Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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By HELENE STAPINSKI IN an office of the American Museum of Natural History, a team of scientists, artists and multimedia experts were discussing what had poisoned Skippy, a cute Jack Russell terrier that had keeled over sick in his virtual backyard. Was it the chocolate he found in the garbage can? Did a snake, or a black widow spider, bite him? Or was a poisonous cane toad to blame? Skippy is just one of many victims in the museum’s show, “The Power of Poison,” opening Nov. 16, to which the staff was busy applying finishing touches. Using iPads, visitors can examine the circumstances surrounding Skippy’s fictional poisoning and, controlling their experience individually, take a crack at solving the mystery. But because the museum is popular with small children, Skippy does not die. Instead, his animated eyes turn into Xs, he runs erratically around the yard, he drools and he vomits a bit. Eventually, though, Skippy rallies to full health. “We were not going to make this a scary show,” said the exhibit’s curator, Dr. Mark Siddall. “Instead you walk out saying, ‘Wow. That was cool.’ ” Dr. Siddall spent two hours enthusiastically discussing poison and its properties at the museum recently, walking through some of the show’s highlights. The exhibit, which takes a look at poison’s role in nature, myth, medicine and human history, examines killer caterpillars, zombie ants and deadly vipers. It also looks at the possible victims, like the heavily slumbering Snow White. Plus the age-old question of what killed Cleopatra. Was it an asp, or something else? And while we’re at it, was Napoleon really poisoned with arsenic? © 2013 The New York Times Company
Link ID: 18837 - Posted: 10.26.2013
by Tina Hesman Saey BOSTON — A variant in a gene involved in breaking down chemicals in smoke triples a smoker’s risk of multiple sclerosis, a study shows. Smoking increases by 30 to 50 percent a person’s risk of multiple sclerosis, a disease in which the immune system attacks a waxy coating around nerve cells. Scientists don’t know exactly how smoking contributes to the disease. Farren Briggs of the University of California, Berkeley and his colleagues searched DNA of thousands of people in Northern California, Norway and Sweden for genetic variants associated with both smoking and multiple sclerosis. The team found hundreds of variants in three genes involved in breaking down chemicals found in smoke, Briggs said October 24 at the annual meeting of the American Society of Human Genetics. In particular, people who smoke and who have two copies of a variant in the NAT1 gene have a risk of getting MS that is three times higher than that of smokers without the variant. For nonsmokers, the variant doesn’t increase MS risk. Citations F.B.S. Briggs et al. NAT1 in an important genetic effect modifier of tobacco smoke exposure in multiple sclerosis susceptibility in 5,453 individuals. American Society of Human Genetics annual meeting, Boston, October 24, 2013. Further Reading N. Seppa. Old drug may have new trick. Science News. Vol. 184, November 2, 2013, p. 16. N. Seppa. Black women may have highest multiple sclerosis rates. Science News. Vol. 183, June 15, 2013, p. 15. © Society for Science & the Public 2000 - 2013
Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.
by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.
By Larry Greenemeier The leaves of the herb kratom (Mitragyna speciosa), a native of Southeast Asia in the coffee family, are used to relieve pain and improve mood as an opiate substitute and stimulant. The herb is also combined with cough syrup to make a popular beverage in Thailand called “4x100.” Because of its psychoactive properties, however, kratom is illegal in Thailand, Australia, Myanmar (Burma) and Malaysia. The U.S. Drug Enforcement Administration lists kratom as a “drug of concern” because of its abuse potential, stating it has no legitimate medical use. The state of Indiana has banned kratom consumption outright. Now, looking to control its population’s growing dependence on methamphetamines, Thailand is attempting to legalize kratom, which it had originally banned 70 years ago. At the same time, researchers are studying kratom’s ability to help wean addicts from much stronger drugs, such as heroin and cocaine. Studies show that a compound found in the plant could even serve as the basis for an alternative to methadone in treating addictions to opioids. The moves are just the latest step in kratom’s strange journey from home-brewed stimulant to illegal painkiller to, possibly, a withdrawal-free treatment for opioid abuse. With kratom’s legal status under review in Thailand and U.S. researchers delving into the substance’s potential to help drug addicts, Scientific American spoke with Edward Boyer, a professor of emergency medicine and director of medical toxicology at the University of Massachusetts Medical School. Boyer has worked with Chris McCurdy, a University of Mississippi professor of medicinal chemistry and pharmacology, and others for the past several years to better understand whether kratom use should be stigmatized or celebrated. © 2013 Scientific American
Keyword: Drug Abuse
Link ID: 18726 - Posted: 10.01.2013
Selectively bred strains of laboratory rats that either prefer or avoid alcohol have been a mainstay of alcohol research for decades. So-called alcohol-preferring rats voluntarily consume much greater amounts of alcohol than do non-preferring rats. Scientists at the National Institutes of Health now report that a specific gene plays an important role in the alcohol-consuming tendencies of both types of rats. “This study advances our understanding of the genetics and neurobiology of alcohol consumption in an important animal model of human alcoholism,” says Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH. As reported online in the Proceedings of the National Academy of Sciences, a diverse team of scientists, led by David Goldman, M.D., chief of NIAAA’s Laboratory of Neurogenetics, used exome sequencing, an approach that comprehensively analyzes the DNA that encodes proteins. They found a severely dysfunctional form of the gene for a brain signaling molecule called metabotropic glutamate receptor 2 (Grm2), known as a stop codon, in alcohol-preferring rats but not in non-preferring rats. The researchers then demonstrated that drugs and genetic changes that block Grm2 increased alcohol consumption in normal rats and mice. “We’ve long known that genes play an important role in alcoholism,” says Dr. Goldman. “However, the genes and genetic variants that cause alcoholism have remained largely unknown. This first discovery of a gene accounting for alcohol preference in a mammalian model illustrates that genomic analysis of a model organism is a powerful approach for a complex disease such as alcoholism.”
The Conservative government is launching a $1.3-billion free market in medical marijuana on Tuesday, eventually providing an expected 450,000 Canadians with quality weed. Health Canada is phasing out an older system on Monday that mostly relied on small-scale, homegrown medical marijuana of varying quality, often diverted illegally to the black market. In its place, large indoor marijuana farms certified by the RCMP and health inspectors will produce, package and distribute a range of standardized weed, all of it sold for whatever price the market will bear. The first sales are expected in the next few weeks, delivered directly by secure courier. "We're fairly confident that we'll have a healthy commercial industry in time," Sophie Galarneau, a senior official with the department, said in an interview. "It's a whole other ball game." The sanctioned birth of large-scale, free-market marijuana production comes as the Conservatives pillory Liberal Leader Justin Trudeau's campaign to legalize recreational marijuana. Health Canada is placing no limits on the number of these new capital-intensive facilities, which will have mandatory vaults and security systems. Private-dwelling production will be banned. Imports from places such as the Netherlands will be allowed. Already 156 firms have applied for lucrative producer and distributor status since June, with the first two receiving licences just last week. © CBC 2013
By JOHN SCHWARTZ Candace Pert, a neuroscientist who helped discover a fundamental element of brain chemistry as a graduate student and went on to become a major proponent of alternative medicine, died on Sept. 12 at her home in Potomac, Md. She was 67. The cause was cardiac arrest, said her sister, Deane Beebe. Dr. Pert was working at the Johns Hopkins University School of Medicine in the 1970s when a team she was on found one of the most sought-after objects in brain research: the receptor in the brain that opiates like morphine fit into, like a key in a lock, allowing the drug’s effects to work. The discovery of the opioid receptor would, in 1978, earn the coveted Albert Lasker Award, often a precursor to the Nobel Prize. The award went to Solomon H. Snyder, who headed the lab. Neither Dr. Pert nor any of the other lab assistants was cited. Such omissions are common in the world of science; the graduate student in the lab rarely gets credit beyond being the first name on the papers describing the research. But Dr. Pert did something unusual: she protested, sending a letter to the head of the foundation that awards the prize, saying she had “played a key role in initiating the research and following it up” and was “angry and upset to be excluded.” Her letter caused a sensation in the field. Some saw her exclusion as an example of the burdens and barriers women face in science careers. In a 1979 article about Dr. Pert in the The Washington Post, Dr. Snyder, who had lauded Dr. Pert’s contributions in his Lasker acceptance speech, argued that “that’s the way the game is played,” adding that today’s graduate students will be tomorrow’s lab chiefs, and that “when they have students, it will be the same.” © 2013 The New York Times Company
Keyword: Pain & Touch
Link ID: 18685 - Posted: 09.21.2013
By Stuart McMillen A classic experiment into drug addiction science. Would rats choose to take drugs if given a stimulating environment and social company?
Keyword: Drug Abuse
Link ID: 18669 - Posted: 09.19.2013
By Sarah Amandolare Decades of research and billions of dollars go into developing and marketing drugs. Here's the life span of a typical brain drug—Cymbalta, a popular antidepressant Tuberculosis researchers discover that a drug that treats infections, called iproniazid, also boosts patients' mood. They learn that iproniazid slows the breakdown of three chemicals in the brain— serotonin, norepinephrine and dopamine. These molecules take center stage in the next two decades, as scientists search for antidepressants. 1974 Eli Lilly researchers develop fluoxetine (Prozac), the first selective serotonin reuptake inhibitor. Fluoxetine thwarts the absorption, or “reuptake,” of serotonin. This boosts levels of the chemical in the pockets of space between neurons. Prozac does not hit drugstore shelves until 1988. 1980s Scientists start tinkering with the reuptake of norepinephrine and dopamine, which, in addition to elevating mood, can relieve muscle and joint pain. They dub this new class of antidepressants serotonin-norepinephrine reuptake inhibitors (SNRIs). At Eli Lilly, scientists begin developing an SNRI with a special focus on norepinephrine. One of their molecules becomes known as duloxetine, later branded Cymbalta. 1986 © 2013 Scientific American
Link ID: 18660 - Posted: 09.18.2013
By JOHN TIERNEY Long before he brought people into his laboratory at Columbia University to smoke crack cocaine, Carl Hart saw its effects firsthand. Growing up in poverty, he watched relatives become crack addicts, living in squalor and stealing from their mothers. Childhood friends ended up in prisons and morgues. Carl Hart, an associate professor of psychology at Columbia, arranged experiments in which drug addicts were offered a choice between a dose of the drug or cash or vouchers. When the dose was smaller, addicts often chose cash or vouchers instead. Those addicts seemed enslaved by crack, like the laboratory rats that couldn’t stop pressing the lever for cocaine even as they were starving to death. The cocaine was providing such powerful dopamine stimulation to the brain’s reward center that the addicts couldn’t resist taking another hit. At least, that was how it looked to Dr. Hart when he started his research career in the 1990s. Like other scientists, he hoped to find a neurological cure to addiction, some mechanism for blocking that dopamine activity in the brain so that people wouldn’t succumb to the otherwise irresistible craving for cocaine, heroin and other powerfully addictive drugs. But then, when he began studying addicts, he saw that drugs weren’t so irresistible after all. “Eighty to 90 percent of people who use crack and methamphetamine don’t get addicted,” said Dr. Hart, an associate professor of psychology. “And the small number who do become addicted are nothing like the popular caricatures.” © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18655 - Posted: 09.17.2013
By Gary Stix New types of drugs for schizophrenia, depression and other psychiatric disorders are few and far between—and a number of companies have scaled back or dropped development of this class of pharmaceuticals. One exception stands out. Ketamine, the anesthetic and illegal club drug, is now being repurposed as the first rapid-acting antidepressant drug and has been lauded as possibly the biggest advance in the treatment of depression in 50 years. A few trials by large pharma outfits are now underway on a new, purportedly improved and, of course, more profitable variant of ketamine, which in its current generic drug form does not make pharmaceutical marketing departments salivate. Some physicians have decided they simply can’t wait for the lengthy protocols of the drug approval process to be sorted out. They have read about experimental trials in which a low-dose, slow-infusion of ketamine seems to produce what no Prozac-like pill can achieve, lifting the black cloud in hours, not weeks. With nothing to offer desperate, sometimes suicidal patients, physicians have decided against waiting for an expensive, ketamine lookalike to arrive and have started writing scripts for the plain, vanilla generic version that has been used for decades as an anesthetic. Ketamine, it seems, has captivated a bunch of white coats with the same grassroots energy that has propelled the medical marijuana movement. © 2013 Scientific American
By Scicurious Effective treatments for drug addiction have been hard to come by. There’s behavioral interventions, methadone maintenance for heroin users, nicotine patches for smokers, antabuse for acoholics, but while all of these are effective in a minority of users, they aren’t effective in all. Many require repeat behaviors that are difficult for addicts. As examples: getting to the methadone center every day can be difficult if you have bad transportation. Alcoholics often need to go to AA meetings several times a week if not several times a day. Antabuse make you feel like crap when you drink…and all you have to do is NOT take it. Nicotine patches don’t tend to scratch the smoking itch in the same way. In the case of cocaine, where is there no drug intervention option at all, when you have someone who is in serious danger of overdose, you need something to take away the effects of the cocaine. Something to work immediately. Enter the idea of a vaccine against cocaine. For those used to thinking about vaccines as things that fight chicken pox and whooping cough, the idea of a vaccine against a drug can seem a little foreign. But it’s a concept that’s been in development for some time. Not so much in the context of vaccinating against potential cocaine use, but as a way to help people get off the drug. But the question still remains: will it work? The idea is to use a vaccine made of a drug that is very close to cocaine (norcocaine), combined with an inactivated virus. The presence of the virus causes the body’s immune system to try and fight it off, creating antibodies to different parts of the molecule, both the cocaine part and the virus part. The antibodies serve as a signal for other immune cells to come along and gobble up the cocaine. After the original vaccine is gone, the antibodies stay circulating in your blood, ready to attack is they see the cocaine signal again. © 2013 Scientific American
by Andy Coghlan Smokers keen to quit are just as likely to be successful if they use electronic cigarettes as they are with nicotine patches, the "gold standard" quitting aid. The findings come ahead of a critical debate in the European Parliament on 8 October to decide whether e-cigarettes should be regulated as medicinal products, which would drastically reduce their availability. When smokers attempt to quit, it is the cutting out of nicotine – the addictive component of tobacco – that triggers withdrawal symptoms. E-cigarettes, which physically resemble real cigarettes, provide a compensatory nicotine hit, without the toxic brew of carcinogenic compounds. Previous studies conducted on e-cigarettes alone have shown that they help smokers quit, but no one knew if they performed as well as nicotine patches. To find out, the New Zealand government funded a head-to-head comparison study. Chris Bullen and his colleagues at the National Institute for Health Innovation in Auckland gave e-cigarettes to 289 smokers who were trying to quit. A separate group of 295 people were given nicotine patches, while 73 received dummy nicotine-free e-cigarettes. Six months later, the team asked participants if their attempts to quit had been a success. Those who had used the nicotine e-cigarettes had the highest success rate: 7.3 per cent had managed to stay away from tobacco. Of the nicotine patch users, 5.8 per cent had quit. And of those taking the placebo around 4 per cent were successful. © Copyright Reed Business Information Ltd.
Keyword: Drug Abuse
Link ID: 18618 - Posted: 09.09.2013
By Scicurious For my food week post, I’m going at it a little differently. We spend a lot of time talking about food, thinking about whether it’s good for us, bad for us, which aspects of it are good or bad for us. We talk about why we crave some foods vs others, and we talk about why some foods taste disgusting. We talk about whether you’d want to replace your entire diet with a chalky fluid substance. Foodies spend a lot of time taking pictures of it, diet mags spend a lot of time talking about how to eat less of it. Food is surrounded by a culture that permeates almost everything we put in our mouths. But food is more than what we like or don’t like. Food is more than a relationship between our stomach and our tongues and noses. There is a very strong relationship between food and your brain, and when it goes wrong, the results can be devastating. There is anorexia, where there is distorted body perception, huge fear of weight gain, and food restriction so severe it can kill. On the opposite end, there is binge eating, uncontrollable eating that people are unable to stop, despite health consequences and social stigma. Critical to both of these problems are issues with “reward”. Food needs to be rewarding, it needs to make you crave it, want more of it, seek it out, work to obtain it. We need to crave food because if we didn’t, we’d all starve to death due to lack of motivation. In binge eating, though, that craving becomes an obsession. And it’s a dangerous one. People who binge eat severely are at risk for obesity, heart problems, diabetes, and other health problems. There is also a lot of anxiety, depression, guilt, and other mental distress that goes along with binge eating. This is more than just a need for portion control or more exercise. It’s a serious compulsion and mental illness, and it shouldn’t be taken lightly. © 2013 Scientific American
By STUART ELLIOTT Electronic cigarettes may be a creation of the early 21st century, but critics of the devices say manufacturers are increasingly borrowing marketing tactics that are more reminiscent of the heady days of tobacco in the mid-1900s. With American smokers buying e-cigarettes at a record pace — annual sales are expected to reach $1.7 billion by year’s end — e-cigarette makers are opening their wallets wide, spending growing sums on television commercials with celebrities, catchy slogans and sports sponsorships. Those tactics can no longer be used to sell tobacco cigarettes, but are readily available to the industry because it is not covered by the laws or regulations that affect the tobacco cigarette industry. The e-cigarette industry is also spending lavishly on marketing methods that are also still available to their tobacco brethren, including promotions, events, sample giveaways and print ads. The Blu eCigs brand — which recently added the actress Jenny McCarthy to its roster of star endorsers, joining the actor Stephen Dorff — spent $12.4 million on ads in major media for the first quarter of this year compared with $992,000 in the same period a year ago, according to the Kantar Media unit of WPP. And ad spending in a category that Kantar Media calls smoking materials and accessories, which includes products like pipes and lighters in addition to e-cigarettes, has skyrocketed: from $2.7 million in 2010 to $7.2 million in 2011 to $20.8 million last year. In the first quarter of 2013, Kantar Media reported, category ad spending soared again, reaching $15.7 million, compared with $2 million in the same period a year ago. In fact, that $15.7 million total exceeded the spending for ads in major media for tobacco cigarettes, at $13.9 million, according to Kantar Media. © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18598 - Posted: 09.03.2013
By Maia Szalavitz That little zing you get when someone “likes” your picture or sings your praises on Facebook? That’s the reward center in your brain getting a boost. And that response can predict how much time and energy you put into the social media site, according to new research. In one of the first studies to explore the effects of social media on the brain, scientists led by Dar Meshi, a postdoctoral researcher at the Freie Universität in Berlin, imaged the brains of 31 Facebook users while they viewed pictures of either themselves or others that were accompanied by positive captions. The research was published in Frontiers in Human Neuroscience. “We found that we could predict the intensity of people’s Facebook use outside the scanner by looking at their brain’s response to positive social feedback inside the scanner,” says Meshi. Specifically, a region called the nucleus accumbens, which processes rewarding feelings about food, sex, money and social acceptance became more active in response to praise for oneself compared to praise of others. And that activation was associated with more time on the social media site. Social affirmation tends to be one of life’s great joys, whether it occurs online or off, so it’s not surprising that it would light up this area. Few people are immune to the lures of flattery, after all. But do these results suggest that the “likes” on Facebook can become addictive? While all addictive experiences activate the region, such activation alone isn’t sufficient to establish an addiction. © 2013 Time Inc
By MIKE STOBBE / AP Medical Writer ATLANTA (AP) — Can’t get enough shuteye? Nearly 9 million U.S. adults resort to prescription sleeping pills — and most are white, female, educated or 50 or older, according to the first government study of its kind. But that’s only part of the picture. Experts believe there are millions more who try options like over-the-counter medicines or chamomile tea, or simply suffer through sleepless nights. ‘‘Not everyone is running out to get a prescription drug,’’ said Russell Rosenberg, an Atlanta-based sleep researcher. The Centers for Disease Control and Prevention study was based on interviews with about 17,000 adults from 2005 through 2010. Study participants were even asked to bring in any medicines they were taking. Overall, 4 percent of adults said they'd taken a prescription sleeping pill or sedative in the previous month. The study did not say whether use is increasing. But a CDC researcher calculated that use rose from 3.3 percent in 2003-2006 to 4.3 percent in 2007-2010. That echoes U.S. market research — as well as studies in some other countries — that indicate an increase in insomnia in recent decades. ‘‘Sleep disorders overall are more prevalent than what they were,’’ said Dr. Ana Krieger, medical director of New York’s Weill Cornell Center for Sleep Medicine. © 2013 NY Times Co.
Link ID: 18588 - Posted: 08.31.2013
As the debate about legalizing marijuana heats up in Canada, a new study suggests the drug might be riskier for teens to consume than had been previously thought. Researchers from the Université de Montréal and New York's Icahn School of Medicine at Mount Sinai Hospital conducted a review of 120 studies examining cannabis and teenage brain development, and concluded there is strong evidence early cannabis use puts some teens at risk of developing addiction and mental health problems as adults. Dr. Didier Jutras-Aswad, with the Université de Montréal's psychiatry department, is a co-author of the review, which was published this month in the journal Neuroparmacology. He says that in adolescence, the brain is still fine-tuning how different areas, such as learning and memory, interact and it appears that marijuana use alters that process. "When you disrupt this, actually, development, during adolescence, notably through cannabis use, you can have very pervasive, very negative effects in the long-term, including on mental health and addiction risk," he told CBC News. Some studies have also found links between early cannabis use and schizophrenia, but Jutras-Aswad says it seems clear there is a wide risk profile that includes genetics and behavioural traits in addition to age. "For me, the question is not about whether cannabis is good or bad, but who is more likely to suffer from problems in cannabis, because we know for most people that will not happen," he said. © CBC 2013
By Stephen L. Macknik A new study in the Journal of Neuroscience suggests that a part of the brain critical to motivation, the substantia nigra, which is famous for its role as a primary culprit in Parkinson’s Disease, is central to the relationship between feeding and drug seeking behavior. Neuroscientists have known for some time that acquisition of drug seeking behavior is higher in people whose food supply is restricted. But nobody knew why. Neuroscientist Sarah Branch and her colleagues at the University of Texas Health Science Center in San Antonio have now discovered a critical neural mechanism that links food restriction to enhanced drug efficacy. They mildly restricted the diet of mice and found that it caused certain neurons in the substantia nigra burst in activity. These neurons, called dopamine neurons, are implicated in the feeling of pleasure felt with drugs of abuse. It’s as if the neurons are preparing to reward their owner the moment that food is found, perhaps to reinforce food acquisition. When the mice were given cocaine as well, the bursty effect in food restricted mice was enhanced even further, which leads to increased drug seeking behavior too. Interestingly, they found that the effects could persist up to ten days after the food restriction ended. The results suggest that there may be a way to enhance drug efficacy in patients with chronic pain. But it also serves as a cogent reminder that the substantia nigra is central to how the brain generates motivational behavior. When the substantia nigra dies, you get Parkinson’s, and you find it difficult to motivate yourself to even pass through a doorway. © 2013 Scientific American