Posts tagged neuroscience
Articles and news from the latest research reports.
Eye movements reveal difference between love and lust
Soul singer Betty Everett once proclaimed, “If you want to know if he loves you so, it’s in his kiss.” But a new study by University of Chicago researchers suggests the difference between love and lust might be in the eyes after all.
Specifically, where your date looks at you could indicate whether love or lust is in the cards. The new study found that eye patterns concentrate on a stranger’s face if the viewer sees that person as a potential partner in romantic love, but the viewer gazes more at the other person’s body if he or she is feeling sexual desire. That automatic judgment can occur in as little as half a second, producing different gaze patterns.
“Although little is currently known about the science of love at first sight or how people fall in love, these patterns of response provide the first clues regarding how automatic attentional processes, such as eye gaze, may differentiate feelings of love from feelings of desire toward strangers,” noted lead author Stephanie Cacioppo, director of the UChicago High-Performance Electrical NeuroImaging Laboratory. Cacioppo co-authored the report, now published online in the journal Psychological Science, with colleagues from UChicago’s Departments of Psychiatry and Psychology, and the University of Geneva.
Previous research by Cacioppo has shown that different networks of brain regions are activated by love and sexual desire. In this study, the team performed two experiments to test visual patterns in an effort to assess two different emotional and cognitive states that are often difficult to disentangle from one another—romantic love and sexual desire (lust).
Male and female students from the University of Geneva viewed a series of black-and-white photographs of persons they had never met. In part one of the study, participants viewed photos of young, adult heterosexual couples who were looking at or interacting with each other. In part two, participants viewed photographs of attractive individuals of the opposite sex who were looking directly at the camera/viewer. None of the photos contained nudity or erotic images.
In both experiments, participants were placed before a computer and asked to look at different blocks of photographs and decide as rapidly and precisely as possible whether they perceived each photograph or the persons in the photograph as eliciting feelings of sexual desire or romantic love. The study found no significant difference in the time it took subjects to identify romantic love versus sexual desire, which shows how quickly the brain can process both emotions, the researchers believe.
But analysis of the eye-tracking data from the two studies revealed marked differences in eye movement patterns, depending on whether the subjects reported feeling sexual desire or romantic love. People tended to visually fixate on the face, especially when they said an image elicited a feeling of romantic love. However, with images that evoked sexual desire, the subjects’ eyes moved from the face to fixate on the rest of the body. The effect was found for male and female participants.
“By identifying eye patterns that are specific to love-related stimuli, the study may contribute to the development of a biomarker that differentiates feelings of romantic love versus sexual desire,” said co-author John Cacioppo, the Tiffany and Margaret Blake Distinguished Service Professor and director of the Center for Cognitive and Social Neuroscience. “An eye-tracking paradigm may eventually offer a new avenue of diagnosis in clinicians’ daily practice or for routine clinical exams in psychiatry and/or couple therapy.”
![The Mediterranean Diet Has Varied Effects on Cognitive Decline Among Different Race-Specific Populations
While the Mediterranean diet may have broad health benefits, its impact on cognitive decline differs among race-specific populations, according to a new study published in the Journal of Gerontology.
The team of researchers, including Ben-Gurion University of the Negev (BGU Prof. Danit R. Shahar RD, Ph.D, analyzed an NIH/NIA prospective cohort study [Health ABC] conducted over eight years in the U.S. to measure the effects of adherence to a Mediterranean diet. Prof. Shahar is affiliated with the BGU S. Daniel Abraham International Center for Health and Nutrition, Department of Public Health, Faculty of Health Sciences.
The Mediterranean-style diet (MedDiet) has fewer meat products and more plant-based foods and monounsaturated fatty acids from olive and canola oil (good) than a typical American diet.
To assess the association between MedDiet score and brain function, the researchers used data of several Modified Mini-Mental State Examinations (3MS) on 2,326 participating older adults (70-79). The 3MS is an extensively used and validated instrument designed to measure several cognitive domains to screen for cognitive impairment and commonly used to screen for dementia.
"In a population of initially well-functioning older adults, we found a significant correlation between strong adherence to the Mediterranean diet and a slower rate of cognitive decline among African American, but not white, older adults. Our study is the first to show a possible race-specific association between the Mediterranean diet and cognitive decline.”
The researchers note that further studies in diverse populations are necessary to confirm association between the MedDiet and cognitive decline, and to pinpoint factors that may explain these results.
(Image: Getty Images)](http://40.media.tumblr.com/b62bebb4855ca153bcf19937110a44fd/tumblr_n8v2orqAJN1rog5d1o1_500.jpg)
While the Mediterranean diet may have broad health benefits, its impact on cognitive decline differs among race-specific populations, according to a new study published in the Journal of Gerontology.
The team of researchers, including Ben-Gurion University of the Negev (BGU Prof. Danit R. Shahar RD, Ph.D, analyzed an NIH/NIA prospective cohort study [Health ABC] conducted over eight years in the U.S. to measure the effects of adherence to a Mediterranean diet. Prof. Shahar is affiliated with the BGU S. Daniel Abraham International Center for Health and Nutrition, Department of Public Health, Faculty of Health Sciences.
The Mediterranean-style diet (MedDiet) has fewer meat products and more plant-based foods and monounsaturated fatty acids from olive and canola oil (good) than a typical American diet.
To assess the association between MedDiet score and brain function, the researchers used data of several Modified Mini-Mental State Examinations (3MS) on 2,326 participating older adults (70-79). The 3MS is an extensively used and validated instrument designed to measure several cognitive domains to screen for cognitive impairment and commonly used to screen for dementia.
"In a population of initially well-functioning older adults, we found a significant correlation between strong adherence to the Mediterranean diet and a slower rate of cognitive decline among African American, but not white, older adults. Our study is the first to show a possible race-specific association between the Mediterranean diet and cognitive decline.”
The researchers note that further studies in diverse populations are necessary to confirm association between the MedDiet and cognitive decline, and to pinpoint factors that may explain these results.
(Image: Getty Images)
Mobile games used for psychology experiments
With its first comprehensive set of results published today, the Great Brain Experiment, a free mobile app run by neuroscientists at the Wellcome Trust Centre for Neuroimaging at UCL, uses ‘gamified’ neuroscience experiments to address scientific questions on a scale that would not be possible using traditional approaches. The app investigates memory, impulsivity, risk-taking and happiness. By playing the games, anyone can anonymously compare their abilities to the wider population and contribute to real scientific research. More than 60,000 people have taken part so far.
The results, published in the journal PLOS ONE, demonstrate that mobile games can be used to reliably conduct research in psychology and neuroscience, reproducing well-known findings from laboratory studies. The small size of standard laboratory studies means they can be limited in their ability to investigate variability in the population at large. With data sent in from many thousands of participants, the scientists at UCL can now investigate how factors such as age and education affect cognitive functions. This new way of doing science enables questions to be addressed which would not previously have been practical.
Writing in the journal PLOS ONE, the researchers explained: “Smartphone users represent a participant pool far larger and more diverse than could ever be studied in the laboratory. By 2015, there will be an estimated two billion smartphone users worldwide. In time, data from simple apps could be combined with medical, genetic or lifestyle information to provide a novel tool for risk prediction and health monitoring.”
The Great Brain Experiment was funded by the Wellcome Trust and first released as part of last year’s Brain Awareness Week. Building on its initial success, the researchers have recently added four new games, including a “coconut shy” which tests people’s ability to perform under pressure. From this, the scientists hope to better understand how people make accurate movements in difficult situations. Going forward, they are calling on the public to download the app and throw coconuts to help science.
Rick Adams, a developer of The Great Brain Experiment based at the Wellcome Trust Centre for Neuroimaging at UCL, said: “The initial aim was simply to make the public more aware of cognitive neuroscience experiments, and how they are conducted. However, with such large numbers of people downloading the app and submitting their results, it rapidly became clear that there was the potential for studying task performance at an unprecedented scale.”
Harriet Brown, a researcher at the Wellcome Trust Centre for Neuroimaging at UCL, said: “It is hoped that carefully measuring performance on a range of tasks may give rise to a better understanding of common mechanisms that underlie performance on these different tasks. Through better understanding of these common mechanisms, we may be able to characterise how they are altered in neurological and psychiatric disease.”
(Source: ucl.ac.uk)
New knowledge about the brain’s effective bouncer
Research from the University of Copenhagen is shedding new light on the brain’s complicated barrier tissue. The blood-brain barrier is an effective barrier which protects the brain, but which at the same time makes it difficult to treat diseases such as Alzheimer’s. In an in vitro blood-brain barrier, researchers can recreate the brain’s transport processes for the benefit of the development of new pharmaceuticals for the brain. The new research findings are published in the AAPS Journal.
Ninety-five per cent of all tested pharmacological agents for treating brain disorders fail, because they cannot cross the blood-brain barrier. It is therefore important to find a possible method for transporting drugs past the brain’s efficient outpost and fervent protector.
Researchers at the Department of Pharmacy at the University of Copenhagen have recreated the complex blood-brain barrier in a laboratory model, which is based on cells from animals. In a new study, the researchers have studied the obstreperous bouncer proteins in the barrier tissue. The proteins protect the brain, but also prevent the treatment of brain diseases:
"The blood-brain barrier is chemically tight because the cells contain transporter proteins which make sure that substances entering the cells are thrown straight back out into the bloodstream again. We have shown that the barrier which we have created in the laboratory contains the same bouncer proteins – and that they behave in the same way as in a ‘real’ brain. This is important, because the model can be used to test drive the difficult way into the brain. Complex phenomena – which we have so far only been able to study in live animals –can now be investigated in simple laboratory experiments using cultivated cells," says postdoc Hans Christian Cederberg Helms from the Department of Pharmacy.
The research team has shown that the transporter proteins P-glycoprotein, breast cancer resistance protein and multidrug resistance-associated protein 1 are active in the artificially created barrier tissue. The proteins pump pharmacological agents from the ‘brain side’ to the ‘blood side’ in the same way as in the human blood-brain barrier.
Collaboration finds a way
The new findings have resulted from collaboration with industrial scientists from the pharmaceutical company H. Lundbeck A/S. “It is important to the treatment of brain diseases such as Alzheimer’s that we find a way of circumventing the brain’s effective defence. The university and industry must work together to overcome the fundamental challenges inherent in developing pharmaceuticals for the future,” says Lassina Badolo, Principal Scientist with H. Lundbeck A/S and an expert on the absorption of medicines in the body.
Associate Professor Birger Brodin adds: “We have shown that the models have the same bouncer proteins as the ones found in the intact barrier. We are now in the process of studying the proteins in the blood-brain barrier that accept pharmacological agents instead of throwing them out. If we can combine a beneficial substance which the brain needs with a so-called ‘absorber protein’, we will in the long term be able to smuggle pharmacological agents across the blood-brain barrier.”
Birger Brodin heads the Drug Transporters in ADME research group which is responsible for the in vitro blood-brain barrier.
(Source: healthsciences.ku.dk)
(Image caption: Whole brain functional connectivity between the nucleus accumbens (NAc) and other brain areas in response to cannabis cues (vs. neutral cues) in all participants)
Dependence Alters the Brain’s Response to Pot Paraphernalia
New research from The University of Texas at Dallas demonstrates that drug paraphernalia triggers the reward areas of the brain differently in dependent and non-dependent marijuana users.
The study, published July 1 in Drug and Alcohol Dependence, demonstrated that different areas of the brain activated when dependent and non-dependent users were exposed to drug-related cues.
The 2012 National Survey on Drug Use and Health shows marijuana is the most widely used illicit drug in the United States. According to a 2013 survey from the Pew Research Center, 48 percent of Americans ages 18 and older have tried marijuana. The National Institute on Drug Abuse says that 9 percent of daily users will become dependent on marijuana.
“We know that people have a hard time staying abstinent because seeing cues for the drug use triggers this intense desire to seek out the drugs,” said Dr. Francesca Filbey, lead author of the study and professor at the Center for BrainHealth in the School of Behavioral and Brain Sciences. “That’s a clinically validated phenomenon and behavioral studies have also shown this to be the case. What we didn’t know was what was driving those effects in the brain.”
To find this effect, Filbey and colleagues conducted brain-imaging scans, called functional magnetic resonance imaging (fMRI), on 71 participants who regularly used marijuana. Just more than half of those were classified as dependent users. While being scanned, the participants were given either a used marijuana pipe or a pencil of approximately the same size that they could see and feel.
A comparison of the images revealed that the nucleus accumbens, the reward region in the brain, was activated in all users in response to the pipe. However, the strengths of the connections with other areas differed between dependent and non-dependent users.
“We found that the reward network is actually being driven by other areas unrelated to reward, like the areas in memory and attention or emotion,” Filbey said.
Non-dependent users showed greater activations in the orbital frontal cortex and hippocampus, suggesting that memory and attention were connected to the activation of the reward network. Dependent users had greater activations in the amygdala and anterior cingulate gyrus, suggesting a more emotional connection.
Additionally, the areas of the brain activated resemble areas activated for other addictions, such as nicotine or cocaine, lending greater support to the addictiveness of marijuana.
These findings suggest that marijuana abuse intervention needs to cater more specifically to a user’s level of addiction.
"Clinicians treating people with problems with marijuana dependence should consider the different processes that trigger the reward response when determining possible pharmacological or behavioral interventions,” Filbey said.
Brain of World’s First Known Predators Discovered
An international team of paleontologists has identified the exquisitely preserved brain in the fossil of one of the world’s first known predators that lived in the Lower Cambrian, about 520 million years ago. The discovery revealed a brain that is surprisingly simple and less complex than those known from fossils of some of the animal’s prey.
The find for the first time identifies the fossilized brain of what are considered the top predators of their time, a group of animals known as anomalocaridids, which translates to “abnormal shrimp.” Long extinct, these fierce-looking arthropods were first discovered as fossils in the late 19th century but not properly identified until the early 1980s. They still have scientists arguing over where they belong in the tree of life.
"Our discovery helps to clarify this debate," said Nicholas Strausfeld, director of the University of Arizona’s Center for Insect Science. "It turns out the top predator of the Cambrian had a brain that was much less complex than that of some of its possible prey and that looked surprisingly similar to a modern group of rather modest worm-like animals."
Strausfeld, a Regents’ Professor in the Department of Neuroscience in the UA College of Science, is senior author on a paper about the findings, which appear in the July 17 issue of Nature.
Brain responses to emotional images predict PTSD symptoms after Boston Marathon bombing
The area of the brain that plays a primary role in emotional learning and the acquisition of fear – the amygdala – may hold the key to who is most vulnerable to post-traumatic stress disorder.
Researchers at the University of Washington, Boston Children’s Hospital, Harvard Medical School and Boston University collaborated on a unique opportunity to study whether patterns of brain activity predict teenagers’ response to a terrorist attack.
The team had already performed brain scans on Boston-area adolescents for a study on childhood trauma. Then in April 2013 two bombs went off at the finish line of the Boston Marathon, killing three people and injuring hundreds more. Even people who were nowhere near the bombing reported distress about the attack and the days-long manhunt for the suspects.
So, one month after the attack, Katie McLaughlin, then at Boston Children’s Hospital and Harvard Medical School and now an assistant professor of psychology at the UW; co-author Margaret Sheridan, of Boston Children’s Hospital and Harvard Medical School; and their fellow researchers sent online surveys to teenagers who had previously participated in studies to assess PTSD symptoms related to the attack.
By using functional Magnetic Resonance Imaging scans from before the attack and survey data from after, the researchers found that heightened amygdala reaction to negative emotional stimuli was a risk factor for later developing symptoms of PTSD.
The research study was published July 3 in the journal Depression and Anxiety.
“The amygdala responds to both negative and positive stimuli, but it’s particularly attuned to identifying potential threats in the environment,” said McLaughlin, the study’s first author. “In the current study of adolescents the more their amygdala responded to negative images, the more likely they were to have symptoms of PTSD following the terrorist attacks.”
The brain scans were conducted during the year prior to the bombing. At that time, the teens were evaluated for their responses to emotional stimuli by viewing neutral and negative images. Neutral images included items such as a chair or button. Negative images showed people who were sad, fighting or threatening someone else. Participants rated the degree of emotion they felt while looking at each image. The MRIs measured whether blood flow increased to the amygdala and the hippocampus when viewing negative images as compared to neutral images.
In the follow-up survey the teens were asked whether they were at the finish line during the bombing, how much media exposure they had after the attack, whether they were part of the lockdown at home or school while authorities searched for the suspects, and how their parents responded to the incident. They also were asked about specific PTSD symptoms, such as how often they had trouble concentrating and whether they kept thinking about the bombing when they tried not to.
Researchers found a significant association between amygdala activation while viewing negative images and whether the teens developed PTSD symptoms after the bombing.
McLaughlin said a number of previous studies have shown that people with PTSD had heightened amygdala responses to negative emotions, but researchers didn’t know whether that came before or after the trauma.
“It’s often really difficult to collect neurobiological markers before a traumatic event has occurred,” she said. By scanning the adolescents’ brains before the bombing, she and her fellow researchers were able to show that “amygdala reactivity before a traumatic event predicts your response to that traumatic event.”
While two-thirds of Americans will be exposed to some kind of traumatic event during their lifetime, most, fortunately, will not develop PTSD.
“The more we understand the underlying neurobiological systems that shape reactions to traumatic events, the closer we move to understanding a person’s increased vulnerability to them,” McLaughlin said. “That could help us develop early interventions to help people who might develop PTSD later.”
(Source: washington.edu)
Variations in Neuronal Networks Could Explain Traumatic Brain Injury Outcomes
A team of researchers at the Neuroscience Institute at Georgia State University has discovered that hidden differences in the properties of neural circuits can account for whether animals are behaviorally susceptible to brain injury. These results could have implications for the treatment of brain trauma.
People vary in their responses to stroke and trauma, which impedes the ability of physicians to predict patient outcomes. Damage to the brain and nervous system can lead to severe disabilities, including epilepsy and cognitive impairment.
If doctors could predict outcomes with greater accuracy, patients might benefit from more tailored treatments. Unfortunately, the complexity of the human brain hinders efforts to explain why similar brain damage can affect each person differently.
The researchers used a unique research animal, a sea slug called Tritonia diomedea, to study this question. This animal was used because unlike humans, it has a small number of neurons and its behavior is simple. Despite this simplicity, the animals varied in how neurons were connected.
Under normal conditions, this variability did not matter to the animals’ behavior, but when a major pathway in the brain was severed, some of the animals showed little behavioral deficit, while others could not produce the behavior being studied. Remarkably, the researchers could artificially rewire the neural circuit using computer-generated connections and make animals susceptible or invulnerable to the injury.
“This study is important in light of the current Obama BRAIN initiative, which seeks to map all of the connections in the human brain,” said Georgia State professor, Paul Katz, who led the research project. “it shows that even in a simple brain, small differences that have no effect under normal conditions, have major implications when the nervous system is challenged by injury or trauma.”
Results of this study were published in the most recent edition of the journal eLife. The lead author on the study, Dr. Akira Sakurai, made this discovery in the course of doing basic research. He was assisted by Ph.D. student Arianna Tamvacakis from Dr. Katz’s lab.
(Source: news.gsu.edu)
(Image caption: In brain cancer cells, the protein PARC plays a key role in long-term cell survival. In both images, the red represents the protein cytochrome c, which is released when mitochondria are damaged and trigger apoptosis – cell suicide. At left, injured brain cancer cells exhibit little cytochrome c; they use the protein PARC to degrade the released cytochrome c, allowing the cancer cells to survive. At right, when researchers reduced PARC, cytochrome c accumulated, allowing apoptosis to carry on)
Neurons, brain cancer cells require the same little-known protein for long-term survival
Researchers at the UNC School of Medicine have discovered that the protein PARC/CUL9 helps neurons and brain cancer cells override the biochemical mechanisms that lead to cell death in most other cells. In neurons, long-term survival allows for proper brain function as we age. In brain cancer cells, though, long-term survival contributes to tumor growth and the spread of the disease.
These results, published in the journal Science Signaling, not only identify a previously unknown mechanism used by neurons for their much-needed survival, but show that brain cancer cells hijack the same mechanism for their own survival.
The discovery will lead to new investigations of brain cancer treatments and provides insight into Parkinson’s disease, including a potential new research tool for scientists.
“PARC is very similar to Parkin, a protein that’s mutated in Parkinson’s disease,” said Mohanish Deshmukh, PhD, a professor of cell biology and physiology and senior author of the Science Signaling paper. “We think they might work in tandem to protect neurons.”
If so, researchers can investigate the interplay between these proteins to create better drugs to treat the second-most prevalent neurodegenerative disease after Alzheimer’s disease.
Vivian Gama, PhD, a postdoctoral fellow in Deshmukh’s lab, led the experiments in cell cultures and animal models. First, she used external stimuli to promote the damage of mitochondria – the energy sources for cells. In most cell types, when mitochondria are damaged, they release a protein called cytochrome c, which triggers a cascade of biochemical steps that end in cell death – a process known as apoptosis.
Working with neurons, though, Gama found that the protein PARC/CUL9 blocked this process; it degraded cytochrome c, halted apoptosis, and allowed for long-term cell survival. “In this setting, we want PARC to do that because we want neurons to survive as long as possible,” said Gama, first author of the Science Signaling paper.
Deshmukh, a member of the UNC Neuroscience Center and the UNC Lineberger Comprehensive Cancer Center, said, “In Parkinson’s disease, we know that Parkin targets damaged mitochondria for degradation. However, exactly what happens to the proteins, such as cytochrome c, that are released from the damaged mitochondria has been unknown. Now, we think PARC plays a role in this process.”
Deshmukh and Gama’s work could lead to an alternative way to study Parkinson’s disease. Other researchers have created mouse models that lack the Parkin gene, but Gama said these models don’t have many of the hallmark symptoms that human patients have, making the model less than desirable for researchers. “Our hypothesis is that in the absence of Parkin, PARC still does the job,” Gama said, “as it may allow cells to survive.”
Gama and Deshmukh are now creating a model that lacks both the Parkin and PARC genes.
They will also investigate PARC as a target for cancer treatment.
“We tested several cancer cell lines and found that PARC degrades cytochrome c in medulloblastoma, a cancer of the central nervous system and in neuroblastoma, a cancer of the peripheral nervous system,” Gama said. “Not all cytochrome c is degraded; there are likely other factors involved. But PARC is an important player.”
When Gama and colleagues triggered the apoptotic process in brain cancer cells, they found that PARC allowed the cells to survive. When PARC was inhibited, the cells were more vulnerable to stress and damage, which means they could be more vulnerable to compounds aimed at destroying them.
Deshmukh said, “We show that brain cancer cells co-opt PARC to bypass apoptosis in the same way that neurons do and for the exact same purpose.”
Mutation stops worms from getting drunk
Neuroscientists at The University of Texas at Austin have generated mutant worms that do not get intoxicated by alcohol, a result that could lead to new drugs to treat the symptoms of people going through alcohol withdrawal.
The scientists accomplished this feat by inserting a modified human alcohol target into the worms, as reported this week in The Journal of Neuroscience.
"This is the first example of altering a human alcohol target to prevent intoxication in an animal," says corresponding author, Jon Pierce-Shimomura, assistant professor in the university’s College of Natural Sciences and Waggoner Center for Alcohol and Addiction Research.
An alcohol target is any neuronal molecule that binds alcohol, of which there are many.
One important aspect of this modified alcohol target, a neuronal channel called the BK channel, is that the mutation only affects its response to alcohol. The BK channel typically regulates many important functions including activity of neurons, blood vessels, the respiratory tract and bladder. The alcohol-insensitive mutation does not disrupt these functions at all.
"We got pretty lucky and found a way to make the channel insensitive to alcohol without affecting its normal function," says Pierce-Shimomura.
The scientists believe the research has potential application for treating people addicted to alcohol.
"Our findings provide exciting evidence that future pharmaceuticals might aim at this portion of the alcohol target to prevent problems in alcohol abuse disorders," says Pierce-Shimomura. "However, it remains to be seen which aspects of these disorders would benefit."
Unlike drugs such as cocaine, which have a specific target in the nervous system, the effects of alcohol on the body are complex and have many targets across the brain. The various other aspects of alcohol addiction, such as tolerance, craving and the symptoms of withdrawal, may be influenced by different alcohol targets.
The worms used in the study, Caenorhabditis elegans, model intoxication well. Alcohol causes the worms to slow their crawling with less wriggling from side to side. The intoxicated worms also stop laying eggs, which build up in their bodies and can be easily counted.
Unfortunately, C. elegans are not as ideal for studying the other areas of alcohol addiction, but mice make an excellent model. The modified human BK channel used in the study, which is based on a mutation discovered by lead author and graduate student Scott Davis, could be inserted into mice. These modified mice would allow scientists to investigate whether this particular alcohol target also affects tolerance, craving and other symptoms relevant to humans.
Pierce-Shimomura speculated that their research could even be used to develop a ‘James Bond’ drug someday, which would enable a spy to drink his opponent under the table, without getting drunk himself. Such a drug could potentially be used to treat alcoholics, since it would counteract the intoxicating and potentially addicting effects of the alcohol.