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Behavioral Epigenetics

Behavioral Epigenetics

Friday, October 29, 2010 - Saturday, October 30, 2010

University Massachusetts Boston Campus Center - Boston, MA

Presented By


The emerging field of epigenetics, the study of how a gene's function or expression can be changed without affecting the gene's basic structure, has forever changed the way we think about our genetic make-up. Epigenetic processes are part of normal development - for example, they occur during cell division. We now know that single nutrients, toxins, prenatal or postnatal environmental exposures can silence or activate a gene without altering its genetic code. No longer can we argue over which has a greater impact, genes or the environment. Both are inextricably linked: environmental events can create biochemical changes that ultimately dictate gene expression, whether at birth or 40 years down the road.

This 2-day conference will be one of the first to focus on a frontier epigenetics field: Behavioral Epigenetics, i.e. the quest to understand how environmental factors can affect alterations in behavior. Epigenetic effects have been studied in animal models of depression, addiction, schizophrenia and neuro-developmental disorders. Human studies on epigenetics and behavior are being conducted as well. Some psychoactive drugs, such as cocaine or anti-psychotics, also cause changes in some of the co-factors involved in this genetic regulatory system. With an understanding of the molecular mechanisms involved in epigenetic modulation, it might be possible to develop targeted therapies for those individuals in whom it malfunctions.

Discussions originating from this symposium, their dissemination through enduring materials, and the collaborations emerging from this forum will foster advancements in the field of Behavioral Epigenetics and will improve our understanding of 1) the fundamental mechanisms that shape development, and 2) individual vulnerability and resilience to adverse behavioral outcome.

Download Epigenetics in the News

Jointly Sponsored by:

Call for Abstracts

The deadline for abstract submission is now closed and we are unable to accommodate any more requests at this time.

Continuing Education Information


This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the Warren Alpert Medical School of Brown University and The New York Academy of Sciences. The Alpert Medical School is accredited by the ACCME to provide continuing medical education for physicians.

This activity is being sponsored by the Massachusetts Psychological Association (MPA) and The New York Academy of Sciences. MPA is approved by the American Psychological Association to sponsor continuing education for psychologists. MPA maintains responsibility for this program and its content

Credit Designation

Warren Alpert Medical School of Brown University designates this educational activity for a maximum of 14 AMA PRA Category 1 Credits.  Physicians should only claim credit commensurate with the extent of their participation in the activity.

The Massachusetts Psychological Association (MPA) designates this educational activity for a maximum of 14 APA Credits. Psychologists should attend the conference in its entirety to receive the credit - APA does not allow partial credit. 

Educational Objectives

Participants in this educational activity will:

• Explore the field of epigenetics, role in normal embryological and fetal development, basic mechanisms and processes including biochemical, cellular, gene transcription and expression, relations to fetal programming and neural plasticity, and better understand non-human and human studies of medical outcomes.

• Improve their understanding of behavioral effects of epigenetic processes and integrate this knowledge into their research and/or medical practice (including both prevention and therapy). Behavioral outcomes include learning, memory, mental illness, normal development and developmental psychopathology.

• Take into account prenatal as well as postnatal factors that may produce epigenetic changes in behavior, and the intergenerational transfer and reversibility of these effects when assessing behavioral outcomes.

• Better their knowledge regarding the implications of pharmacotherapy.

• Design and implement changes in medical practice so that epigenetics can be considered in the prevention and treatment of behavioral alterations.

• Identify pending questions, more gaps in this field, and steps moving forward.

• Identify new multidisciplinary research opportunities and collaborations.

      Presented by


      For a complete list of supporters, please click the Supporters tab.



      *Presentation times are subject to change.

      Day 1: Friday, October 29, 2010

      8:00 am

      Registration and Breakfast

      9:00 am

      Opening Remarks

      Session I: Background and Perspectives

      Chair: Barry M. Lester, PhD, Warren Alpert Medical School of Brown University

      9:15 am

      What is Behavioral Epigenetics?
      Barry M. Lester, PhD, Warren Alpert Medical School of Brown University

      9:45 am

      Epigenetics: Basic Processes and Mechanisms
      Eric J. Nestler, MD, PhD, Mount Sinai School of Medicine

      10:45 am

      Coffee Break

      11:15 am

      Epigenetics, Intergenerational Inertia, And Human Adaptation: Hypotheses And Policy Implications
      Christopher W. Kuzawa, PhD, MsPH, Northwestern University

      12:00 pm

      Panel and Audience Discussion

      1:15 pm


      Session II: Learning and Memory

      Chair: J. David Sweatt, PhD, University of Alabama at Birmingham

      2:15 pm

      Epigenetic Mechanisms in Memory Formation
      J. David Sweatt, PhD, University of Alabama at Birmingham

      3:00 pm

      The Role of Chromatin-Modifying Enzymes in Long-Term Memory Processes
      Marcelo Wood, PhD, University of California, Irvine

      3:45 pm

      Coffee Break

      4:15 pm

      Signaling and Epigenetic Mechanisms in Stress-Related Memory Formation
      Johannes M. H. M. Reul, PhD, University of Bristol, UK

      5:00 pm

      Panel and Audience Discussion

      6:15 pm


      8:15 pm

      Day 1 Concludes

      Day 2: Saturday, October 30, 2010

      8:00 am

      Registration and Breakfast

      Poster Set-up

      Session III: Development

      Chair: Edward Tronick, PhD, University of Massachusetts Boston and Children's Hospital Boston

      8:30 am

      Alterations of DNA Methylation Associated with Growth Restriction and Infant Neurobehavior
      Carmen J. Marsit, PhD, Brown University

      9:15 am

      Epigenetic Mechanisms Underlying Persistent Alterations in Medial Prefrontal Cortical Function in Mice Exposed to Cocaine in Utero
      Barry Kosofsky, MD, PhD, Weill Cornell Medical College

      10:00 am

      Coffee Break and Poster Viewing

      10:30 am

      Epigenetic Programming by Maternal Care
      Michael Meaney, PhD, McGill University

      11:15 am

      Panel and Audience Discussion

      1:00 pm

      Lunch and Poster Session

      Session IV: Neuropsychiatry

      Chair: Eric J. Nestler, MD, PhD, Mount Sinai School of Medicine

      2:00 pm

      Histone Methylation-Dependent Transcriptional Regulation of Cocaine-Induced Behavioral And Structural Plasticity
      Ian Maze, PhD, Rockefeller University

      2:45 pm

      Epigenetic Targets in Neurodegenerative and Psychiatric Disorders
      Ted Abel, PhD, University of Pennsylvania

      3:30 pm

      Coffee Break and Poster Viewing

      4:00 pm

      Epigenetic Mechanisms Regulating Synapse Function And Behavior
      Lisa Monteggia, PhD, University of Texas Southwestern Medical Center

      4:45 pm

      Epigenetic Risk Factors in Social-Communication Disorders
      David H. Skuse, MD, PhD, University College London, UK

      5:30 pm

      Panel and Audience Discussion

      6:45 pm

      Closing Remarks
      Edward Tronick, PhD, University of Massachusetts Boston and Children's Hospital Boston

      7:00 pm

      Conference Concludes

      Poster Breakdown



      Barry M. Lester, PhD

      Warren Alpert Medical School of Brown University

      Edward Tronick, PhD

      University of Massachusetts Boston and Children's Hospital Boston

      Eric J. Nestler, MD, PhD

      Mount Sinai School of Medicine


      Ted Abel, PhD

      University of Pennsylvania

      Barry Kosofsky, MD, PhD

      Weill Cornell Medical College

      Christopher W. Kuzawa, PhD

      Northwestern University

      Ian Maze, PhD

      Rockefeller University

      Carmen Marsit, PhD

      Brown University

      Michael Meaney, PhD

      McGill University

      Lisa Monteggia, PhD

      University of Texas Southwestern Medical Center

      Johannes M. H. M. Reul, PhD

      University of Bristol, UK

      David H. Skuse, MD, PhD

      University College London, UK

      J. David Sweatt, PhD

      University of Alabama at Birmingham

      Marcelo Wood, PhD

      University of California, Irvine


      Presented by

      Jointly Sponsored by

      The New York Academy of Sciences and The Warren Alpert Medical School of Brown University.

      For opportunities to support this educational activity, please contact Marta Murcia at or 212.298.8641.

      Silver Supporters

      This event is funded in part by the Life Technologies™ Foundation.

      Bronze Supporters

      Massachusetts Life Sciences Center

      Grant Support

      Funding for this conference was made possible (in part) by 1 R13 DA029985-01 from the National Institute on Drug Abuse, Eunice Kennedy Shriver National Institute of Child Health & Human Development, National Institute on Mental Health and National Institutes of Health Office of the Director. The views expressed in written conference materials or publications and by speakers and moderators do not necessarily reflect the official policies of the Department of Health and Human Services; nor does mention by trade names, commercial practices, or organizations imply endorsement by the U.S. Government

      This activity has been funded in part by an Independent Medical Education Grant from AstraZeneca.

      Supported in part by March of Dimes Foundation Grant No. 4-FY10-458.

      This activity has been funded in part by a charitable contribution from Bristol-Myers Squibb Research and Development.

      Supported by an educational grant from Janssen, Division of Ortho-McNeIl-Janssen Pharmaceuticals, Inc., administered by Ortho-McNeIl Janssen Scientific Affairs, LLC


      Genomatix Software, Inc

      Massachusetts Life Sciences Center

      Promotional Partners

      Alzheimer’s Research Forum

      American Academy of Addiction Psychiatry


      Biological Psychiatry

      Clinical Epigenetics Journal

      Clinical Epigenetics Society

      Epigenetics and Chromatin

      Epigenetics Journal


      Fondation IPSEN

      Harvard Catalyst | The Harvard Clinical and Translational Science Center

      Journal of Developmental & Behavioral Pediatrics

      Massachusetts Life Sciences Center

      New York Alliance Against Chronic Disease

      New York State Foundation for Science, Technology, and Innovation

      Massachusetts Neuropsychological Society

      The Dana Foundation

      The Massachusetts Chapter of the American Academy of Pediatrics

      The New York Academy of Medicine

      Day 1: Friday, October 29, 2010

      Session I: Background and Perspectives

      What is Behavioral Epigenetics?

      Barry M. Lester PhD
      Warren Alpert Medical School of Brown University, Providence, RI

      The emergence of the field of epigenetics has forever changed the way we think about how we are affected by our genetic make-up. Although scientists have known about epigenetic marks since the 1970s there has been a more recent explosion of work on epigenetic mechanisms. There are ongoing discussions about how to define epigenetics including attempts to develop a consensus definition of “epigenetics” for consideration by the broader research community. The application of epigenetics to the study of behavior has ushered in the new fast-growing field of behavioral epigenetics but this field has not been described. In this presentation, we attempt to characterize and describe behavioral epigenetics as a discipline. We will provide an overview of the work that has been done in this field including behavioral processes, epigenetic mechanisms, species, tissues and “stressors” that have been studied. This review will help us understand how far we have come. It will also highlight some of the special issues and problems that are unique to the study of behavioral epigenetics and suggest directions for future work in this relatively new frontier. Some of these issues will be discussed here and will also be discussed throughout this conference.

      Epigenetics: Basic Processes and Mechanisms

      Eric J. Nestler MD, PhD
      Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY

      Epigenetic regulation, also known as chromatin remodeling, in neurons describes a process where the activity of a particular gene is controlled by the structure of chromatin in that gene’s proximity. Chromatin remodeling is complex and involves multiple covalent modifications of histones (e.g., acetylation, phosphorylation, methylation), ATPase-containing protein complexes which move histone oligomers along a strand of DNA, methylation of DNA, and the binding of numerous transcription factors and transcriptional co-activators and co-repressors, all of which act in a concerted fashion to determine the activity of a given gene. Epigenetic regulation is crucial for nervous system development, and several common mental retardation syndromes and related neurodevelopmental disorders are caused by abnormalities in chromatin remodeling mechanisms. Epigenetic regulation also occurs in the mature, fully differentiated brain, and provides unique mechanisms which may underlie stable changes in gene expression in brain both under normal conditions (e.g., learning and memory) and in several pathological states (e.g., depression, drug addiction, and schizophrenia). In some rare cases (e.g., gene imprinting), epigenetic modifications can be transmitted to offspring, which raises the possibility that behavioral experience in adult life might influence gene expression in subsequent generations. However, there has not to date been definitive evidence for epigenetic transmission of behavioral experience. While work on epigenetic mechanisms in brain is still in early stages, it promises to improve our understanding of brain plasticity and the pathophysiology of psychiatric disorders as well as possibly lead to the development of fundamentally new treatments for these conditions.

      Epigenetics, Intergenerational Inertia, And Human Adaptation: Hypotheses And Policy Implications

      Christopher W. Kuzawa PhD MSPH1
      1Department of Anthropology, Northwestern University, Evanston, IL
      2Cells 2 Society: The Center for Social Disparities and Health at the Institute of Policy Research, Northwestern University, Evanston, IL

      The rapid pace of human evolutionary expansion has provided minimal opportunities for genetic adaptation to the diverse social and ecological conditions that human populations inhabit. As such, the success of our species has largely relied upon non-genomic adaptive mechanisms that allow more rapid adjustment than that afforded by natural selection. The capacity to modify developmental biology in response to environmental change (developmental plasticity), undergirded by epigenetic and other processes, is one such adaptive mode and an important contributor to modern human biological variation. Although plasticity allows tailoring of behavior and biology to local conditions, many important developmental decisions are made early in development and may not be reversed (e.g. critical periods). Because the human lifespan lasts for multiple decades and ecological change is often stochastic rather than predictable, it follows that the suitability of a behavioral or developmental phenotype established in response to early environments will invariably decline with age. In this talk, I will review evidence that a subset of epigenetic processes work around this problem by integrating information across generations, thereby yielding relatively stable signals of typical social or physical conditions in the recent past. The tendency for parental experiences to leave a lingering imprint on developmental and epigenetic settings in offspring and grandoffspring (phenotypic inertia) could help lineages track more durable, sustained ecological trends, and thereby provide the developing organism with a higher fidelity cue of conditions likely to be experienced across its lifecycle. Predictions of this model and policy implications will be discussed.

      Session II: Learning and Memory

      Epigenetic Mechanisms In Memory Formation

      J. David Sweatt, PhD
      UAB School of Medicine, Birmingham, AL

      This presentation will address the idea that conservation of epigenetic mechanisms for information storage represents a unifying model in biology, with epigenetic mechanisms being utilized for cellular memory at levels from behavioral memory to development to cellular differentiation.

      The area of epigenetics is unfamiliar to many neurobiologists: epigenetic mechanisms typically involve alterations in chromatin structure, which in turn regulate gene expression. “Epigenetics” is functionally equivalent to the mechanisms allowing stable maintenance of gene expression that involve physically “marking” DNA or its associated proteins through post-translational modification. Thus, regulation of chromatin structure and regulation of direct methylation of DNA are the principal mechanisms of epigenetic regulation.

      Do epigenetic mechanisms operate in behavioral memory formation? We have generated several lines of evidence that support this idea. 1. Contextual fear conditioning triggers alterations in hippocampal histone acetylation, and contextual latent inhibition training triggers similar but distinct changes in histone acetylation. 2. The methyl-DNA binding protein MeCP2 (the Rett mental retardation syndrome gene product) alters chromatin structure and regulates hippocampal LTP and memory formation. 3. Inhibitors of DNA methylation block both hippocampal LTP and associative learning in vivo.

      Conclusions - An emerging idea is that the regulation of chromatin structure, mechanistically via histone modification and DNA methylation, may mediate long-lasting behavioral change and learning and memory. We find this idea fascinating because similar mechanisms are used for triggering and storing long-term "memory" at the cellular level, for example when cells differentiate.

      The Role Of Chromatin Modifying Enzymes In Long-Term Memory Processes

      Marcelo Wood PhD
      University of California-Irvine, Irvine, CA

      Chromatin, the complex of DNA and associated proteins, is a physical barrier to transcription mechanisms. The manipulation of chromatin is critically involved in regulating gene expression for a number of processes including the formation of long-term memory. Chromatin modifying complexes, which contain histone-modifying enzymes, regulate access to the underlying genomic DNA by relaxing chromatin structure and providing docking sites for additional regulatory factors. The enzymes that regulate levels of histone acetylation are histone acetyltransferases (HATs) and histone deacetylases (HDACs), and the interplay between HATs and HDACs is pivotal for the regulation of gene expression required for long-term memory processes. The alluring aspect of investigating these enzymes is that chromatin modifications may provide transient, and subsequently, potentially stable epigenetic marks in the service of activating and/or maintaining transcriptional processes. These in turn may ultimately participate in the molecular mechanisms required for neuronal changes subserving long-lasting changes in behavior. As an epigenetic mechanism of transcriptional control, chromatin modification has been shown to participate in maintaining cellular memory (e.g. cell fate) and may underlie the strengthening and maintenance of synaptic connections required for long-term changes in behavior. We use a combined genetic, molecular, pharmacological, and behavioral approach to examine the role of specific HATs and HDACs in learning and memory. Our results demonstrate that the CREB-binding protein (CBP) is a key HAT necessary for long-term memory formation and that histone deacetylase 3 (HDAC3) is a key negative regulator of long-term memory. Further understanding of these mechanisms promise to elucidate basic mechanisms underlying learning and memory and provide novel therapeutic strategies for treatment of cognitive disorders.

      Signaling and Epigenetic Mechanisms in Stress-Related Memory Formation

      Johannes M. H. M. Reul PhD
      Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, University of Bristol, United Kingdom

      Adaptation to emotionally stressful events is thought to involve changes in gene expression in limbic brain regions such as the amygdala and hippocampus. We identified distinct signaling and epigenetic mechanisms in hippocampal dentate gyrus granule neurons that are critical for appropriate behavioral adaptation including memory formation of stressful events. We found that stressful challenges such as forced swimming (FS), novelty, Morris water maze (MWM) and fear conditioning (FC) training evoke specific post-translational changes (i.e. Serine10 phosphorylation (S10p) and Lysine14 acetylation (K14ac)) in the nucleosomal protein histone H3. These epigenetic changes were only observed in dentate gyrus neurons and resulted in the induction of c-Fos and other gene products. Signaling to the chromatin occurred through glucocorticoids and glutamate acting via glucocorticoid receptors (GRs) and NMDA receptors (NMDA-Rs), respectively. NMDA-R activation led to activation of the ERK MAPK pathway in these dentate neurons resulting in the activation of at least two downstream kinases, i.e. mitogen- and stress-activated kinase1 (pMSK1) and Ets-like protein-1 (pElk-1). Formation of pMSK1 (a H3 kinase) and pElk-1 (through recruitment of p300, a histone acetyl transferase) resulted in the phospho-acetylation of H3 and induction of gene expression (e.g. c-Fos). GRs strongly facilitated pMSK1 and pElk-1 formation in dentate neurons. Furthermore, a series of studies of us and others showed that these dentate epigenetic mechanisms are critical for the formation of memories associated with stressful events such as FS, MWM and FC.
      Support: BBSRC and MRC, UK

      Conference Location:

      UMass Boston Campus Center
      100 Morrissey Blvd.
      BALLROOM 3550
      3rd Floor
      Boston, MA 02125


      Public Transportation (Recommended)

      Take the Red Line to JFK/UMass Station. A free shuttle bus will carry you to the campus.

      For more information click here.

      Commuter Rail:
      Take the commuter rail to the JFK/UMass station from the South Shore on the Middleboro and Plymouth lines.

      Kenmore Square stop (service all day): Take the Number 8 bus; the last one leaves campus at 1 a.m.
      Forest Hills stop (rush hour only):Take the Number 16 bus

      Taxi services

      Bay State Taxi: 617-566-5000

      Metro Cab: 617-782-5500

      Independent Cab: 617-426-8700

      Checkered Cab: 617-536-7000

      Calling from the Campus Center:
      Next to the elevator bank located on the UL level of the Campus Center (entry level from the parking lots) there is a phone with 3 pre-programmed phone numbers for taxi services. Those wishing to use a cab service can call any of these numbers indicating both pick-up and drop-off locations, and form of payment.

      Driving Directions

      From the North:
      Take Interstate 93 South through Boston to exit 15 (JFK Library/South Boston/Dorchester) and follow the University of Massachusetts signs along Columbia Road and Morrissey Boulevard to the campus.

      From the South:
      Take Interstate 93 North to exit 14 (JFK Library/Morrissey Boulevard) and follow Morrissey Boulevard north to the campus.

      From the West:
      Take the Massachusetts Turnpike (Interstate 90) east to Interstate 93. Take I-93 South one mile to exit 15 (JFK Library/South Boston/Dorchester) and follow the University of Massachusetts signs along Columbia Road and Morrissey Boulevard to the campus.

      Parking on Campus

      All visitors to the Campus Center are encouraged to park in the North Lot (see Map) $6 per single use Pickup/drop off is allowed at the Main entrance on the circular road in front of the building.

      Suggested Hotel Accommodations in Downtown/Financial District and Back Bay
      (within walking distance of the T’s Red line or Green line)

      Club Quarters in Boston
      161 Devonshire Street
      Boston, MA 02110
      Phone: 617-357-6400

      Boston Marriott Copley Place
      110 Huntington Avenue Boston
      Boston, MA 02116
      Phone: 617-236-5800

      The Boston Park Plaza Hotel & Towers
      50 Park Plaza at Arlington Street
      Boston, MA 02116
      Phone: 617-426-2000

      Copley Square Hotel
      47 Huntington Avenue
      Boston, MA 02116
      Phone: 617-536-9000

      Courtyard by Marriott, Boston Copley Square
      88 Exeter Street
      Boston, MA 02116
      Phone: 617-437-9300

      The Eliot Hotel
      370 Commonwealth Ave
      Boston, MA 02215
      Phone: 617-267-1607

      Fairmont Copley Plaza Hotel
      138 Saint James Avenue
      Boston, MA 02116
      Phone: 617-267-5300

      The Lenox Hotel
      61 Exeter Street
      Boston, MA 02116
      Phone: 617-536-5300

      For more information about these and other hotels in the Downtown/Financial district or Back Bay area please click here

      Suggested Hotel Accommodations around UMass Campus Center

      DoubleTree Club Hotel Boston Bayside
      240 Mount Vernon Street
      Boston, MA 02125
      Phone: 617-822-3600

      Comfort Inn Boston
      900 Morrissey Boulevard,
      Boston, MA 02122
      Phone: 617-287-9200

      Ramada Boston
      800 Morrissey Boulevard
      Freeport St
      Boston, MA 02122
      Phone: 617-287-9100

      General Information about Boston

      Please click here

      Special Needs and Additional Information

      For any additional information and for special needs, including child/family care resources available to conference attendees, please e-mail Deanna Vollmer or call Deanna Vollmer 212.298.8611.