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In This Issue...
- Interview with Dr. Elena Choleris
- Neurobiology of Drug Instrumentalization
- Social Networking at IBNS Banquets: Be Careful!
- IBNS Fellows
- Trending Science
- Member News
Interview with Dr. Elena Choleris
by Anandakumar Shunmugavel
 One of the several factors that contribute to the success of a meeting organized by IBNS, is the selection of speakers. The process comprises of several meticulous steps in nominating and choosing speakers for the special occasion. In this issue, I had the chance to interview Dr. Elena Choleris, IBNS Chair, Program Committee 2018, on the process involved in having deserving speakers for various IBNS events.
AS: It's obvious that of the six different committees [Membership & Communication, Education & Training, Finance & Fund Raising, Local Organizing and Program] the Program Committee is involved in selecting speakers for IBNS events. Can you please share the events in which the Program Committee selects the speakers?
EC: The Program Committee selects speakers at five levels. Travel Award and Data Blitz, Presidential Speaker, Keynote Speaker, Speakers of Symposia and oral sessions.
AS: By the name implies, I guess Travel Award/Data Blitz speakers will be the Travel Award [TA] winners? Do all the TA winners will get a chance to be a speaker?
EC: Yes, all of those trainees who receive a travel award will give a brief oral overview of their poster.
AS: The TA Blitz session is scheduled before the poster session. Is there any special reason to have the TA Blitz before poster session?
EC: In preparing the program, we ensure the Travel Award Blitz is scheduled before the poster sessions so that the speakers can refer the audience to their posters.
AS: That is great! Coming to the Presidential Speaker, do all the members of IBNS contribute to the selection of the speaker?
EC: No - Presidential Speaker is chosen by the president of IBNS. Even though they don't have to, traditionally, the President consults with the Program Committee Chair and Co-Chair for this choice.
AS: Keynote address disseminates the core message of the event. I think choosing a keynote speaker could be a challenging process to the Committee. Can you explain how a key note speaker is chosen?
EC: Keynote Speakers are chosen by the Program Committee. It is a three-step process. First, all members of the Program Committee are asked to make suggestions of people they think would be great Keynote Speakers. Second, all members of the Program Committee rank-order the proposed Keynote Speakers. All ranks are averaged, and an overall ranked-ordered list is produced. Last, the Program Committee Chair and Co-Chair and the IBNS President contact the top ranked individuals and invite them to present their work at our annual meeting as a Keynote Speaker.
AS: Now I understand why the IBNS Keynote Speakers are always distinguished, inspirational and motivational speakers! What are the other IBNS events that involve a selection of speaker?
EC: There are two more events from IBNS. 1) Symposia: IBNS conducts an invitation to submit symposium proposals. [This] is emailed to the IBNS members and posted on the IBNS website. Anyone can submit a symposium proposal by the given deadline, IBNS members and non-members alike. The members of the Program Committee are then asked to read all proposals and rank them in order. Again, an average rank is calculated and those symposia that were ranked at the top receive an invitation from the Chair and Co-Chair of the Program Committee. 2) Oral sessions: These are for talks that people specifically request at the time of abstract submission. We typically can accommodate most, if not all, of those who request to give an oral session instead of a poster. If there were to be more requests than slots to accommodate into the program, then I'd ask the Program Committee to rank order the oral presentations.
AS: Thanks, Elena, for sharing the process of the IBNS speaker selection. Can you summarize the overall role of the Pogram Committee in the speaker selection process?
EC: As you may have guessed, the Program Committee plays a major role in taking all of these decisions. For this reason, it is important that we have wide representation of different areas of Behavioral Neuroscience research in our Committee, as well as diversity. This ensures the IBNS meeting program is as representative of the interests of our members as possible, stimulating and exciting as it has been over the 27 years of IBNS conferences!
I would like to take the opportunity to thank current and past members of the IBNS Program Committee, and Editor and Guest Editor of the IBNS newsletter for the given chance to share the process of speaker selection, and all the IBNS members. I also invite anyone who may be interested, to volunteer for this key committee of our society.
Neurobiology of Drug Instrumentalization
by Christian P. Müller
Section of Addiction Medicine, Department of Psychiatry and Psychotherapy, Friedrich-Alexander-University of Erlangen-Nuremberg, Erlangen, Germany
([email protected])
Psychoactive drugs can cause addiction, a major psychiatric disorder. However, the vast majority of humans who consume drugs regularly are actually not addicts nor are they becoming addicted. Pharmacological reinforcement theories explain this by the drug's positive and/or  negative reinforcing actions. However, non-addicted psychoactive drug use is usually a rather complex behavior, well organized, and occurring under certain environmental and mental conditions, and with a specific benefit. This complexity cannot be readily explained by pharmacological reinforcement theories. To better capture the phenomenon of non-addicted drug use, a few years ago we developed a theoretical framework called "drug instrumentalization" (Müller & Schumann, 2011). In recent years, my group at the University of Erlangen-Nuremberg, Germany, focused on finding neurobiological mechanisms for drug instrumentalization.
One can assume that for a specific goal directed behavior, there is always one mental state in which an organism performs the behavior most efficiently. In addition, there are numerous other mental states in which the behavior can still be performed, but less efficiently or requiring more effort. Thus, maintaining or achieving an optimal mental state for a desired behavior has a clear adaptive value.
Given that mental states change continuously over the day, an organism is frequently not in the optimal mental state for a desired behavior. This is where psychoactive drugs are used in a controlled way, i.e. in order to shift a given mental state into a desired mental state in a short and predictable time frame. Mental states were suggested to have their neurobiological base in the summatory activity of modulatory neurotransmitter systems in the brain.
Importantly, functional proteins in these systems, such as neurotransmitter transporters or receptors, are interaction targets of virtually all known psychoactive drugs. By this way, drugs can change activity in several modulatory systems at the same time, and modulate efficacy of sensory processing and goal-directed behavior.
There are several instrumentalization goals well documented. One is the self-medication for an innate or acquired aversive mental state as, e.g., experienced in psychiatric disorders. At the clinical level, depression frequently emerges co-morbid with alcohol abuse. Thereby, patients report to dampen ruminating negative thinking and to ameliorate suffering from bad mood with alcohol. It was shown that a dysfunction in lipid homeostasis, affecting in particular sphingolipid systems of the brain, can be a major pathway into innate- and stress-induced depression (Gulbins et al., 2013). Thereby, depression was associated with an increase of the sphingolipid ceramide in the brain and a reduction of hippocampal neurogenesis.
We recently reported that mice with a hyperfunction of the enzyme acid sphingomyelinase (ASM), which leads to enhanced turnover of sphingomyelin to ceramide, are not only depressive but also consume significantly more alcohol and escalate consumption after withdrawal. Interestingly, free-choice alcohol consumption, but not forced injections, reversed the ASM hyperfunction and normalized the depressive symptoms. This was achieved by the re-establishment of sphingolipid- and subsequent monoamine homoeostasis in the brain. Interestingly, free-choice alcohol drinking had no effect on ASM activity and no anti-depressive effect in wild type mice (Müller et al., 2017).
This study showed, in particular, that it is not only the pharmacological effect of a psychoactive drug that matters, but the possibility for the organism to self-titrate consumed amount. It also highlights that psychoactive drugs can have quite distinct effects depending on the mental state of an organism (Müller and Kornhuber, 2017).
If we, in the future, wish to improve our understanding of how the brain organizes systematic consumption of psychoactive drugs, I strongly believe that it may become unavoidable to look at model systems that mimic the actual drug user’s pathological conditions, may it be genetically-, developmentally-, or environmentally-induced (Müller, 2017). In our group, we will expand our focus also to other instrumentalization goals, and the interplay between sphingolipids and classical neurotransmitter systems in the brain.
References:
Gulbins E, Palmada M, Reichel M, Lüth A, Böhmer C, Amato D, Müller CP, Tischbirek CH, Groemer TW, Tabatabai G, Becker KA, Tripal P, Staedtler S, Ackermann SF, Brederode H v., Alzheimer C, Weller M, Lang UE, Kleuser B, Grassmé H, Kornhuber J (2013) Acid sphingomyelinase/ceramide system mediates effects of antidepressant drugs, Nature Med 19: 934-938.
Müller CP, Schumann G (2011) Drugs as an instrument: A new framework for non-addictive psychoactive drug use. Behav Brain Sci 34(6):293-347.
Müller CP, Kalinichenko LS, Tiesel J, Witt M, Stöckl T, Sprenger E, Fuchser J, Beckmann J, Praetner M, Huber SE, Amato D, Mühle C, Büttner C, Ekici AB, Smaga I, Pomierny-Chamiolo L, Pomierny B, Filip M, Eulenburg V, Gulbins E, Lourdusamy A, Reichel M, Kornhuber J (2017) Paradoxical antidepressant effects of alcohol are related to acid sphingomyelinase and its control of sphingolipid homeostasis. Acta Neuropathol 133(3): 463-483.
Müller CP, Kornhuber J (2017) Biological evidence for paradoxical improvement of psychiatric disorder symptoms by addictive drugs. Trends Pharmacol Sci 38(6): 501-502.
Müller CP (2017) Animal models of psychoactive drug use and addiction – present problems and future needs for translational approaches. Behav Brain Res, doi: 10.1016/j.bbr.2017.06.028.
Social Networking at IBNS Banquets: Be Careful!
by Larry Young
IBNS 2017 was a great experience, with outstanding scientific session throughout and ending with a particularly spectacular banquet. The size and atmosphere of IBNS meetings, in my experience, are a much better setting than the Society for Neuroscience meetings for sharing the latest discoveries in behavior neuroscience and social networking.
The IBNS banquets are notoriously exhilarating, spurring lots of late night social networking that can lead to new scientific and personal connections. In Hiroshima, the banquet included traditional dance of Japanese "devils" and invigorating discussions that lasted through the night. Hiroshima was my second IBNS meeting, where I had the opportunity to speak on the topic of the 'Neurobiology of Pair Bonding.' Speaking on this topic conjured up memories of my my first IBNS meeting, 15 years ago in Capri, Italy.
As a young Assistant Professor, I was excited to be invited to speak in a symposium organized by Anne Murphy. Anne did her postdoc with Geert Holstege, in the Netherlands, studying the neurocircuity of male sexual behavior. At that time, I was studying the neural consequences of mating (e.g. pair bonding in prairie voles), so I was a perfect fit for her symposium. Anne and I had never met prior to this IBNS meeting. The banquet was the night before the last day of sessions and, of course, our session was scheduled at 8 AM that following morning. Naturally, the speakers in our symposium, Anne, Jill Schneider, Jennifer Swann and I enjoyed the banquet festivities and danced until the music ended. Afterward, we all enjoyed each other's company at a villa, which overlooked the Mediterranean and had a private pool. Anne and I were absorbed by the relationship between our two areas of our research. We talked science and sipped the local limoncello deep into the night.
At 5AM, we all called it a night. Fun, right? Unfortunately, there was our 8AM symposium in the Italian amphitheater. When we arrived for our session, the auditorium was already filled with our science idols. Understandably, we were slightly (very) sleep deprived, but yet excited to share our research with the audience. Back in those days, you saved your talk on a CD. Normally, you just pop the CD into the organizers computer, your talk loads, and you’re good to go. However, for some baffling reason, the session's computer would not let us insert our CDs. In fact - it was as if there was an invisible barrier blocking the CD from going in. To this day, I do not understand what happened; although, Anne and I are pretty sure it was punishment from the gods of Capri for our escapade the night before. So, there we are in the middle of a huge auditorium with spotlights beaming directly at us, and with the audience staring at us with disapproval and disappointment that four PhD’s could not figure out how to insert a CD into the computer. After 20 minutes, we finally got the talks to load and were able to proceed with our session. The relief we all felt as the session ended was palpable.
Our session was the last of the meeting and it was time to return home. I’m not really sure how it happened, but the next thing I know I was lugging Anne’s 40kg suitcase in the sweltering heat across the hilly cobblestone streets to the ferry back to Naples. We hugged goodbye and went our separate ways. Well, kind of. Pair bonding is a funny thing and it's strength should never be underestimated. In 2004, just two years after the IBNS meeting, Anne and I were married on one of the most beautiful beaches in Costa Rica. Thirteen years later, we are still pair bonded and living in Atlanta, GA.
So in conclusion, IBNS meetings, and in particular the closing banquets, are excellent places for social networking and establishing collaborations. I am sure many new relationships were created in Hiroshima, and maybe even a few of you were lucky enough to leave the meeting feeling bonded with others. IBNS banquets can literally change your life. My advice for future IBNS banquets: be open to and embrace these life changing opportunities, but stay away from the limoncello!
IBNS Fellows
A warm congratulations to the IBNS 2017 Fellows!
Fellows of IBNS have been awarded to outstanding members since 1992. These are individuals who have made substantial contributions to the Society and to the field of Behavioral Neuroscience.
Our past-president, Dr. Misha, handed the Fellows title to Dr. Markus Fendt and Dr. Mike Hennessy at the 2017 Annual Meeting.
Trending Science
In this column, we will share the latest research, interesting scientific articles and news you can use.
Landmark Study
A recent landmark study “Correction of a Pathogenic Gene Mutation in Human Embryos” demonstrates a method for repairing genes in human embryos that prevent inherited diseases. The research team of Dr. Shoukhrat Mitalipov, Ph.D, Director, Center for Embryonic Cell and Gene Therapy at Oregon Health and Science University, OR, USA has corrected the heterozygous MYBPC3 mutation (that causes hypertophic cardiomyopathy) in human periimplantation embryos with CRISPR-Cas9 based gene targeting technique with high efficiency and accuracy. This research significantly advances our knowledge in germline gene correction and opens an avenue to treat people with known heritable disease causing gene-mutations with a risk of transfer to the next generation.
The results of the study are now published in the journal Nature. Ma, H. et al. Correction of a pathogenic gene mutation in human embryos. Nature (2017). doi:10.1038/nature23305
Member News
Lorenzo More
Dr. Lorenzo More, M.Sc, Ph.D, FHEA has been promoted to Senior Lecturer, School of Pharmacy and Biomedical Sciences at the University of Central Lancashire, Preston, UK. He chose to share, with fellow IBNS readers, more on The Nature and Nurture of Psychopathy: A Long Road Behind A Simple Idea:
"During my life, I have always been fascinated by how the brain learns, stores and retrieves information. During my career, I have tried to answer this question by approaching it from many viewpoints: physiological, pharmacological, behavioral/cognitive and genetic.
The heterogeneous training I have undergone has the downside to require much time invested; but on the flip side, it has led me to be a comprehensive professional figure, able to deal proficiently with scientists of very different backgrounds (e.g. molecular biologists with cognitive psychologists).
I have been appointed Senior Lecturer in Neuroscience and I will be working of psychopathy, enhanced cognition and epigenetics. The idea I am pursuing with this project is simple: the environment shapes behavior; and thus, psychopathy can be seen as the enduring outcome of Gene-by-Environment interaction, for which a systematic behavioral and epigenetic analysis will tell us what the key molecular mechanisms of this processes are.
I will use the mouse as model, in first instance, with an outlook to apply findings to humans and generating an enviro-mimetic drug, aka an 'enviro-pill.' The road to this (little, but important to me) achievement has been long and somewhat difficult.
I am happy to say that IBNS meetings and the IBNS community have contributed a great deal to improving my chances of success. IBNS meetings have been fundamental, in many occasions, by allowing me to meet with top scientists, keynote speakers and colleagues. They have all listened to my ideas, gave precious feedback and support, and nevertheless became important collaborators and friends. Such a level of personal interaction is rarely possible in the bigger meetings."
Byron Jones
Dr. Byron Jones became a New Investigator for Department of Defense, and received funding from the DoD to study individual differences in susceptibility to Gulf War illness.
Of the 700,000 troops that the United States sent to Kuwait and Iraq from 1990-1991, between 25-30% suffered from chronic illnesses. So, with all things being equal, DoD wants to know why some personnel became (and still are) sick, while others did not.
It is likely that the basis for the sickness behavior and other neurological signs stems from exposure-based neuroinflammation. The key issue is what were the troops exposed to in Kuwait and Iraq that caused the neuroinflammation?
My colleagues, Diane Miller and Jim O’Callaghan at CDC-NIOSH, developed a mouse model that features exposure to organophosphorus compounds. The US troops were exposed to two different kinds, possibly three: insecticides, prophylaxis against nerve gas, and possibly trace amounts of nerve gas. They also reasoned that mere exposure to these compounds, as toxic as they are, was not sufficient to explain the syndrome.
Folks in an active combat area are likely to have high circulating stress-related steroid hormones, so Diane and Jim reasoned that high-circulating cortisol somehow enhances the inflammatory effect of the organophosphorus compounds.
In fact, this is exactly what they found when mice were exposed with high circulating corticosterone (rodent cortisol) to a potent organophosphorus compound (DFP). While DFP increases, signs of neuro-inflammation, adding corticosterone produces a synergistic enhancement.
So what about those who don’t become sick – is there a mouse model for that? Indeed there is, and this is where my labs come in collaboration with Jim and Diane. It turns out that the mouse strain that Diane and Jim used is the industry standard, C57BL/6J. As many of you know, this is one of the parental strains of the BXD panel of recombinant inbred strains (more than 150 at this time). The other strain is DBA/2J mouse and on almost any behavioral, physiological, etc. measure you can think of, these two mice strains are like day and night. The BXD are derived from mating these two strains, and the genetic variants (about 5 million) between the two are redistributed in all kinds of combinations among the BXD strains.
So, I proposed to Diane and Jim that we test the DBA mice in the same system; and lo and behold, these mice are very much less sensitive to the combination of corticosterone and DFP than are the C57 mice. And more, we also tested females and in both strains, the females were less affected than males.
These results piqued the interest of the DoD and we landed a grant to apply this model to 30 of the BXD recombinant strains, in a systems genetics, systems biology approach. We expect to see continuously distributed results, indicating many genes at work with the environment. We aim to identify genes and gene networks underlying the syndrome and what we learn from the mice will likely inform the genetic involvement in humans and identify risk-associated biomarkers.
Hopefully, we will be able to assess a prioi those who are resistant and those who are susceptible to the combined exposures, and perhaps other exposures as well. The ultimate goal will be to develop preventative measures and treatments, or even rethink the whole exposure-exposome business altogether.
Larry Reid
Dr. Larry Reid, alongside Alicia Walf and, undergraduate, Faith Avens, have a new article appearing in the latest issue of Behavioural Brain Research, titled Cognitive Behavioral Therapy (CBT) for Preventing Alzheimer's Disease. The abstract: "This review provides the rationale for implementing cognitive behavioral therapy (CBT) for the prevention of Alzheimer's disease (AD)."
There are known risk factors associated with the development of AD, some of which may be ameliorated with CBT. We posit that treating the risk factors of inactivity, poor diet, hyposmia and anosmia, sleep disorders and lack of regularly engaged challenging cognitive activity will modify the physiology of the brain sufficiently to avoid the accumulation of excess proteins, including amyloid beta, casual events in the development of AD. Further, the successful treatment of the listed risk factors is well within our technology to do so and, even further, it is cost effective.
Also, there is considerable scientific literature to support the proposition that, if implemented by well-established practices, CBT will be effective and will be engaged by those of retirement age. That is, we present a biologically informed CBT for the prevention of the development of AD, i.e., an aspect of applied behavioral neuroscience.
Although not advocated in the article, we are busy developing a website to provide education and advocacy with the hope that such counseling will induce retirees to engage in selected actions that will reduce the risk of Alzheimer’s disease.
We would appreciate any who might share our interest in preventing Alzheimer’s disease and would care to share their ideas on our article’s content, to send your ideas to [email protected]. We guess that the article’s content is somewhat different than what is usually held about how to deal with the looming crisis of a large proportion of the population of prosperous nations developing incurable Alzheimer’s disease
Markus Wöhr
Markus Wöhr, along with Sören Krach, edited the book, "Social Behavior from Rodents to Humans: Neural Foundations and Clinical Implications." This book is part of the series, "Current Topics in Behavioral Neurosciences." This compelling volume provides a broad and accessible overview on the rapidly developing field of social neuroscience.
A major goal of the volume is to integrate research findings on the neural basis of social behavior across different levels of analysis, from rodent studies on molecular neurobiology to behavioral neuroscience to fMRI imaging data on human social behavior. More than fifty authors have contributed their work to the volume, including: Wim Crusio, Christian Keysers, Yasushi Kiyokawa, Jaak Panksepp, Sergio Pellis, Carmen Sandi, Tania Singer.
Central Office
The IBNS Central Office has not been affected by the recent catastrophic flooding in Texas. Please note that we have offices in three locations, including Texas and Kentucky. We thank you for the numerous emails and phone calls of concern.
Do you have an interesting hobby or member news to share?
Let us know at [email protected]
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