Neuroimmune Mechanisms Contributing to Addiction Neurobiology - Brain Function and Alcohol Use Disorders

From the National Institute on Alcohol Abuse and Alcoholism (NIAAA), this is an all-day conference on the role of the neuroimmune system in addiction neurobiology.

The field of psychoneuroimmunology has been around for a couple of decades (the term was coined in 1975 Robert Ader and Nicholas Cohen at the University of Rochester), but we are only now beginning to really grasp the implications of immune system function of mental health.

Neuroimmune Mechanisms Contributing to Addiction Neurobiology

Tuesday, September 02, 2014
Runtime: 05:07:43

Description:
The purpose of this workshop is to highlight recent progress in the understanding of neuroimmune mechanisms contributing to brain function and alcohol use disorders. It will bring together scientists from both alcohol and other research fields to highlight recent science advances, identify research gaps, and discuss possible challenges in this area.

Full Program:

8:30 AM - Welcome/Opening Remarks - George Koob, Ph.D., Director, NIAAA

8:40 AM - Introduction: Neuroimmune, Brain Function, and Alcohol Use Disorders - Changhai Cui, Ph.D., Program Director, Division of Neuroscience and Behavior, NIAAA

8:50 AM - Neuroimmune regulation in alcohol consumption: from gene to behavior - Adron Harris, Ph.D., Director, Waggoner Center for Alcohol & Addiction Research, University of Texas at Austin

9:20 AM - Mechanisms of Ethanol Activation of Neuroimmune Signaling and Neurodegeneration - Fulton Crews, Ph.D., Professor, Department of Pharmacology, Director, Bowles Center for Alcohol Studies, University of North Carolina, Chapel Hill

9:50 AM - Innate Immune Factors Modulate Ethanol Interaction with GABAergic Transmission in the Central Amygdala - Marisa Roberto, Ph.D., Associate Professor, Committee On The Neurobiology Of Addictive Disorders, Scripps Research Institute

10:20 AM - Break

10:35 AM - Microglia in learning dependent synaptic remodeling - Wen-Biao Gan, Ph.D., Professor, Skirball Institute of Biomolecular Medicine, New York University

11:05 AM - Neural-glial interactions in addiction: modulation by early-life experience - Staci Bilbo, Ph.D., Associate Professor, Psychology & Neuroscience, Arts & Sciences, Duke University

11:35 AM - Immune signaling, emotions/stress, and addiction - Rajita Sinha, Ph.D., Director of Interdisciplinary Stress Center, Yale University School of Medicine

12:05 PM - Lunch Break

1:05 PM - Panel Discussion - Antonio Noronha, Ph.D., Director of Division of Neuroscience and Behavior, NIAAA - Panelists: Drs. Dorit Ron, Kathy Grant, Cynthia Kane, Dipak Sarkar, Gyongi Szabo

2:05 PM - Closing Remarks

This is a brief and basic article, but the idea behind it, that we need to stop distinguishing between biological and social (especially as causes in dysfunctional behavior), is spot on - and I really like the term they mention, “neuropsychosocial.”

Why ‘Nature Versus Nurture’ Often Doesn’t Matter

By Michael White • August 22, 2014


(Photo: abstract/Shutterstock)
Sometimes it just doesn’t make any sense to try to separate the social and the biological.
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Every Friday this month we’re taking a look at the relationship between the social and the biological—specifically, how and why the former becomes the latter. Check back next week for the final installment.

When it comes to understanding ourselves, we tend to be splitters: mind and body, nature and nurture, or genes and environment. We take such a split for granted when we ask how the social becomes biological, but sometimes it’s not so useful to dichotomize the world into society and biology. Instead of looking for distinct social and biological influences (and believing that we can change one but not the other), we should recognize that the factors that drive our social behavior can, like a Zen koan, be two things at once.

Take the case of teen alcohol abuse. In a study published last week, an international team of researchers reported the “neuropsychosocial” factors that identify teens who are likely to abuse alcohol. The word “neuropsychosocial” does away with the common nature/nurture divide, and so did the researchers. Rather than asking whether teens abuse alcohol because of social influences or innate biology, the scientists looked at those variables that could be measured, regardless of whether the variables were social, biological, or a mix of both.

The study is part of a long-term European project called IMAGEN, established to understand the “biological and environmental factors that might have an influence on mental health in teenagers.” The project enrolled 2,000 14-year-olds, from whom were collected several types of data, including personal histories, psychological assessments of behavior, brain images, and genetic data. The researchers asked theses teens about their alcohol consumption at the beginning of the study, and then again at age 16. Armed with this data and a relatively large sample size, the scientists set out to answer the question: What neuropsychosocial factors identify teens who abuse alcohol?

In one analysis, the researchers looked for the factors that identified “current” drinkers, 14-year-olds who were already abusing alcohol when the study data were collected. They compared “binge drinkers” (defined as having been drunk at least three times by age 14) to non-drinkers (teens who drank no more than twice before age 16). In a second analysis, they attempted to identify future alcohol abusers—teens who were not drinking at age 14, but went on to get drunk multiple times by age 16. For each of these analyses, they built a computer model that used the measured neuropsychosocial variables to classify teens as drinkers or non-drinkers. The first model correctly identified 82 percent of current binge-drinking teens and 89 percent of non-drinking teens. The second model, predicting future drinkers, didn’t fare quite as well: 66 percent of drinkers and 73 percent of non-drinkers were correctly classified.

The most important identifying factors of current and future alcohol abusers were an inseparable mix of the social and the biological. A look at those factors shows how teasing out distinct social and biological causes would be an analytical nightmare: the different genetic, neurological, and life history variables are linked together in a thicket of feedback connections. For example, a history of romantic or sexual relationships strongly predicted current and future binge drinking behavior. But teen sexual behavior is surely influenced by other variables the researchers measured, like personality (which has a substantial genetic component), and “reward anticipation” or “emotional reactivity,” which were measured using brain imaging. It’s important to keep in mind that the study was not designed to discover which factors cause teen drinking, a much more difficult task. Instead, the researchers focused on what they could measure—an approach that, while it has its limits, is one of science’s most successful strategies.

What are the neuropsychosocial factors that best identify current and future teen drinkers? Some predictive traits include the volume and activity level of certain brain areas: “Future binge drinkers had reduced grey matter volume but increased activity when receiving a reward in the superior frontal gyrus compared to controls.” A personality trait characterized by “searching for, and feeling rewarded by, novel experiences” predicts both current and future teen drinkers. Other factors, like disruptive family events and more developed pubertal status identify current (but not future) drinkers, while “anxiety sensitivity” predicts only future drinkers. Notably, one set of factors that are not very predictive are specific genetic variants associated with alcohol dependence. This isn’t surprising because the individual effect of any one gene on a behavior like alcohol abuse is likely to be small.

With these results, we can we say about the biological basis for the social phenomenon of teen alcohol abuse? Not much more than, “it’s complicated.” And anyway, framing the question like this is a mistake.

We often approach a social problem by splitting it into its social and biological root causes, and assuming that we can change the social ones while working around the supposedly irreversible biological ones. But when it comes to human behavior, this is often not very useful or informative. As the authors write, their data “speak to the multiple causal factors for alcohol misuse,” and, in fact, any one variable, taken in isolation, had a small influence in their study. The predictive power of their computer model came from combining variables that were measurable—regardless of whether they could be neatly categorized as social or biological—into a single risk profile. This profile offers clues for how to find and help at-risk teens, and the most effective interventions may turn out to have little to do with directly treating some key social or biological cause of alcohol abuse. As we think about the connection between our social behavior and our biology, we should, like good scientists, be pragmatic, and abandon the distinction between society and biology when it’s not useful.



Michael White is a systems biologist at the Department of Genetics and the Center for Genome Sciences and Systems Biology at the Washington University School of Medicine in St. Louis, where he studies how DNA encodes information for gene regulation. He co-founded the online science pub The Finch and Pea. Follow him on Twitter @genologos.

More From Michael White

• Why Our Molecular Make-Up Can't Explain Who We Are
• How the Sexes Evolved
• How Tiny Genetic Changes Have Massive Behavioral Effects

Recap of Cognitive Neuroscience Society’s Annual Meeting (Scientific American Mind)

Here is a summary of some of the research presented at the 2014 Cognitive Neuroscience Society Annual Meeting. Daisy Yuhas at Scientific American Observations blog does the summarizing.

Brains in Boston: Weekend Recap of Cognitive Neuroscience Society’s Annual Meeting

By Daisy Yuhas | April 8, 2014



Greetings from Boston where the 21st annual meeting of the Cognitive Neuroscience Society is underway. Saturday and Sunday were packed with symposia, lectures and more than 400 posters. Here are just a few of the highlights.

The bilingual brain has been a hot topic at the meeting this year, particularly as researchers grapple with the benefits and challenges of language learning. In news that will make many college language majors happy, a group of researchers led by Harriet Wood Bowden of the University of Tennessee-Knoxville have demonstrated that years of language study alter a person’s brain processing to be more like a native speaker’s brain. They found that native English speaking students with about seven semesters of study in Spanish show very similar brain activation to native speakers when processing spoken Spanish grammar. The study used electroencephalography, or EEG, in which electrodes are placed along the scalp to pick up and measure the electrical activity of neurons in the brain below. By contrast, students who have more recently begun studying Spanish show markedly different processing of these elements of the language. The study focused on the recognition of noun-adjective agreement, particularly in gender and number.

Accents, however, can remain harder to master. Columbia University researchers worked with native Spanish speakers to study the difficulties encountered in hearing and reproducing English vowel sounds that are not used in Spanish. The research focused on the distinction between the extended o sound in “dock” and the soft u sound in “duck,” which is not part of spoken Spanish. The scientists used electroencephalograms to measure the brain responses to these vowel sounds in native-English and native-Spanish speakers. The Spanish speakers responded just like English speakers to the “dock” vowel sound, but not to the “duck,” sound, which was harder for the former group to identify. The finding is part of a larger body of research hinting at the possibility that vowel sounds like the o in dock that are produced on the periphery of the vocal tract are easier to perceive than the soft u sound produced in the middle of the vocal tract. By identifying these kinds of preferences, the researchers hope to better train language-learners to attune to sounds beyond their native tongue’s typical repertoire.

Birth control does not appear to effect cognition, according to Lena Ficco and colleagues of the University of Massachusetts Amherst. In one of the few neuroendocrinological studies presented, Ficco investigated whether contraception containing ethinyl estradiol changed the mental map-making or verbal abilities of women who had been taking this form of birth control for several years. Both verbal and navigation tasks are supported by estrogen. But because ethinyl estradiol suppresses estrogen, Ficco wondered whether there might be cognitive costs in taking contraception. Instead she observed no differences between women on these pills and a control group of non-pill-using women during the low-estrogen phase of their menstrual cycle. In future, Ficco hopes to assess whether length of pill use in an older population relates to any cognitive changes.

Researchers at Notre Dame University have some preliminary evidence that alcohol can set your body’s internal alarm clock. It can, in fact, make a relaxing Sunday morning seem like a manic Monday. The group wanted to investigate how alcohol, a physiological stressor, would alter the body’s cortisol awakening response, in which a flood of the stress hormone cortisol peaks as a person wakes up. Earlier work has demonstrated that this response is tied to psychological stress, prompting earlier rising on weekdays or during other anxious time periods. The Notre Dame group found that college students who consumed about four drinks on a weekend evening would awaken the next morning with significantly higher cortisol levels than non-drinkers. In fact, the researchers suggest that the stress-inducing effect is similar to that produced by cortisol levels on a weekday.

Finally, researchers have worked out a new nuance of the sound-induced flash illusion. In this illusion, an individual will either see a flash of light and hear two beeps or see two flashes and hear one beep. The curious thing is that people will report seeing two flashes if they hear two beeps, and just one flash if they heard one beep. Scientists at the University of Milan-Bicocca in Italy decided to replicate this illusion with a slight twist. Instead of actually flashing lights, they asked their subjects to keep their eyes closed and then used magnetic fields to change the electric currents surrounding neurons and stimulate the occipital lobe (a technique called transcranial magnetic stimulation). This stimulation triggered phosphenes, or the sensation of a flash of light—albeit without any actual light flashing. Because of how these phantom flashes are induced directly in the visual system, this approach enabled the researchers to time the stimuli and response to decipher whether this illusion depended on visual processing shortly after encountering a flash or beep. Indeed, they found that their subjects would report seeing two phosphenes after the researchers had induced just one flash with two auditory beeps, provided the stimuli were presented within relatively short succession. This suggests that the experiences in the brain’s early visual cortex can be modulated by sound. Lead author Silvia Convento explains that this kind of sensory overlap likely reflects brain organization that was beneficial to our ancestors. Even if it introduces some errors, the linkage would allow our brains gather and organize information from the environment more rapidly.

The lectures and symposia thus far have brought together a nice mix of history and hypotheses. Jon Kaas, who studies the organization of the mammalian brain at Vanderbilt University, for example, presented some of his ongoing work mapping the possible “sub-regions” of the motor cortex. The idea was inspired in part by research done in 2009 by neuroscientist Michael Graziano at Princeton University, who demonstrated that by stimulating a specific location on the motor cortex of an anaesthetized monkey, the animal would carry out a behavior such as bringing its hand to its mouth. Kaas has since investigated this and similar behaviors —including grasping, reaching, and climbing behaviors— in several primate species, including galagos, squirrel monkeys and owl monkeys. His findings have led him to the conclusion that the motor cortex may be divided into functional sub-regions with a specific active purpose, that direct movement across the body, and that the organization of these sub-regions could be consistent across primates.

In a totally different vein, a symposium on developmental cognitive neuroscience reflected on how lessons in this field could potentially guide policy on education and the justice system. For example, Margaret Sheridan of Harvard University reviewed the most recent published findings from the Romanian Orphanage Study, which reveal how extreme deprivation brutally inhibits mental development. This research complements ongoing study of the cognitive struggles of children growing up in poverty. On a more positive note, there are interventions that could help these children close the gap. Neuropsychologist Helen Neville of the University of Oregon discussed how her group has succeeded in training young children to improve their attention skills, often through simple and fun activities that ask children to concentrate and ignore distractions.

One of the most moving moments of the conference was in the opening keynote address by MIT neuroscientist Suzanne Corkin. Corkin spoke about the legacy of H.M., a patient who underwent a procedure to prevent epileptic seizures that left him unable to form new memories. Corkin, who spent decades studying H.M., discussed how he helped illuminate the distinctions between different memory forms and where they are located in the brain (to learn more about H.M., check out the May/June issue of Scientific American Mind). But Corkin also discussed the man behind the initials, describing his gentle and remarkably upbeat disposition, given that he was repeatedly confronting a confusing, context-free present. Her talk included a poignant and powerful audio recording of Corkin and H.M. chatting in 1992. In the excerpt, H.M. professes to “not mind” all of the tests and studies, saying simply, “I figure what’s wrong about me helps you help others.”


About the Author: Daisy Yuhas is an associate editor at Scientific American Mind. You can follow her on Twitter, @daisyyuhas

~ The views expressed are those of the author and are not necessarily those of Scientific American.