddique Magic mushrooms may effectively “reset” the activity of key brain circuits known to play a role in depression, the latest study to highlight the therapeutic benefits of psychadelics suggests. Psychadelics have shown promising results in the treatment of depression and addictions in a number of clinical trials over the last decade. Imperial College London researchers used psilocybin – the psychoactive compound that occurs naturally in magic mushrooms – to treat a small number of patients with depression, monitoring their brain function, before and after. Images of patients’ brains revealed changes in brain activity that were associated with marked and lasting reductions in depressive symptoms and participants in the trial reported benefits lasting up to five weeks after treatment. Dr Robin Carhart-Harris, head of psychedelic research at Imperial, who led the study, said: “We have shown for the first time clear changes in brain activity in depressed people treated with psilocybin after failing to respond to conventional treatments. “Several of our patients described feeling ‘reset’ after the treatment and often used computer analogies. For example, one said he felt like his brain had been ‘defragged’ like a computer hard drive, and another said he felt ‘rebooted’. “Psilocybin may be giving these individuals the temporary ‘kick start’ they need to break out of their depressive states and these imaging results do tentatively support a ‘reset’ analogy. Similar brain effects to these have been seen with electroconvulsive therapy.” © 2017 Guardian News and Media Limited

Keyword: Depression; Drug Abuse
Link ID: 24189 - Posted: 10.13.2017

Dean Burnett Another day, another powerful man embroiled in a sinister sexual scandal decades in the making. This time it’s powerful Hollywood figure Harvey Weinstein. The moral, ethical and political aspects of this whole mess have been covered extensively elsewhere, and will no doubt continue to be so over the coming days and weeks. However, recent reports suggest that Weinstein has checked himself into a European rehab clinic for sex addiction. This has been met with some not-inconsiderable cynicism, but, even if it is true, wondering whether Weinstein is a sex addict overlooks a more fundamental question: is anyone a sex addict? Because that diagnosis, as commonplace as it may seem, is far from established psychiatric fact. Many people do believe sex addiction is real and serious problem, while others dismiss it outright. Despite it being a widely-used term, it doesn’t feature in either the DSM-V or ICD-10, the two main sources for officially-recognised psychiatric disorders the world over (although that’s not a guarantee of consensus either). How can something that seems, to many, to be so straightforward be the subject of so wide a debate? We all know what sex is, we all know what addiction is, what’s the issue? First, sex is a fundamental drive inherent in practically every human. A large percentage of our brain’s systems are responsible for or at least involved in it. An underlying need to seek out sex and an ability to engage in it as and when we like is a remarkably human trait (well, maybe bonobos too). This has many significant consequences for how our societies and cultures work, but one relevant problem is, at what point do you want sex too much? Because that’s not an easy thing to pin down. Those who don’t support the idea of sex addiction often argue that it’s another attempt to pin a clinical diagnosis on “normal” human behaviour (like the dispute around grief in the DSM-V). Some even compare it to gay conversion therapy, in how it medicalises and tries to undo what is an expression of human sexuality. © 2017 Guardian News and Media Limited

Keyword: Sexual Behavior; Drug Abuse
Link ID: 24185 - Posted: 10.12.2017

By Neuroskeptic A curious flurry of headlines in praise of beer appeared this week: Beer really DOES make you happier! Key molecule boosts brain’s reward centre Drinking Beer Makes You Really Happy, Confirms Awesome New Study Drinking beer can make you happy, researchers claim It was reported that scientists from Germany have discovered that a molecule in beer called hordenine activates dopamine receptors in the brain, and thus produces a positive mood. The research in question was published back in March of this year, so I’m not sure why it only made the headlines this week – maybe Oktoberfest had something to do with it. Either way, the study did indeed find that hordenine is a dopamine D2 receptor agonist, but it’s not clear this has any relevance to beer drinkers. The German researchers, Sommer et al., are chemists, not neuroscientists. They used computational simulations to model whether 13,000 known ‘food-derived’ molecules would bind to the D2 receptor. The hordenine molecule was predicted to fit the receptor, and follow-up experiments showed that it does indeed bind to it, suggesting possible psychoactive properties.

Keyword: Drug Abuse
Link ID: 24162 - Posted: 10.09.2017

By JAIME LOWE WHEN I was 16, I was admitted to U.C.L.A.’s neuropsychiatric institute. I’d been suffering from increasing paranoia (I thought war was imminent; I thought I would be called into battle) and lack of sleep (I paced our staircase into the early hours of morning). Most profoundly, I thought my parents were actually secret agents, wearing masks, sent to monitor my behavior. My hallucinations encompassed a wide range of cultural references — Michael Jackson, the Muppets, the Night Stalker, Bob from “Twin Peaks” and the clown from “It.” My parents told the doctors at U.C.L.A. that my behavior had been erratic for two months — I was obsessing over odd things, I wasn’t eating and I was convinced that the end of the world was on its way. In short, I was manic. I was hospitalized for almost a month, and I left the institute with a diagnosis of bipolar disorder. My cure came in the form of three pink pills: 900 milligrams of lithium. It worked when I was on it. But a few years ago, my general practitioner had discovered heart-attack-level blood pressure and high creatinine measures — side effects that I couldn’t feel but were serious enough to warrant a visit to the E.R. As a result of my taking lithium, my kidneys were breaking down — I basically had a 60-year-old’s kidneys in my 37-year-old body. I was given a choice: I could stay on the lithium and get a kidney transplant eventually, or I could switch medication and risk having mania return. I chose to try a new medication. No drug could ever be as cool as lithium, a mysterious element that was present during the Big Bang and lingers throughout the galaxy as primordial stardust. Lithium has a medicinal history that dates to the Greeks and Romans, yet no doctor or researcher knows exactly how or why it works. It just does. It’s on the periodic table of elements, unpatentable and therefore cheap. Depakote, a drug officially approved for bipolar patients in the United States in the mid-1990s, has none of this cachet, and yet it’s known to be as effective as lithium in bipolar cases like mine. So my psychiatrist prescribed it to replace my pink pills. © 2017 The New York Times Company

Keyword: Schizophrenia
Link ID: 24141 - Posted: 10.03.2017

By Claudia Wallis, A funny thing happened in the Dutch city of Maastricht in the fall of 2011. A policy went into effect banning the sale of marijuana at the city’s 13 legal cannabis shops to visitors from most other countries. The goal was to discourage disruptive drug tourism in a city close to several international borders. The policy had its intended effect, but also a remarkable unintended one: foreign students attending Maastricht University starting getting better grades. According to an analysis published earlier this year in Review of Economic Studies, students who had been passing their courses at a rate of 73.9% when they could legally buy weed were now passing at a rate of 77.9% — a sizeable jump. The effect, which was based on data from 336 undergraduates in more than 4,000 courses, was most dramatic for weaker students, women, and in classes that required more math. Some of this falls in line with past research: marijuana use has been linked to inferior academic achievement (and vice versa), so it makes sense that poorer students might benefit most from a ban, and the drug is known to have immediate effects on cognitive performance, including in math. But what’s really unusual about the study, notes one of its authors, economist Ulf Zoelitz of the Briq Institute on Behavior and Inequality, is that rather than merely correlating academic performance with cannabis use, as much past research has done, “we could cleanly identify the causal impact of a drug policy.” Zoelitz co-authored the study with Olivier Marie of Erasmus University Rotterdam. © 2017 KQED Inc.

Keyword: Learning & Memory; Drug Abuse
Link ID: 24139 - Posted: 10.03.2017

by Emilie Reas Paranoia. Munchies. Giggles. Sleepiness. Memory loss. Although the effects of cannabinoids–the active components of marijuana–are familiar to many, their neurobiological substrates are poorly characterized. Perhaps the effect of greatest interest to both neuroscientists and to cannabis users hoping to preserve their cognitive function, is short-term memory impairment that often accompanies marijuana use. Our partial understanding of its physiological and behavioral effects is not for want of studies into its neural effects. Ample research has shown a range of changes to neurotransmission, receptors, ion channels and mitochondria following cannabinoid exposure. However, knowledge of its cellular and molecular properties alone cannot offer a complete picture of its system-wide effects leading to cognitive and behavioral changes. A recent study published in PLOS Computational Biology took a novel approach to address this issue, combining computational modeling with electrophysiological brain recordings from rats performing a memory task, to unravel the dynamics of neural circuits under the influence of cannabinoids. To assess memory changes induced by cannabinoids, the scientists injected tetrahydrocannabinol (THC), the main psychoactive compound in marijuana, into rats before they performed a “delayed-nonmatch-to-sample” working memory task. In this task, rats are cued with one of two levers, and after a delay, are required to select the opposite lever. Compared to sober sessions, performance under THC was impaired by 12%, confirming the all-too-familiar memory impairment associated with cannabis use. THC alters hippocampal activity

Keyword: Learning & Memory; Drug Abuse
Link ID: 24087 - Posted: 09.21.2017

Paula Span In the summer, Henry Wrenn-Meleck likes to sit on the stoop of his building on the Upper West Side of Manhattan, observing the passing urban parade. One day in late July, “one of my neighbors could see something was wrong,” he recently recalled. “I was sort of rolling around, obviously in a lot of pain. He said, ‘I have to call 911,’ and he did.” Mr. Wrenn-Meleck, 63, an independent music publisher and dealer in rare guitars, spent three weeks in a hospital, being treated for trauma from a fall he does not recall. But the underlying problem was “40 years of being a very serious alcoholic,” he said. “My body finally said no more.” Discharged from the hospital after detoxing, Mr. Wrenn-Meleck went to the New Jewish Home in Manhattan for physical therapy. He also entered its geriatric substance abuse recovery program where, he found, he was one of the younger participants. Epidemiologists at the National Institute on Alcohol Abuse and Alcoholism last month reported a jarring trend: Problem drinking is rising fast among older Americans. Their study, published in JAMA Psychiatry, compared data from a national survey taken in 2001 and 2002 and again in 2012 and 2013, each time with about 40,000 adults. Drinking had increased in every age group, the researchers found. Those over 65 remained far less likely to drink than younger people — about 55 percent of older participants told interviewers they’d imbibed in the past year. Still, that was a 22 percent increase over the two periods, the greatest rise in any age group. More troublingly, the proportion of older adults engaged in “high-risk drinking” jumped 65 percent, to 3.8 percent. The researchers’ definition: for a man, downing five or more standard drinks in a day (each containing 14 grams of alcohol) at least weekly during the past year; for a woman, four such drinks in a day.

Keyword: Drug Abuse
Link ID: 24066 - Posted: 09.15.2017

By Diana Kwon Lying in a room at Imperial College London, surrounded by low lighting and music, Kirk experienced a vivid recollection of visiting his sick mother before she passed away. “I used to go and see my mum in the hospital quite a lot,” recalls Kirk, a middle-aged computer technician who lives in London (he requested we use only his first name). “And a lot of the time she’d be asleep . . . [but] she’d always sense I was there, and after about five minutes she’d wake up, and we’d interact. I kind of went through that again—but it was a kind of letting go.” Kirk choked up slightly while retelling his experience. “It’s still a little bit emotional,” he says. “The thing I realized [was that] I didn’t want to let go. I wanted to hold on to the grief, because that was the only connection I had with my mum.” While this may sound like an ordinary therapy session, it was not what you would typically expect. Kirk was experiencing the effects of a 25-mg dose of psilocybin—the active ingredient in psychedelic “magic” mushrooms—which he had ingested as part of a 2015 clinical trial investigating the drug’s therapeutic potential. After his mother died, Kirk says, he fell into a “deep, dark pit of grief.” Despite antidepressants and regular sessions with a therapist, his condition was not improving. “I was stuck in it for years,” he recalls. So when he heard Imperial College London was recruiting participants for an upcoming trial studying the impact of psilocybin on depression, Kirk decided to sign up. © 1986-2017 The Scientist

Keyword: Depression; Drug Abuse
Link ID: 24064 - Posted: 09.14.2017

By Michelle Roberts Health editor, BBC News online There is "surprisingly limited" evidence that light drinking during pregnancy poses any risk to the baby, say UK researchers. They reviewed all the available studies done on the topic since the 1950s and found no convincing proof that a drink or two a week is harmful. The Bristol University team stress this does not mean it is completely safe. They say women should avoid all alcohol throughout pregnancy "just in case", as per official guidelines. But women who have had small amounts to drink in pregnancy should be reassured that they are unlikely to have harmed their baby. The Chief Medical Officer for the UK, Prof Dame Sally Davies, updated her advice last year to advocate total abstinence. Before that, pregnant women had been told they could drink one or two units - equivalent to one or two small glasses of wine - a week. There is no proven safe amount that women can drink during pregnancy, although the risks of drinking heavily in pregnancy are well known. Getting drunk or binge drinking during pregnancy increases the risk of miscarriage and premature birth and can lead to mental and physical problems in the baby, called foetal alcohol syndrome. The risks associated with light drinking, however, are less clear. Dr Luisa Zuccolo and colleagues found 26 relevant studies on the topic. Their review found no overwhelming proof of harm - but, in seven of the studies, light drinking was associated, on average, with an 8% higher risk of having a small baby, compared with drinking no alcohol at all. The review, in BMJ Open, also notes it appeared to increase the risk of having a premature birth. © 2017 BBC.

Keyword: Development of the Brain; Drug Abuse
Link ID: 24057 - Posted: 09.12.2017

By JOSH KATZ The first governmental account of nationwide drug deaths in 2016 shows overdose deaths growing even faster than previously thought. Drug overdoses killed roughly 64,000 people in the United States last year, according to the first governmental account of nationwide drug deaths to cover all of 2016. It’s a staggering rise of more than 22 percent over the 52,404 drug deaths recorded the previous year — and even higher than The New York Times’s estimate in June, which was based on earlier preliminary data. Drug overdoses are expected to remain the leading cause of death for Americans under 50, as synthetic opioids — primarily fentanyl and its analogues — continue to push the death count higher. Drug deaths involving fentanyl more than doubled from 2015 to 2016, accompanied by an upturn in deaths involving cocaine and methamphetamines. Together they add up to an epidemic of drug overdoses that is killing people at a faster rate than the H.I.V. epidemic at its peak. This is the first national data to break down the growth by drug and by state. We’ve known for a while that fentanyls were behind the growing count of drug deaths in some states and counties. But now we can see the extent to which this is true nationally, as deaths involving synthetic opioids, mostly fentanyls, have risen to more than 20,000 from 3,000 in just three years. Deaths involving prescription opioids continue to rise, but many of those deaths also involved heroin, fentanyl or a fentanyl analogue. There is a downward trend in deaths from prescription opioids alone. At the same time, there has been a resurgence in cocaine and methamphetamine deaths. Many of these also involve opioids, but a significant portion of drug deaths — roughly one-third in 2015 — do not. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 24027 - Posted: 09.02.2017

By Colin Hendrie and Alisdair Pickles The current global crisis of depressive illness has a simple root cause: a failure of treatment. This is the result of a broken scientific process that has for nearly 70 years fallen short in delivering the drug therapies it was set up to provide. Given existing antidepressants don’t work for many people, the excitement surrounding the development of a new class of treatments from recreational drugs such as magic mushrooms is understandable. But there are strong reasons to doubt they will have the kind of impact hoped for. Instead, we are more likely to be seeing the latest episode in a long-running saga of repeated disappointment. This saga began when antidepressant use became widespread in the 1950s and 1960s. It was hoped they would have the same transformative effect on mental illness that antibiotics had on non-viral infectious diseases. As it turned out, antidepressants were only of value to some people with depression. Studies involving thousands of people with the condition reveal that the proportion seeing a clinically significant response to antidepressants is often very similar to that seen with a placebo, which is about 40 per cent. In double-blind, placebo-controlled studies, antidepressants don’t fare well. This helps to explain why, by the end of the 20th century, Big Pharma was floundering over the development of new drugs for depression. In 2010, many companies stopped such work. © Copyright New Scientist Ltd.

Keyword: Depression; Drug Abuse
Link ID: 24017 - Posted: 08.31.2017

By Meredith Wadman Luca Rossi tried to hang himself in a bedroom in Perugia, Italy, in 2012. Suspended by his belt from a wardrobe, he had begun to choke when his fiancée unexpectedly walked in. He struggled to safety, defeated even in this intended last act. The 35-year-old physician had everything to live for: a medical career, plans for a family, and supportive parents. But Rossi* was addicted to crack cocaine. He had begun his habit not long after medical school, confidently assuming that he could control the drug. Now, it owned him. Once ebullient and passionate, he no longer smiled or cried. He knew he might be endangering his patients, but even that didn’t matter. He was indifferent to all except obtaining his next fix. “It pushes you to suicide because it fills you with your own emptiness,” he says. In the first months after his near suicide, Rossi didn’t drop his $3500-a-month habit. Early in 2013, he learned that his fiancée was pregnant. Frightened by impending fatherhood, he smoked even more. He didn’t—couldn’t—stop. Then, in April 2013, Rossi’s father, a chemist, happened upon a local newspaper article describing work just published in Nature. Neuroscientists led by Antonello Bonci and Billy Chen at the National Institute on Drug Abuse (NIDA) in Baltimore, Maryland, had studied rats trained to seek cocaine compulsively—animals so powerfully addicted that they tolerated repeated electric shocks to their feet to get their fixes. The rats had also been genetically engineered so that their neurons could be controlled with light. When the researchers stimulated the animals’ brains in an area that regulates impulse control, the rats essentially kicked their habit. “They would almost instantaneously stop searching for cocaine,” Bonci says. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging; Drug Abuse
Link ID: 24013 - Posted: 08.30.2017

Nicola Davis An article suggesting that sugar should be considered an addictive substance, and could even be on a par with abusive drugs such as cocaine, has sparked a furious backlash with experts describing the claims as “absurd”. In a narrative review published in the British Journal of Sports Medicine the authors write that sugar could act as a gateway to alcohol and other addictive substances, adding that like sugar, like cocaine and opium, is refined from plants to yield pure white crystals – a process they say “significantly adds to its addictive properties.” Too much sugar could increase depression risk in men, study suggests Read more The article was co-authored by cardiovascular research scientist James J DiNicolantonio and cardiologist James H O’Keefe, both from Saint Luke’s Mid America Heart Institute in Kansas, together with William Wilson – a physician with the nonprofit US group practice Lahey Health. “Consuming sugar produces effects similar to that of cocaine, altering mood, possibly through its ability to induce reward and pleasure, leading to the seeking out of sugar,” they write, citing rodent studies which show that sweetness is preferred even over cocaine, and that mice can experience sugar withdrawal. Speaking to the Guardian, DiNicolantonio said that the consumption of sugar was a grave concern. “In animals, it is actually more addictive than even cocaine, so sugar is pretty much probably the most consumed addictive substance around the world and it is wreaking havoc on our health.” © 2017 Guardian News and Media Limited

Keyword: Drug Abuse; Obesity
Link ID: 23999 - Posted: 08.26.2017

By Emily Underwood It doesn’t take long for tropical zebrafish to get hooked on hydrocodone. Within a week, they will risk their lives thousands of times per hour to get a dose of the opioid, shows the first study that let the fish themselves choose when to take a hit. To train them, researchers released 1.5 milligrams of hydrocodone per liter of water every time they swam over a shallow platform. The drug quickly filtered out of the tank, so they had to keep going back if they wanted to maintain their high. After just 5 days, the trained fish were visiting the opioid-delivering platform almost 2000 times every 50 minutes, the team reports online today in Behavioral Brain Research. When no drug was present, they visited the platform only about 200 times. Fish normally avoid shallow water, where they’re more likely to be spotted by predators. But over and over again, the jonesing zebrafish left the safety of deep water for the shallow platform. When the team rigged the tank so it took several visits to get a hit, the fish ramped up their efforts, returning as many as 20 times for one dose. Previous studies have shown that zebrafish exposed to opioids become stressed and anxious when the drug is taken away, displaying symptoms of withdrawal. But this is the first time scientists have shown that zebrafish will expend effort—and even court danger—to get a dose. Because zebrafish and humans share the same opioid receptor in their brains, as well as neurotransmitters such as dopamine and serotonin that signal pleasure and reward, the team hopes to use them to screen for new treatments for opioid addiction. © 2017 American Association for the Advancement of Science

Keyword: Drug Abuse
Link ID: 23998 - Posted: 08.26.2017

By Jessica Hamzelou People who use methamphetamine are almost five times more likely to have a stroke caused by a bleed in the brain, many of which are fatal. “We can add stroke to the list of terrible and devastating things that methamphetamine does,” says Damian Zuloaga, of the University at Albany, New York. Beyond the signature tooth decay known as “meth mouth”, methamphetamine also increases heart rate and blood pressure, and can trigger heart attacks. The drug can lead to psychosis, and has been linked to anxiety disorders, depression, and problems with movement similar to those seen in Parkinson’s disease. A handful of studies have also linked methamphetamine use to strokes. To explore further, Julia Lappin and her colleagues at the Australian National Drug and Alcohol Research Centre in Sydney sifted through published research on the topic. The team specifically looked for research into people under the age of 45 – a group less likely to be affected by age-related causes of stroke. They assessed the results of 77 studies in total. Most of these studies were conducted in the US, where, in 2012, around 1.2 million people reported using methamphetamine in the past year. Several of the studies the team looked at reported that strokes are responsible for between one and five per cent of methamphetamine-related deaths. And other studies found that methamphetamine was to blame for between two and six per cent of all strokes caused by a blockage in the brain’s blood flow in under 45s. © Copyright New Scientist Ltd.

Keyword: Drug Abuse; Stroke
Link ID: 23988 - Posted: 08.24.2017

Richard Harris It's always appealing to think that there could be an easy technical fix for a complicated and serious problem. For example, wouldn't it be great to have a vaccine to prevent addiction? "One of the things they're actually working on is a vaccine for addiction, which is an incredibly exciting prospect," said Dr. Tom Price, secretary of Health and Human Services. He was talking to reporters earlier this week, after the White House discussed the recommendations from a government commission tasked with suggesting ways to cope with the nation's opioid epidemic. Trump Says He Intends To Declare Opioid Crisis National Emergency But, as is so often the case, there's no quick fix on the horizon for an epidemic that is now killing more Americans than traffic accidents. Researchers have been working on vaccines against addictive drugs, including nicotine, cocaine and heroin, for almost two decades. "Like any other vaccine, you inject the vaccine and you use your immune system to produce antibodies," says Dr. Ivan Montoya, acting director of the division of Therapeutics and Medical Consequences at the National Institute on Drug Abuse. "In this case, the antibodies are against the drugs of abuse." © 2017 npr

Keyword: Drug Abuse
Link ID: 23980 - Posted: 08.22.2017

By Aggie Mika | In a report published today (August 16) in Nature, researchers uncover the mechanisms by which the psychoactive and addictive drug fenethylline, trade name Captagon, exerts its potent stimulating effects. Essentially, one component of the drug, theophylline, boosts the effects of another, amphetamine. “This combination greatly enhances amphetamine’s properties,” says coauthor and Scripps Research Institute researcher Kim Janda in a press conference this week, Reuters reports. “So this now makes sense why it’s being so heavily abused.” In exploring fenethylline’s mode of action, the researchers came upon a method to vaccinate against the drug in mice using small, antibody-eliciting molecules called haptens that target the drug’s chemical components. Once antibodies for a specific chemical are prompted by a vaccine, they bind to and prevent it from interacting with its receptors in the body, thus preventing the effects of the drug driven by that chemical. Fenethylline’s use is mostly confined to the Middle East, where approximately 40 percent of young adult drug users in Saudi Arabia are addicted to the drug, the authors write in their report. According to Reuters, the drug initially sparked Janda’s interest because of its use by Islamic State jihadists. According to the San Diego Union-Tribune, “Syrian civil war combatants and Islamic State terrorists have reportedly used the drug to boost their fighting ability and to lessen fear.” © 1986-2017 The Scientist

Keyword: Drug Abuse; Neuroimmunology
Link ID: 23971 - Posted: 08.18.2017

By Megan Scudellari Neuropharmacology postdoc Nick DiPatrizio was stumped. His advisor, University of California, Irvine, researcher Daniele Piomelli, had discovered eight years earlier that hungry rats have high levels of endocannabinoids, endogenous molecules that bind to the same receptors as the active ingredient in marijuana. Now, in 2009, DiPatrizio was trying to identify exactly where and how those molecules were controlling food intake in rats. But under specific feeding conditions, he couldn’t locate any changes in endocannabinoid levels in the brain, which is flush with endocannabinoid receptors and the obvious place to look for behavioral signals. Piomelli gently chastised his mentee. “He said, ‘You’re being neurocentric. Remember, there’s a body attached to the head. Look in the other organs of the body,’ ” recalls DiPatrizio. So the young scientist persisted, and eventually discovered that hunger—and the taste of fat—leads to increased endocannabinoid levels in the jejunum, a part of the small intestine. Endocannabinoid signaling in the gut, not the brain, was controlling food intake in the rodents in response to tasting fats.1 The evolution of endocannabinoid research has mirrored DiPatrizio’s early thinking: ever since the first endocannabinoid receptor was identified in the late 1980s, the field has been overwhelmingly focused on the central nervous system. The main endocannabinoid receptor, CB1, was first discovered in a rat brain and is now known to be among the most abundant G protein–coupled receptors in neurons there. Plus, cannabis is well-known for its psychotropic effects. “That has led the research field to be very CNS-oriented,” says Saoirse O’Sullivan, who studies endocannabinoids at the University of Nottingham in the U.K. © 1986-2017 The Scientist

Keyword: Drug Abuse
Link ID: 23954 - Posted: 08.14.2017

By Kerry Grens The popular chemogenetic technique for controlling cells does not operate in vivo in the way scientists had assumed. Reporting in Science yesterday (August 3), researchers show that CNO, a drug used in the DREADDs method (designer receptors exclusively activated by designer drugs), is not actually responsible for the effects scientists observe. Rather, it’s clozapine, a metabolite of CNO with numerous cellular targets, that binds the receptors. These results make it imperative for researchers to do proper controls with clozapine, and indicate that they should change their protocols altogether. “I’m glad I don’t own stock in CNO,” says Scott Sternson, a neuroscientist at the Janelia Research Campus. “There’s no reason to use CNO anymore.” Although it may be the end of CNO in these studies, coauthor Mike Michaelides of the National Institute on Drug Abuse tells The Scientist the results don’t necessarily mean the end of DREADDs. In fact, his findings might simplify things. Rather than using CNO, researchers can just administer clozapine instead because it’s the real actuator of the technique. “If they use proper controls, then hopefully it should be fine,” he says. The idea behind DREADDs is that a receptor is introduced into cells that will only respond to a particular drug, in this case CNO. Likewise, the drug will only target that receptor. The technique allows researchers to control neural activity. Michaelides says that although it’s a commonly used method, no one had done the critical experiments to observe CNO interacting directly with DREADDs in vivo. © 1986-2017 The Scientist

Keyword: Miscellaneous
Link ID: 23931 - Posted: 08.08.2017

/ By Robin Lloyd While broadly welcomed by public health advocates as an important step to further curb tobacco use, many of the commitments in a new plan to tackle the problem, announced last Friday by Food and Drug Administration Commissioner Scott Gottlieb, actually involve gathering more input for future policies, rather than taking action now. “We expect to take meaningful steps in 2017 to advance important regulatory components that address the key aspects of this new policy,” FDA spokesman Michael Felberbaum said in an email message to Undark. “We do not have any additional details to share at this time.” That strikes some public health advocates as a bit of foot-dragging. “A lot of these issues they’re raising that they say they have to consider have been considered, have been researched, have been studied,” says Eric Lindblom, director for tobacco control and food and drug law at the O’Neill Institute for National and Global Health Law at Georgetown University. Lindblom has a long resume for developing tobacco control policies to improve public health, including a 2011-2014 stint at the FDA’s Center for Tobacco Products. “FDA saying that ‘We’re going to look into nicotine reduction,’ without also saying, ‘We’re going to issue a proposed rule before the end of this year, or before June of next year,’ just opens the door to continued discussion and talking and all the rest, without actually ever getting anything done,” Lindblom said. Copyright 2017 Undark

Keyword: Drug Abuse
Link ID: 23928 - Posted: 08.08.2017