Robert Gerlai received his Ph.D. from the Hungarian Academy of Sciences with the highest distinction in 1989.  He has held numerous academic positions in Europe and North America (Eötvös University of Budapest, Mount Sinai Hospital Research Institute of Toronto, Indiana University Purdue University, University of Hawaii) and he also held leadership positions in the US biotechnology and pharmaceutical research industry working as a senior research scientist and Vice President (Genentech Inc., Eli Lilly & Co., Saegis Pharma) before joining University of Toronto in 2004 where he is now Associate Chair of the Department of Psychology and Full Professor of Psychology.  Dr. Gerlai has published over 100 papers in refereed scientific journals and several book chapters and he is a member of the editorial board of Cognitive Processing, and of Genes Brain and Behavior.  He has edited several special issues of scientific journals and served as co-editor of a large handbook on molecular genetic approaches in behavioural neuroscience.  He is currently editing a multivolume Handbook on mouse neurogenetics for Cambridge University Press and is writing a Behaviour Genetics Textbook for the same publisher.  He has been serving as a scientific referee for more than 50 scientific journals.  Dr. Gerlai has been advising major grant funding agencies and evaluated grant proposals, e.g., as permanent member of the reviewing panels BBBP-1 and BRLE-1 of the National Institutes of Health (NIH, USA), Canadian Institutes of Health (CIHR), and as ad hoc referee for numerous other NIH panels, and the National Science Foundation (NSF,  USA), Wellcome Trust (UK), Israeli Science Foundation, and CIHR, and the Natural Sciences and Engineering Research Council of Canada (NSERC).  He is founding member of the International Behavioral and Neural Genetics Society, IBANGS, is past-treasurer and member-at-large of this society.  He was USA Councilor of the International Behavioral Neuroscience Society (IBNS) and has also served as Chair of several committees of IBNS.  He became Fellow of IBNS in 2005 and currently he is the President-of IBNS.  Dr. Gerlai’s research has been focusing on the biological and genetic mechanisms of behaviour.  He is most known for his work on behavioural phenotyping and the use of genetically engineered mice.  For example, his paper on the pros and cons of gene targeting published in Trends in Neurosciences in 1996 has received thousands of citations.  He is also known for his work on the Eph tyrosine kinase receptors and their roles in learning and memory in mammals (papers in J. Neuroscience, Nature Reviews Neuroscience, and Trends in Neurosciences) a research line in which he employed a novel alternative to gene targeting.  Dr. Gerlai’s current research at U of T concerns novel phenotyping approaches and forward genetics for and the behavioural characterization of zebrafish.

 

Joseph P. Huston is Professor and Chair of the Institute of Physiological Psychology at the University of Düsseldorf in Düsseldorf, Germany. He received a B.A. in Psychology from the University of Maryland, and the Ph.D in Experimental Psychology at Tufts University in Medord, Mass. in 1969 with a thesis entitled "The psychophysics of energizing and reinforcing stimulation of the brain". He then spent two years (1970-71) at the Institute of Physiology in Prague with Jan Bures, supported by the National Academy of Sciences - Czechoslovac Academy of Sciences Exchange Program, where he learned electrophysiology. He then worked for 5 years with Alex Borbely at the Institute of Pharmacology in Zürich, Switzerland where he delved into sleep research, took up intracranial self-stimulation work again, and learned some behavioral pharmacology. After serving as Chair of Experimental Psychology at the University of Zürich, he moved to the University of Düsseldorf in 1978. There, Joe initially focused on anatomical tracing and intracranial self-stimulation, rodent models of Parkinson’s disease, the relationship between reinforcement and memory processes, and the role of neuropeptides in learning and emotionality. Later he shifted to behavioural neurochemistry, using in vivo microdialysis and HPLC. Current research interests of his institute include the behavioural and neurochemical phenotyping of genetically manipulated mice, neuronal histamine, neurokinins, episodic memory, gap-junction connexins, extinction-induced depression, serotonin-cocaine interactions, ageing-related deficits, and the intranasal application of drugs. He is chief editor of Behavioural Brain Research, Reviews in the Neurosciences, and the new book series, Handbook of Behavioral Neuroscience. He has published about 400 peer-reviewed papers and books and received the Myers Lifetime Achievement Award for Outstanding Scientific Contributions to the Field of Behavioral Neuroscience in 2003.

Robert Adamec, Ph.D. is currently a University Research Professor (a rank above full Professor) in Psychology and Basic Medical Science at Memorial University of Newfoundland. Dr. Adamec is a founding member and Fellow of IBNS as well as a Fellow of CPA in recognition of his contribution to Psychology as a science in Canada. As a behavioural neuroscientist, Dr. Adamec’s contributions are to three areas of study: substrates of fearful temperament; epilepsy and affect; stress and affect. Initial interest lay in the neural basis of individual differences in the degree to which cats were inhibited by threatening environments. The work suggested that behavioral inhibition was fearful and that the temperamental trait emerged early in life independently of experience.  Adamec then showed that more fearful cats possessed a natural increase in amygdala excitability and potentiation of transmission between limbic areas in response to naturally threatening or electrical stimuli. The work pointed to inherited excitability in particular limbic circuits as a substrate for behavioral inhibition. This idea influences current theoretical and experimental thinking.  Behavioral inhibition is studied as a putative predispositional factor in stress precipitation of anxiety disorders. Early studies in temperament led to work by Adamec changing limbic correlates of the trait to determine their contribution to the trait. The idea was to turn an uninhibited cat into an inhibited (frightened) cat by permanently changing limbic excitability with kindling. Partial kindling without motor convulsive seizures changed behavior and produced potentiated amygdala efferent transmission like that seen in naturally inhibited cats, implicating pathway potentiation as a dispositional mechanism. This work stimulated international work on effects of kindling on affect. It also introduced the idea that traces of repeated seizures, expressed as changes in limbic transmission, might underlie affective psychopathology experienced by epileptics, for which there is evidence in humans (Trimble). Adamec then showed that low frequency stimulation (LFS) of amygdala reversed kindling induced amygdala efferent potentiation and fearfulness in cats. Importantly, neural effects were confined to the right hemisphere. This study along with others pointed to the possible involvement of periaqueductal gray (PAG) in neuroplastic changes in anxiety disorders, currently a growth area of interest. The importance of right amygdala in Adamec’s work influenced investigators such as Lalumiere who finds right rodent amygdala facilitation of the formation of fear memories. The third area of study examines effects of stress on affect and neural plasticity. Adamec found that single and brief pharmacological stress (with FG7142 in cats) and experiential stress (predator stress in rats) produces lasting changes in fearfulness and anxiety.  These lasting changes in affect in the cat depend on right lateralized NMDA receptor dependent potentiation of amygdala efferents to the PAG. This work is one of the first demonstrations that stress effects on affect involve limbic neuroplastic changes, now a growth area of study. It stimulated many studies of lasting after effects of brief stressors on affect as a model of PTSD (e.g. Cohen and colleagues).  It led to further work by Adamec implicating pCREB expression, protein synthesis and NMDA receptor dependent potentiation of right limbic pathways in anxiogenic effects of predator stress in rats. Work on right lateralized neural effects of stress provide neurobiological face validity to these animal models of PTSD in view of work implicating hyperexcitability of right human amygdala in the etiology of PTSD. Currently funded by CIHR, the work on stress continues.

C. Sue Carter, Ph.D. is Professor of Psychiatry and Co-Director of Brain-Body Center at the University of Illinois at Chicago.   Dr Carter was Distinguished University Professor (1997-2001) and Professor (1985-1997) in the Department of Biology at the University of Maryland.   She also held a Guest Researcher appointment (1985-2001) in the NICHD-NIH (Developmental Endocrinology Branch).   Dr. Carter was a faculty member at the University of Illinois in Champaign-Urbana (1972-1985), where she held joint academic positions through the level of Professor in the Department of Psychology and Department of Ecology, Ethology and Evolution.  She was one of the founders of the Program in Neural and Behavioral Biology at UIUC.   In 1982-1983 she held a visiting position as a program officer in Psychobiology at the National Science Foundation. Dr. Carter currently directs a NIH Program Project Grant that deals with the Developmental Consequences of Oxytocin.  She has been a recipient of a NIH Research Scientist Award (1993-1998) and has a history of funding for research in the general area of social behavior and behavioral endocrinology throughout her academic career.  Much of her past research has been done in animal models.   Her research career has been focused on the study of social behaviors, and especially reproductive behaviors and the novel traits of monogamous mammals.  Her laboratory began studies of the physiological basis of social attachment in voles in the late 1970s, conducted the first studies of the role of peptides (oxytocin, vasopressin and CRH) in pair bond formation between adults, and has used this model to document the importance of stress and stress hormones in social bond formation. Dr. Carter has been involved for over two decades in studies of human behavior, including research on the behavioral effects of male and female sex steroids, and more recently the role of lactation in stress management.

Bob Blanchard is Professor of Psychology and Neuroscience at the University of Hawaii, a site from which both east and west excursions are equally feasible.  Demonstrating this, he has been a National Academy of Science - Soviet Academy of Sciences Exchange Fellow in Moscow; a Japan Society for the Promotion of Science Visiting Fellow at Tokyo University; and a Guest Professor at the University of Bergen (Norway) and the University of Göttingen (Germany).  He has also served as both Executive Secretary, and as President, of the International Society for Research on Aggression.  His research is on aggression and defense, utilizing an ethoexperimental approach that combines ethology (evaluation of behavior in natural or seminatural settings; detailed description and measurement of behavior based initially on direct observation; a focus on interacting conspecific or nonconspecific animals; attention to natural outcomes) with standard experimental methodologies.  A particular focus of his work on aggression involves the distinction between offensive and defensive aggression, based on both behavioral and physiological factors.  He is also very interested in the cross-species generality of this distinction, and of other emotion-linked behaviors.  With reference to defensive behavior, his work has identified a pattern of risk assessment activities that are pivotal in the decision-making process that may either lead to specific defensive responses to threat, or, to a reduction in defensiveness and return to normal, depending on information obtained from the process.  Work from his and other laboratories indicates that particular defensive behaviors may be selectively sensitive to drugs that are effective against specific anxiety-related psychopathologies; risk assessment and defensive threat/attack respond selectively to drugs effective against generalized anxiety, while flight responds to antipanic drugs.  Such results suggest that hyperexpression of specific defensive behaviors may be important in the etiology of particular anxiety disorders, again illustrating a potential conservatism of emotional response across mammalian species.

Mark Geyer is Professor and Vice-Chair for Research in the Department of Psychiatry at the University of California San Diego.  A pioneer in the translational study of sensorimotor gating deficits in schizophrenia and related animal models, Dr. Geyer is the Director of the Neuropsychopharmacology Unit of the VISN 22 VA’s Mental Illness Research, Clinical, and Education Center and Associate Chief of the Psychophysiology Unit of the VA Center of Excellence for Stress and Mental Health.  He has published over 330 peer-reviewed papers and many reviews and chapters.  Dr. Geyer is an Associate Editor of Neuropsychopharmacology, Fellow of ACNP, IBNS, and AAAS, Past-President of the international Serotonin Club, and a member of the Scientific Council of NARSAD.  Dr. Geyer’s laboratory uses behavioral measures and psychopharmacological manipulations in rodents and humans to examine the roles of neurotransmitters in behavior, to develop animal models of human drug effects, and to explore information-processing deficits in psychiatric disorders.  He uses startle measures of habituation and prepulse inhibition, which are deficient in people with schizophrenia and mimicked in rodents by pharmacological, developmental, and genetic manipulations.  His group is using a battery of startle tests in a prospective longitudinal Marine Resilience Study, paralleled by neurobiological studies of CRF systems in rodents.  He has developed a Behavioral Pattern Monitor for use in rats, mice, and humans.  These methods provide translational and multivariate assessments of spatio-temporal patterns of exploratory behavior and are being used in comparisons of schizophrenia and bipolar mania in relationship to corresponding animal models.  
Dr. John P. Bruno received his Ph.D. in Psychology from The Johns Hopkins University in 1980.  His post-doctoral training was with Ted Hall (North Carolina Division of Mental Health) and Ed Stricker/ Michael Zigmond (University of Pittsburgh).  He has been on the faculty of The Ohio State University since 1986, where he is currently a professor of Psychology, Psychiatry and Neuroscience.  Dr. Bruno’s current research focuses on the neurobiology of cognitive deficits in  schizophrenia.  The research embraces a distributed neural systems approach to studying the top-down and bottom-up regulation of attentional processing and cognitive flexibility in several different animal models of schizophrenia (i.e. inactivation of hippocampal efferents during development; elevated brain kynurenic acid levels; and perinatal immune activation) .  The research centers on the role that alpha7 nicotinic and mGluR 2 receptors play in the regulation of glutamate release in prefrontal cortex.  These two receptor systems are targets for the development of novel antipsychotic medications with cognition-enhancing properties.  The laboratory utilizes techniques such as in vivo microdialysis, enzyme selective biosensors, and a variety of behavioral paradigms to study cognitive deficits and therapeutic efficacy in these animal models.

Jacqueline N. Crawley, Ph.D., is Chief of the Laboratory of Behavioral Neuroscience at the National Institute of Mental Health Intramural Research Program in Bethesda, Maryland, USA.  Dr. Crawley received a B.A. in Biology from the University of Pennsylvania in 1971, a Ph.D. in Zoology from the University of Maryland in 1976, was a postdoctoral fellow in Neuropsychopharmacology at Yale University School of Medicine 1976-79, spent two years in the Neurobiology central research program at the DuPont Company, and has been a faculty member at NIMH since 1983.  Her laboratory investigates the biological causes of mental illnesses, employing behavioral assays in rodent models of neuropsychiatric disorders.  Approaches include behavioral neuropharmacology and behavioral genetics.  Transgenic and knockout mice, with mutations for genes expressed in the brain, provide powerful tools for understanding the genetic substrates of behavior.  Current studies are focused on mouse models of autism.  This neurodevelopmental disorder is the most heritable of all mental illnesses, displaying up to 90% concordance between monozygotic twins for autism spectrum disorders.  Dr. Crawley's laboratory is developing a comprehensive set of mouse behavioral tasks that are relevant to the three diagnostic symptoms of autism: 1) abnormal reciprocal social interactions, 2) impaired communication, and 3) repetitive behaviors, insistence on sameness, and restricted interests.  A new automated three-chambered social approach task developed by the lab is now in wide use by many mouse modeling groups in the autism research community.  Discovering robust measures of olfactory and vocalization communication in mice is a challenging need for the field that is being pursued in Dr. Crawley's lab.  Lines of mice with mutations in candidate genes for autism are being tested for the phenotypic outcome of null and humanized mutations, including synaptic genes such as neuroligins and shanks that were identified in some autistic individuals.  Inbred strains with autism-relevant behavioral phenotypes, such as BTBR T+tf/J, are being used to discover background genes mediating normal and abnormal social and repetitive behaviors. Mouse models of autism with sufficient face validity for the symptoms of autism are being employed as translational tools to evaluate behavioral and pharmacological treatments for autism.  Dr. Crawley is the author of the book "What's Wrong With My Mouse? Behavioral Phenotyping of Transgenic and Knockout Mice."  She served as IBNS President in 2000. 

László Lénárd was born in 1944 in Pécs, Hungary. He received MD degree in 1969 (Pécs University), PhD in 1980 and DMSC in 1989 (HAS) and was elected as a member of the Hungarian Academy of Sciences in 2001. He was appointed as full professor of Physiology in 1990. He has been the chairman of the Institute of Physiology, Pécs University Medical School, and the director of the Neurophysiology Research Group of the HAS since 1990. He was the vice-rector (1997-2000) and the dean (2002) of the Medical School and he has been the rector (president) of the Pécs University since 2003. László Lénárd’s research focuses on the central regulatory processes of feeding and body weight, the mechanisms of sensorimotor integration and the processes of learning and memory. On the basis of his results it has been revealed that the globus pallidus plays an essential role in the regulation of sensory-motor and metabolic processes. He demonstrated that neurochemical lesions of the globus pallidus are followed by sex-dependent body weight changes and that sensory neglect develops after selective neurochemical lesion of the mesolimbic dopaminergic system. The existence and the importance of a functional balance mechanism of dopaminergic and noradrenergic systems in the control of body weight regulation was also shown by his works. He demonstrated that the mesolimbic dopaminergic system acts as an interface in limbic and motor functions. He is a co-author of the first description of intracerebral amphetamine self stimulation and showed that insulin and glucose induce reverse changes of extracellular dopamine level. Based on collaborative research he described glucose-sensitive neurons in the monkey hypothalamus and later in the amygdaloid body, globus pallidus and orbitofrontal cortex. On the basis of these data and related results obtained in other labs, he elaborated a hypothesis of a hierarchically organized glucose-monitoring system integrating visceral signals with taste and odor information. He described the satiation effect of direct intra-amygdaloid application of different bombesin-like peptides. He has been teaching physiology since 36 years and the leader of the Neuroscience PhD program since 10 years. He published 115 papers and book chapters and 248 abstracts and was invited speaker or plenary lecturer in 32 cases. He has had extensive worldwide research collaborations.  He received the Pro Sciencia (twice) and Teaching Master awards from the HAS, Széchenyi Professorship,  Szentá-gothai Price and Grastyán Price.

Michael L. Woodruff received his A.B. in Psychology from the University of Michigan and M.S. and Ph.D. degrees in Psychology and Neurosciences from the University of Florida. He held faculty positions at the University of Florida and Middlebury College.  He is presently Vice Provost for Research, Professor of Anatomy and Cell Biology and Professor of Psychology at East Tennessee State University.  He is also the executive director of the ETSU Research Foundation with responsibility for technology transfer and oversight of the ETSU business incubator.  His research interests include mechanisms of inducing recovery of function after brain injury or degeneration. He has received competitive extramural funding to support his research from the American Heart Association, the Alzheimer's Disease Association, the NIH.  He is a fellow of the American Psychological Association, of the International Behavioral Neuroscience Society, and of the American Society for Neurotransplantation, and a member of the Society for Neuroscience. In addition to serving as President of IBNS he was its treasurer and was also treasurer of the American Society for Neurotransplantation. In 1990 he received the Foundation Research Award from East Tennessee State University and has received six “Excellence in Teaching” awards from the Quillen College of Medicine.

Robert Isaacson attended the University of Michigan from which he obtained his undergraduate and graduate degrees.  Between the time of receiving his Bachelors' degree and starting his graduate work, he was commissioned as an officer in the United States Navy, serving in the Korean war.  After obtaining his Ph. D. in 1958 he stayed on at the University of Michigan where he advanced to a full professorship.  He moved to the University of Florida in 1968, becoming a Graduate Research Professor at that Institution.  In 1978 he moved to Binghamton University as a Distinguished Professor. He has been a visiting professor at the Universities of Utrecht (NL) and Cordoba (Arg.).  He is the author or coauthor of more than 275 scientific publications and 20 books.  He has held committee memberships in the American Psychological Association and the Society for Neuroscience.  His service to the scientific community includes membership on nine editorial boards for professional journals as well as serving on advisory committees for NIMH and NIH.  He served as President of the Alachua County (FL) Association for Retarded Children and the Governor's Blue Ribbon Committee (FL) for Mental Retardation.  He was elected President of the International Behavioral Neuroscience Society in 1998. The Marjorie Myers Lifetime Achievement Award was presented to him in 2001. At present he is serving on a National Research Council  committee considering certain agents with possible neurotoxic effects.

After receiving his medical degree from the University of Pennsylvania in 1960, Dr. Gerard R. Smith did two years of training in internal medicine at the New York Hospital.  He spent the next two years at the Walter Reed Army Institute of Research where he showed that psychological stress in monkeys did not increase gastric acid secretion. In 1964, he returned to Pennsylvania to join the Department of Physiology.  During the next four years, he initiated the program of research in the controls of eating in monkeys and rats that he would pursue for the next 34 years.  His first important result showed that the glucostatic control of eating, then considered the only short-term control of eating, operated only in metabolic emergencies.  In 1968, he joined the Department of Psychiatry at Cornell (now Weill) Medical College and within a year became the Director of the Bourne Laboratory.  In 1971, he and his postdoctoral fellow, James Gibbs, discovered that cholecystokinin (CCK), a peptide secreted in response to food stimuli contacting the mucosal surface of the upper small intestine, decreased food intake.  Experiments over the next twenty years in rodents, monkeys, and humans proved that CCK was the first physiological mechanism for the satiation of eating. His laboratory also demonstrated the satiating effect of other peptides, such as glucagon, bombesin, and gastrin-releasing peptide, as well as the role of mesolimbic dopamine in the central mediation of the stimulating effect of sweet taste on eating. In 2000, he resigned the Directorship.  He closed his laboratory in 2002.  He is currently Professor Emeritus of Behavioral Neuroscience in Psychiatry.


Linda Patia Spear, Distinguished Professor of Psychology at Binghamton University, received her B.S. in Psychology from Western Illinois University, and her Ph.D. in Psychology at the University of Florida where she also received postdoctoral training in Neuroscience.  Dr. Spear has published over 200 peer-reviewed publications in the areas of developmental psychobiology, psychopharmacology, and toxicology.  Her current research uses animal models to examine fundamental characteristics of adolescence, including adolescent sensitivity to ethanol, the neurobiology of risk taking and the contribution of adolescent-relevant motivational strategies, stressors and peer affiliations to risk taking, alcohol/drug use, and other problem behaviors of adolescence.  Her research is currently supported by grants from NIDA and NIAAA, including a MERIT award from NIAAA.  Dr. Spear has served as President of a number of societies, including the International Behavioral Neuroscience Society, the International Society for Developmental Psychobiology, and the Neurobehavioral Teratology Society.  Dr. Spear’s service to NIH has included 4-year terms as a member of study sections for NIDA, NIAAA, and the NIH Center for Research Resources, and service on the NIDA External Advisory Board and the NIAAA’s Underage Drinking Steering Committee.  She is currently serving on the External Advisory Board of NIAAA.  Dr. Spear was the 2005 recipient of the Keller Award, an award given annually by NIAAA to “an outstanding alcohol researcher who has made significant and long-term contributions” to the study of alcohol abuse and alcoholism. 

 

Robert D. Myers received his Ph.D. degree from Purdue University in 1956.  He then was a fellow in neurophysiology at the Johns Hopkins School of Medicine, later spending three years as a visiting scientist in physiology and pharmacology and as a visiting professor of neuropharmacology at the National Institute for Medical Research in Mill Hill, England.  He was professor of psychological and biological sciences at both Colgate and Purdue universities and served as director of the psychobiology and neurobiology programs at Purdue.  In 1978, he was appointed professor of psychiatry and pharmacology at the University of North Carolina School of Medicine and director of the Bowles Biomedical Research Laboratory.  In 1987, he became joint professor pharmacology and psychiatric medicine at the East Carolina University School of Medicine and director of the research division of the University Center for Alcohol and Drug Abuse Studies.  In 1996 he was appointed university distinguished research professor of pharmacology and then in 1998 emeritus professor. Myers was elected a fellow of CINP in 1978.  Myers is the author of about 500 scientific publications, including 50 chapters, and has written or edited six books.  He is the founder and now editor-in-chief emeritus of the biomedical journal, Alcohol.  Among his major research contributions are:  (1) identification of site in brain where pyrogens cause fever; (2) monoamine theory of thermo regulation; (3) drugs to treat alcohol drinking; (4) CNS mechanisms for set-points for body temperature and weight; (5) identification of subtrates in brain during hunger and satiety; (6) discovery of factors in brain that cause addictive drinking of alcohol; (7) induction of a hibernation in primates; (8) multiples metabolite theory of alcoholism; (9) chemical profile theory of feeding; (10) discovery of non PGE system in brain underlying fever; and (11) discovery of a new class of 5-HT drugs for treating alcoholism.

Paul R. Sanberg is Distinguished University Professor and Director of the Center for Aging and Brain Repair and Associate Vice President for Innovation at the University of South Florida Office of Research and Innovation.  Dr. Sanberg trained at York University, the University of British Columbia, the Australian National University and at the Johns Hopkins University School of Medicine.  Dr. Sanberg has held academic positions at the Ohio University, the University of Cincinnati, and Brown University prior to his current position.  His industry experience has included being Scientific Director for CytoTherapeutics, Inc., (Providence, Rhode Island), now Stem Cells, Inc., (Palo Alto, California) and was CSO and on the Board of Directors for Layton BioScience, Inc. (Atherton, California), and is currently Chairman and Founder of  Saneron CCEL Therapeutics, Inc. (Tampa, Florida).  The companies are involved in cell therapy for degenerative disorders. Dr. Sanberg is Editor-in-Chief of Cell Transplantation, Executive Director of the American Society for Neural Transplantation and Repair, and past president of the International Behavioral Neuroscience Society and the Cell Transplant Society.  He is the author of more than 450 scientific articles and has published thirteen books including, Neural Stem Cells for Brain and Spinal Cord Repair (Humana Press, 2003) and Cell Therapy, Stem Cells and Brain Repair (Humana Press, 2006) and is an inventor on over 25 U.S. patents.  His early work was pioneering in understanding a role for excitotoxicity in neurological disorders and was involved in some of the first clinical trials of neural transplantation in Parkinson’s, Huntington’s and stroke patients.


Matthew J. Wayner, Blumberg Professor of Life Sciences at the University of Texas at San Antonio, was elected the first president of the IBNS in 1992.  He was officially recognized by the IBNS as the Founding President of the Society and for his major contributions to behavioral neuroscience in 2002.  His distinguished career includes several other awards; beginning as one of the first graduate students to receive a NSF Pre-doctoral Fellowship (1952); the Golden Pick Axe Award from Dartmouth College (1996), the Marjorie Myers Lifetime Achievement Award in Behavioral Neuroscience, that was awarded for the first time by the IBNS in 1998, and the UTSA Presidents Distinguished Achievement Award in Recognition of Research Excellence (2000).  He also served as the Executive Director of the IBNS and Central Office until 2002.  His research career began at Syracuse University where he established the Brain Research Laboratory and in 1966 began his long scientific publishing career which included Brain Research Publishing Inc., Ankho International Inc., and Fayetteville Typesetting Inc. Twelve highly respected scientific journals were published; including the four he personally edited, Physiology and Behavior, Pharmacology Biochemistry and Behavior, Brain Research Bulletin, and Neuroscience and Biobehavioral Reviews.  In 30 years at Syracuse University, at least 32 doctoral degrees were awarded under his supervision; with most of his former students still significantly involved in basic neuroscience research. In 1982 he was recruited by UTSA to help transform the Division of Life Sciences from primarily a teaching program into one with a top notch research component.  His proposal to establish the University's first doctoral program in biology was approved in 1992. In 1997, his first UTSA doctoral student received his degree.  During his career he also arranged many important international conferences and published over 230 research articles; and presented 150 abstracts at scientific meetings.  His early seminal work was on the role of drinking in the regulation of body fluids. He was also co-author of one of the most important technical developments in electrophysiology; the glass fiber method of back filling glass micropipette recording electrodes.  In 1990 he added the hippocampus to his long time interest in the lateral hypothalamus.  In his present position at UTSA, he continues to do research and teach at both the undergraduate and graduate levels.