Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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By Amelia Nierenberg A couple of glasses of wine or a few drinks in the evening will probably make you fall asleep faster than normal. Who among us hasn’t left the dishes for the next morning or neglected a skin-care routine after a dinner party or festive night out? But even if you thud into dreamland, there’s a good chance that too much alcohol will mean a fitful night of sleep. That’s because alcohol disrupts what’s known as your sleep architecture, the normal phases of deeper and lighter sleep we go through every night. A night of drinking can “fragment,” or interrupt, these patterns, experts say, and you may wake up several times as you ricochet through the usual stages of sleep. “You pay for it in the second half of the night,” said Dr. Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles. Alcohol is “initially sedating, but as it’s metabolized, it’s very activating.” Here’s how it breaks down. In the first half of the night, when fairly high levels of alcohol are still coursing through your bloodstream, you’ll probably sleep deeply and dreamlessly. One reason: In the brain, alcohol acts on gamma-aminobutyric acid, or GABA, a neurotransmitter that inhibits impulses between nerve cells and has a calming effect. Alcohol can also suppress rapid eye movement, or REM sleep, which is when most dreaming occurs. Later in the night, as alcohol levels drop, your brain kicks into overdrive. You may toss and turn as your body undergoes a rebound arousal. “As the levels decline, you’re going to get more issues with the fragmentation,” said Dr. R. Nisha Aurora, a member of the board of directors of the American Academy of Sleep Medicine. You’ll also probably have more vivid or stressful dreams and — because fitful sleep means that you’re waking up more regularly — you are more likely to remember them.

Keyword: Sleep; Drug Abuse
Link ID: 28183 - Posted: 02.02.2022

ByRobert F. Service More than 50 years after the Summer of Love, psychedelics are again the rage. This time the love comes from doctors beginning to embrace psychedelics such as LSD and psilocybin to treat depression, substance abuse, and other serious mental health conditions. But because the drugs cause hallucinations, their medical use requires intensive monitoring by clinicians. That drives up treatment costs, making psychedelics impractical for widespread therapeutic use. In recent years, researchers have begun to tweak psychedelics’ chemical structures, aiming to make analogs that retain medical usefulness but don’t cause hallucinations. Now, researchers report in Science they’ve teased apart the molecular interactions responsible for psychedelics’ antidepressive effects from those that cause hallucinations. They used that knowledge to make new compounds that appear to activate brain cellular circuits that help relieve depression without triggering a closely related pathway involved in hallucinations. So far, the compounds have only been studied in mice. But if such psychedelic analogs work in humans, they could spawn new families of pharmaceuticals. “This work is going to generate a lot of interest,” says Bryan Roth, a pharmacologist at the University of North Carolina School of Medicine, whose lab is also seeking nonhallucinogenic psychedelic analogs. The need is profound. Mental or neurological disorders are estimated to affect roughly one-quarter of U.S. adults every year, and therapies often don’t work. LSD, psilocybin (the main ingredient in magic mushrooms), and other psychedelics might do better. Studies have shown a single dose of psilocybin can offer relief from depression for months at a time, and last year, a clinical trial of 3,4-methylenedioxymethamphetamine, or ecstasy, showed it can alleviate posttraumatic stress disorder. © 2022 American Association for the Advancement of Science.

Keyword: Depression; Drug Abuse
Link ID: 28177 - Posted: 01.29.2022

Sung Han & Shijia Liu You’re startled by a threatening sound, and your breath quickens. You smash your elbow and pant in pain. Why does your breathing rate increase dramatically when you’re hurting or anxious? As neurobiologists studying how the brain responds to environmental threats and the neural circuitry of emotion, we were curious about the answer to this question ourselves. In our recently published study, we discovered that one particular circuit of the brain in mice underlies this tight connection between pain, anxiety and breathing. And this discovery may eventually help us develop safer pain killers for humans. One of the most common symptoms of both pain and anxiety disorders is shortness of breath, or hyperventilation. On the other hand, slow, deep breathing can reduce pain and distress. The simplest way to explain this, we reasoned, is the existence of a common pathway in the brain that regulates breathing, pain and anxiety simultaneously. So we searched for brain regions previously reported to regulate breathing, pain and emotion. A small area in the brainstem called the lateral parabrachial nucleus caught our attention. Not only is it part of the breathing regulation center of the brain, it also mediates pain and negative emotions like fear and anxiety. Searching through a public database of gene expression patterns, or how genetic material is translated into proteins that let cells function, in the mouse brain, we serendipitously found that one type of opioid receptor called the µ-opioid receptor is highly expressed in parabrachial neurons. © 2010–2022, The Conversation US, Inc.

Keyword: Emotions; Drug Abuse
Link ID: 28167 - Posted: 01.22.2022

By Lisa Sanders, M.D. The mother stood in the baggage-claim area of the Buffalo Niagara International Airport, waiting for her 37-year-old son, who had just flown in from North Carolina. The carousel was nearly empty by the time she caught sight of him. She was shocked by how sick he looked. His face was pale and thin, his hair and clothes rumpled as if he felt too awful to care. Most surprising of all: He was being rolled toward her in a wheelchair. “I had some trouble with the stairs,” he explained. He thanked the attendant and then struggled to get to his feet. He didn’t make it. Before he got more than a few inches off the seat, his arms and then his legs began to shake and wobble, and he fell heavily back into the chair. His mother collected his bag and pushed him out to where her husband was waiting in the car. On the drive home, the young man struggled to explain what was going on. He had always considered himself to be pretty strong and healthy, but these past few weeks had been rough. It started in his legs. He felt wobbly. When he walked, his hips, legs and especially his feet felt as if they might not be able to hold him up. He saw his physician assistant about it — he worried that it was caused by the cholesterol-lowering medication he had started taking — but the P.A. assured him it wasn’t. He was running a few times a week, but he had to stop because his legs were done well before the run was. And he didn’t feel as sharp as he used to be. His brain seemed foggy and slow. Then this morning he had trouble climbing the stairs to the plane. That was scary. The guy behind him helped by holding up his backpack, but his feet felt like dead weights. He had to use his arms to help get his body up high enough to take each step. Once on the plane, he supported himself on the headrests to get to his assigned seat. They offered the wheelchair when he arrived in Buffalo, and he gratefully accepted. His mother tentatively asked if he thought he should see a doctor. She knew he hated it when she tried to tell him what to do. He had flown up to see a football game with her ex-husband, his father, and a hockey game with his stepbrother. If he didn’t feel any better after that, he conceded, it would be time to see a doctor. © 2022 The New York Times Company

Keyword: Movement Disorders; Drug Abuse
Link ID: 28150 - Posted: 01.12.2022

By Charles F. Zorumski One minute you’re enjoying a nice buzz, the next your brain stops recording events that are taking place. The result can mean having vague or no memory of a time period ranging anywhere from a few minutes up to several hours. Scary—isn’t it? Unfortunately, alcohol-induced blackouts aren’t a rarity, either. A 2015 survey of English teenagers who drank showed 30 percent of 15-year-olds and 75 percent of 19-year-olds suffered alcohol-induced blackouts. In medical terms this memory loss is a form of temporary anterograde amnesia, a condition where the ability to form new memories is, for a limited time, impaired. That means you can’t remember a stretch of time because your brain was unable to record and store memories in the first place. Neuroscientists do not fully understand how blackouts occur. Researchers long assumed alcohol impairs memory because it kills brain cells. Indeed, long-standing alcohol abuse can damage nerve cells and permanently impact memory and learning. It is unlikely, however, that brain damage is behind acute blackouts. It is clear that processes in the hippocampus—the area of brain involved in the formation, storage and retrieval of new memories—are disturbed. Specifically, it appears alcohol impairs the so-called long-term potentiation of synapses at the pyramidal cells in the hippocampus. Alcohol alters the activity of certain glutamate receptors, thereby boosting the production of specific steroid hormones. This in turn slows the long-term potentiation of hippocampal synapses. Normally this mechanism, responsible for strengthening the synaptic transfer of information between neurons, is the basis of memory formation. © 2022 Scientific American,

Keyword: Drug Abuse; Learning & Memory
Link ID: 28142 - Posted: 01.08.2022

By Emily Witt In the fall of 1972, a psychiatrist named Salvador Roquet travelled from his home in Mexico City to the Maryland Psychiatric Research Center, an institution largely funded by the United States government, to give a presentation on an ongoing experiment. For several years, Roquet had been running a series of group-therapy sessions: over the course of eight or nine hours, his staff would administer psilocybin mushrooms, morning-glory seeds, peyote cacti, and the herb datura to small groups of patients. He would then orchestrate what he called a “sensory overload show,” with lights, sounds, and images from violent or erotic movies. The idea was to push the patients through an extreme experience to a psycho-spiritual rebirth. One of the participants, an American psychology professor, described the session as a “descent into hell.” But Roquet wanted to give his patients smooth landings, and so, eventually, he added a common hospital anesthetic called ketamine hydrochloride. He found that, given as the other drugs were wearing off, it alleviated the anxiety brought on by these punishing ordeals. Clinicians at the Maryland Psychiatric Research Center had been studying LSD and other psychedelics since the early nineteen-fifties, beginning at a related institution, the Spring Grove Hospital Center. But ketamine was new: it was first synthesized in 1962, by a researcher named Calvin Stevens, who did consulting work for the pharmaceutical company Parke-Davis. (Stevens had been looking for a less volatile alternative to phencyclidine, better known as PCP.) Two years later, a doctor named Edward Domino conducted the first human trials of ketamine, with men incarcerated at Jackson State Prison, in Michigan, serving as his subjects. At higher doses, Domino noticed, ketamine knocked people out, but at lower ones it produced odd psychoactive effects on otherwise lucid patients. Parke-Davis wanted to avoid characterizing the drug as psychedelic, and Domino’s wife suggested the term “dissociative anesthetic” to describe the way it seemed to separate the mind from the body even as the mind retained consciousness. The F.D.A. approved ketamine as an anesthetic in 1970, and Parke-Davis began marketing it under the brand name Ketalar. It was widely used by the U.S. military during the Vietnam War, and remains a standard anesthetic in emergency rooms around the world. © 2021 Condé Nast.

Keyword: Depression; Drug Abuse
Link ID: 28132 - Posted: 12.31.2021

By Vanessa Barbara JUIZ DE FORA, Brazil — My first encounter with ketamine did not go well. A lifelong depressive — I picked up the habit of despairing sadness in early adulthood, and it remained faithfully with me — I’d turned to a more experimental form of treatment: ketamine infusions, in which a kindly anesthesiologist funnels the drug into a sad person’s veins for around 50 minutes and hopes it perks her up. Forty-five minutes into my first session, I rather anxiously asked my partner, who was in the room with me, if our 3-year-old daughter was fine. He decided it was the perfect time for a joke. Our daughter, he answered, was safe at home — and as a matter of fact, he added, she was already a very independent 15-year-old. I panicked. While under the strong, dissociative effect of the drug, patients sometimes enter what’s called a k-hole, in which their sense of time and space is distorted or eliminated. In that state of oblivion, I found it entirely plausible that my daughter was not a toddler anymore, but a strong-willed teenager. I became very distressed. My heartbeat accelerated. The anesthesiologist hurriedly ended the session as my partner said: “I’m kidding! Sorry! She’s still 3!” It was an inauspicious start, but I was determined to make the best of it. Ketamine, long used as an anesthetic but better known as an illegal party drug and, of course, a horse tranquilizer, has in recent years been gaining traction as an antidepressant. People have written enthusiastic accounts of their experiences, and researchers and psychiatrists, in a cascade of studies, have pointed to its possible benefits, not least the speed with which it can alleviate symptoms. Today, hundreds of clinics around the world provide infusions to people who have found little, if any, improvement with other treatments. That’s where I come in. Over the years, apart from the good old psychotropic medications, I have tried several types of talk therapy, meditation, acupuncture, singing lessons, bungee jumping and transcranial magnetic stimulation. (I still have sweet memories of the woodpecker sounds tapped into my brain.) © 2021 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 28130 - Posted: 12.29.2021

By Gretchen Reynolds People who work out regularly and are aerobically fit tend to guzzle a surprising amount of alcohol, according to a new study, well timed for the holidays, of the interplay between fitness, exercise and imbibing. The study, which involved more than 40,000 American adults, finds that active, physically fit men and women are more than twice as likely to be moderate or heavy drinkers as people who are out of shape. The results add to mounting evidence from previous studies — and many of our bar tabs — that exercise and alcohol frequently go hand in hand, with implications for the health effects of each. Many people, and some researchers, might be surprised to learn how much physically active people tend to drink. In general, people who take up one healthy habit, such as working out, tend to practice other salubrious habits, a phenomenon known as habit clustering. Fit, active people seldom smoke, for instance, and tend to eat healthful diets. So, it might seem logical that people who often exercise would drink alcohol sparingly. But multiple studies in recent years have found close ties between working out and tippling. In one of the earliest, from 2001, researchers used survey answers from American men and women to conclude that moderate drinkers, defined in that study as people who finished off about a drink a day, were twice as likely as those who didn’t drink at all to exercise regularly. Later studies found similar patterns among college athletes, who drank substantially more than other collegians, a population not famous for its temperance. © 2021 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 28121 - Posted: 12.22.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 28117 - Posted: 12.18.2021

By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

Keyword: Depression; Drug Abuse
Link ID: 28099 - Posted: 12.04.2021

By Ariana Remmel Scientists have finally sniffed out the molecules behind marijuana’s skunky aroma. The heady bouquet that wafts off of fresh weed is actually a cocktail of hundreds of fragrant compounds. The most prominent floral, citrusy and piney overtones come from a common class of molecules called terpenes, says analytical chemist Iain Oswald of Abstrax Tech, a private company in Tustin, Calif., that develops terpenes for cannabis products (SN: 4/30/18). But the source of that funky ganja note has been hard to pin down. Now, an analysis is the first to identify a group of sulfur compounds in cannabis that account for the skunklike scent, researchers report November 12 in ACS Omega. Oswald and colleagues had a hunch that the culprit may contain sulfur, a stinky element found in hops and skunk spray. So the team started by rating the skunk factor of flowers harvested from more than a dozen varieties of Cannabis sativa on a scale from zero to 10, with 10 being the most pungent. Next, the team created a “chemical fingerprint” of the airborne components that contributed to each cultivar’s unique scent using gas chromatography, mass spectroscopy and a sulfur chemiluminescence detector. As suspected, the researchers found small amounts of several fragrant sulfur compounds lurking in the olfactory profiles of the smelliest cultivars. The most dominant was a molecule called prenylthiol, or 3-methyl-2-butene-1-thiol, that gives “skunked beer” its notorious flavor (SN: 11/27/05). © Society for Science & the Public 2000–2021

Keyword: Chemical Senses (Smell & Taste); Drug Abuse
Link ID: 28092 - Posted: 12.01.2021

By Kim Tingley When they first appeared in the United States in the mid-2000s, “electronic nicotine delivery systems” — e-cigarettes, vapes, e-liquids and other wares that contain the stimulant found in tobacco — were subject to little federal oversight. Their makers could incorporate countless other ingredients and flavorings. Like cigarettes before them, the devices proved extremely attractive to young people; in 2018, the surgeon general declared youth vaping an “epidemic” and noted that one in five high schoolers and one in 20 middle schoolers used e-cigarettes. Nicotine can harm the developing brain, and e-cigarettes contain potentially harmful toxins like heavy metals; the long-term effects of vaping — the heating of nicotine to create an inhaled aerosol — are uncertain. Despite these concerns, public-​health officials in the U.S. hope that, given a choice in the open market, people already addicted to nicotine will choose e-cigarettes over cigarettes — a deadly consumer product so successful at attracting and retaining users that it has killed as many as 24 million Americans over the past six decades. Because e-cigarettes generally contain fewer toxic chemicals than tobacco smoke, they are believed to be less damaging than cigarettes. If a sizable number of the one in seven adults in the U.S. who smoke switched to e-cigarettes, the theory goes, significantly fewer people might suffer from cancer and cardiovascular and respiratory diseases. In 2016, in an effort to mitigate the potential harms of e-cigarettes, the Food and Drug Administration began regulating them as “new tobacco products.” It became illegal to sell e-cigarettes to anyone under 18 (a cutoff that rose nationally to 21 in late 2019), and the agency was empowered to require warning labels. The F.D.A. also gained the authority to keep products out of the marketplace, unless it could be demonstrated that their public-health benefit outweighed their risks. (As a result of legislation passed in 2009, this condition applies to new tobacco products in general; cigarettes themselves, and other tobacco products on the market before Feb. 15, 2007, don’t have to meet the same standard.) As of last month, the agency had denied nearly a million applications. But a vaporizer and two liquids, in regular tobacco and menthol flavors, were authorized, after the F.D.A. declared that data submitted by their manufacturer showed that they were indeed less toxic than cigarettes and could, in the words of the agency’s news release, “benefit addicted adult smokers who switch to these products.” This would “outweigh the risk to youth” and lead to an overall “protection of the public health.” © 2021 The New York Times Company

Keyword: Drug Abuse
Link ID: 28090 - Posted: 11.24.2021

By Emily Willingham As with most decision points around pregnancy, cannabis use is a fraught subject. Researchers can’t assess it in randomized trials because dosing pregnant people with the psychoactive substance is unethical. The next best thing is studies with enough participants who use cannabis on their own, allowing for comparisons with those who do not. The findings of one such study, published on November 15 in the Proceedings of the National Academy of Sciences USA, highlight symptoms of increased anxiety, hyperactivity and aggression in children whose parents used cannabis during pregnancy. And its analysis of placental tissue points to changes in the activity of immunity-related genes. Today pregnant people “are being bombarded with a lot of ads to treat nausea and anxiety during pregnancy” with cannabis, says the paper’s senior author Yasmin Hurd, director of the Addiction Institute at Mount Sinai. “Our studies are about empowering them with knowledge and education so that they can make decisions.” The results are “very striking, very much a first,” says Daniele Piomelli, a professor and director of the Center for the Study of Cannabis at the University of California, Irvine, who was not involved in the work. Pregnancy studies in rodents and even in sheep, which have a placenta more like ours, have required cautious interpretations of findings that show effects on offspring behavior and function, he says. The new study is one of the first to tackle the question in people “in a systematic way,” Piomelli adds. © 2021 Scientific American

Keyword: ADHD; Drug Abuse
Link ID: 28078 - Posted: 11.17.2021

Sarah Marsh and Hannah Devlin A growing number of private clinics are offering ketamine for depression, according to experts who warn of a potential “wild west” of providers with no national register of patients’ treatment being integrated into overall NHS care. At least six private providers in the UK offer the drug for depression. In March the first service that also includes psychotherapy opened in Bristol, charging £6,000 for a course of low-dose treatments and talking therapy. But health experts expressed concern about creating a two-tier system in which the novel treatment is unavailable to NHS patients. They also warned of “doctor shopping”, where patients go to a ketamine clinic one day and another the next without health professionals being able to keep track of who is getting the drug. Scientists said the NHS healthcare watchdog was taking too long to update its guidance informing clinical practice on prescribing antidepressants in the UK. It was last updated in 2009. Ketamine has a reputation as a party drug because of its short-term dissociative effects but is licensed as an anaesthetic. When abused, the drug can cause long-term problems such as ulcers, pain in the bladder and kidney problems. But it has shown potential in depression treatment trials for those who are resistant to other treatments. Because ketamine is licensed to be used by doctors as an anaesthetic it can be prescribed off-licence for depression, which is what is happening in private clinics. To be prescribed on the NHS, it would need to be approved by the National Institute for Health and Care Excellence (Nice) as a cost-effective treatment. Ketamine would also need to be authorised by the Medicines and Healthcare Regulatory Agency to be marketed as a treatment for depression. © 2021 Guardian News & Media Limited

Keyword: Depression; Drug Abuse
Link ID: 28073 - Posted: 11.13.2021

By Andrew Jacobs APPLE VALLEY, Calif. — Jose Martinez, a former Army gunner whose right arm and both legs were blown off by a roadside bomb in Afghanistan, has a new calling: He’s become one of the most effective lobbyists in a campaign to legalize the therapeutic use of psychedelic drugs across the country. On a Zoom call this spring with Connie Leyva, a Democratic legislator in California who has long opposed relaxing drug laws, Mr. Martinez told her how psilocybin, the psychoactive ingredient in “magic” mushrooms, had helped to finally quell the physical pain and suicidal thoughts that had tormented him. Ms. Leyva says she changed her mind even before the call ended, and she later voted yes on the bill, which is expected to become law early next year. “We ask these men and women to go fight for our freedoms,” she said in an interview. “So if this is something that is helping them live a more normal life, I feel like I shouldn’t stand in the way.” In the two years since Oregon, Washington, D.C., and a half-dozen municipalities decriminalized psilocybin, vets have become leading advocates in the drive to legalize psychedelic medicine, which they credit with helping ease the post-traumatic stress, anxiety and depression that are often tied to their experiences in the military. The campaign has been propelled by the epidemic of suicides among veterans of Iraq and Afghanistan, but also by the national reckoning over the mass incarceration of people on drug charges that has softened public attitudes on prohibition. More than 30,000 service members have taken their own lives in the years since Sept. 11 — four times the number of those who died on the battlefield — and the Department of Veterans Affairs has struggled to address the crisis with the traditional repertoire of pharmacological interventions. © 2021 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 28072 - Posted: 11.13.2021

By Brianna Randall Inside the Big Sky Ketamine Care clinic in Missoula, Montana, a woman relaxes in a leather recliner as soothing classical music pipes through the speakers. She watches nature scenes flicker across a TV screen as a low dose of ketamine drips into her arm for 40 minutes. A nurse monitors vitals and sits beside the woman as her mind drifts — and hopefully heals. The Montana business is just one example of the recent boom in ketamine treatment, which uses a sedative also known as an animal tranquilizer or a club drug nicknamed “Special K.” This alternative therapy option for treating mood disorders has grown in popularity as patients and medical providers look to fast-acting options for the 264 million people worldwide who suffer from depression. It’s the only legal psychedelic currently available in the U.S., though psilocybin was recently legalized for therapy in Oregon. Providers and many researchers say ketamine can alleviate anxiety or depression symptoms, including suicidality, in a matter of hours; commonly prescribed oral antidepressants, like Zoloft or Prozac, on the other hand, often take weeks before they kick-in. Still, along with its promise in psychiatric treatment, ketamine faces cultural distrust and lingering questions, especially surrounding its main side effect: feeling high, or a dissociated sense that you are separate from your mind, body and surroundings. Scientists still don’t know the exact pathways by which ketamine alleviates mood disorders, but recent research about how ketamine works in the brain — as well as how best to use it in clinical settings — may help overcome some of the distrust. © 2021 Kalmbach Media Co.

Keyword: Depression; Drug Abuse
Link ID: 28048 - Posted: 10.23.2021

By Matt Richtel and Sheila Kaplan The Food and Drug Administration for the first time on Tuesday authorized an electronic cigarette to be sold in the United States, a significant turn in one of the most contentious public health debates in decades. In greenlighting a device and tobacco-flavored cartridges marketed by R.J. Reynolds under the brand name Vuse, the agency signaled that it believed that the help certain vaping devices offer smokers to quit traditional cigarettes is more significant than the risks of ensnaring a new generation. “The authorized products’ aerosols are significantly less toxic than combusted cigarettes based on available data,” the F.D.A. said in a statement announcing the decision. The statement concluded, “The F.D.A. determined that the potential benefit to smokers who switch completely or significantly reduce their cigarette use, would outweigh the risk to youth.” The watershed decision could pave the way for authorization of some other electronic cigarettes, including those of the once-dominant maker Juul, to stay on the market. For more than a year, the manufacturers of e-cigarettes have been in a holding pattern — most of their products on the market but awaiting official authorization — as the F.D.A. has investigated whether they were a benefit or a danger to public health. “The importance of the F.D.A. authorizing a vaping product as ‘appropriate for the protection of public health’ should not be understated,” said Gregory Conley, president of the American Vaping Association, an industry group. He added, “Now that the F.D.A. has acted, we are hopeful that adult consumers and health communicators will begin to understand the harm reduction benefits offered by these and other smoke-free products.” © 2021 The New York Times Company

Keyword: Drug Abuse
Link ID: 28032 - Posted: 10.13.2021

By Erin Blakemore Methamphetamine overdoses are on the rise, a study published in JAMA Psychiatry says. When researchers from the National Institute on Drug Abuse (NIDA) and the Centers for Disease Control and Prevention analyzed data from 2015 to 2019, they found that meth overdose deaths in the United States had almost tripled. During that time span, meth-related overdoses rose from 5,526 to 15,489. This was accompanied by a 43 percent increase in people reporting meth use. Researchers believe over 2 million adults used meth during the period, up from 1.4 million. They used data from the National Vital Statistics System, which tracks births, deaths and the reasons people die. Then they looked at data from the National Survey on Drug Use and Health, which analyzes a random sample of adults in the United States. Advertisement The study shows stark differences in who uses meth. American Indians and Alaska Natives were the most likely to report methamphetamine-use disorder, meth injection and overall meth use. Black people who don’t inject meth also experienced a sharp rise in meth use, which increased more than tenfold. Gay men had the highest prevalence of meth injection. More than three times the women who reported meth use in previous years said they used the drug between 2015 and 2019. Age was a factor, too. Young adults 18 to 23 showed a fourfold increase in meth use without injection. Overall, the number rose by nearly half for all U.S. adults.

Keyword: Drug Abuse
Link ID: 28020 - Posted: 10.06.2021

Emma Yasinski Some genetic risk factors for alcohol use disorder overlap with those for neurodegenerative diseases like Alzheimer’s, scientists reported in Nature Communications on August 20. The study, which relied on a combination of genetic, transcriptomic, and epigenetic data, also offers insight into the molecular commonalities among these disorders, and their connections to immune disfunction. “By meshing findings from genome wide association studies . . . with gene expression in brain and other tissues, this new study has prioritized genes likely to harbor regulatory variants influencing risk of Alcohol Use Disorder,” writes David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in an email to The Scientist. “Several of these genes are also associated with neurodegenerative disorders—an intriguing connection because of alcohol’s ability to prematurely age the brain.” Over the past several years, researchers have published a handful of massive genome-wide association studies (GWAS) studies identifying loci—regions of the genome that can contain 10 or more individual genes—that likely influence a person’s risk of developing an alcohol use disorder (AUD). In a study published two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and first author on the new paper, and his team found evidence that the immune system might be overactive in people with AUD, but the finding left him with more questions. The first was whether excessive drinking directly causes immune dysfunction, or if instead some people’s genetic makeup puts them at risk for both simultaneously. The second was which of the dozen or so genes at each previous GWAS-identified locus actually influences drinking behaviors. Lastly, he wanted to know if there is a genetic difference between people who consume higher numbers of alcoholic beverages per week but are not diagnosed with AUD and those who have received the diagnosis. © 1986–2021 The Scientist.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27995 - Posted: 09.18.2021

David Kleinfeld My colleagues and I recently found that we were able to train mice to voluntarily increase the size and frequency of seemingly random dopamine impulses in their brains. Conventional wisdom in neuroscience has held that dopamine levels change solely in response to cues from the world outside of the brain. Our new research shows that increases in dopamine can also be driven by internally mediated changes within the brain. Dopamine is a small molecule found in the brains of mammals and is associated with feelings of reward and happiness. In 2014, my colleagues and I invented a new method to measure dopamine in real time in different parts of the brains of mice. Using this new tool, my former thesis student, Conrad Foo, found that neurons in the brains of mice release large bursts of dopamine – called impulses – for no easily apparent reason. This occurs at random times, but on average about once a minute. Pavlov was famously able to train his dogs to salivate at the sound of a bell, not the sight of food. Today, scientists believe that the bell sound caused a release of dopamine to predict the forthcoming reward. If Pavlov’s dogs could control their cue-based dopamine responses with a little training, we wondered if our mice could control their spontaneous dopamine impulses. To test this, our team designed an experiment that rewarded mice if they increased the strength of their spontaneous dopamine impulses. The mice were able to not only increase how strong these dopamine releases were, but also how often they occurred. When we removed the possibility of a reward, the dopamine impulses returned to their original levels. In the 1990s, neuroscientist Wolfram Schultz discovered that an animal’s brain will release dopamine if the animal expects a reward, not just when receiving a reward. This showed that dopamine can be produced in response to the expectation of a reward, not just the reward itself – the aforementioned modern version of Pavlov’s dog. © 2010–2021, The Conversation US, Inc.

Keyword: Drug Abuse; Learning & Memory
Link ID: 27993 - Posted: 09.15.2021