University of Wisconsin–Madison


Eventbrite - Wisconsin Symposium on Emotion - WSoE 2018

Thursday, April 19, 2018

7:30 – 8:30am: Breakfast & Registration
8:30 – 8:45am: Welcome – Ned Kalin, MD and Richie Davidson, PhD
8:45 – 9:45am: Elisabeth Binder, MD, PhD
Molecular Mechanisms of Gene X Environment Interactions:
Possible Relevance for Prevention, Diagnosis and Treatment of Psychiatric Disorders

9:45 – 10:30am: Discussion
10:30-11:00am: Break
11:00 – 12:00pm: Martin Paulus, MD
Computational Dysfunctions in Anxiety: Failure to Differentiate Signal from Noise
12:00 – 12:45pm: Discussion
12:45 – 2:30: Lunch Break
2:30 – 3:30pm: Kristen Brennand, PhD
Modeling Predisposition to Schizophrenia Using Stem Cells
3:30 – 4:15pm: Discussion
4:30 – 6:30pm: Poster Session & Reception


Friday, April 20, 2018

7:30 – 8:00am: Breakfast
8:00 – 9:00am:  Frances Champagne, PhD
Dynamic Epigenetic Pathways in Development
9:00 – 9:45am: Discussion
9:45 – 10:45am: Breakout Session Discussions
10:45 – 11:45am: Kevin LaBar, PhD
Fear Generalization and Contextualization
11:45 – 12:30pm – Discussion
12:30pm: Symposium Adjourns

Thursday, April 19, 2018
4:30 – 6:30pm
Varsity Hall 2 

* For Registered Attendees of the Symposium *

A hallmark of the Wisconsin Symposium on Emotion is the poster session and reception held on the first evening of the conference. Attendees gather to discuss posters, drink beverages, and nosh on appetizers. This intimate evening allows participants a special opportunity to meet and discuss their work with the speakers and fellow colleagues.

The poster session will be held in Varsity Hall 2 on the second floor of Union South. All travel award winners present a poster and all other attendees are encouraged to present posters as well. Poster abstracts should be limited to 250 words and should include a title.

The deadline for participation is April 1, 2018.
To register your poster, please submit a completed WSoE Poster Registration Form to the symposium coordinator:

Poster dimensions: stands are 48″ x 48″ and useable space is 46″ x 46″

Friday, April 20, 2018
9:45 – 10:45am

*Students may select 1-2 presenters when registering for the symposium*

Students and trainees attending the symposium are invited to participate in small group discussion sessions with 2 presenters of their choosing. Breakout discussions give attendees an opportunity to participate in further in-depth conversations with experts in the field of affective neuroscience.

Student attendees may select up to two presenters for the breakout discussion sessions. Please make your selection when you register for the symposium, or by contacting the symposium coordinator:

Elisabeth Binder, MD, PhD
Thursday, April 19, 2018
8:45am – 9:45am



Molecular Mechanisms of Gene X Environment Interactions:
Possible Relevance for Prevention, Diagnosis and Treatment of Psychiatric Disorders

Early adverse exposures, such as maternal stress during pregnancy and child abuse, are thought to result in long-lasting consequences on neural circuit function and stress hormone regulation and ultimately in an increased risk for psychiatric but also medical disorders later in life. Overall, this presentation will describe putative molecular mechanisms how genetic variants and exposure to adversity interact to shape risk and resilience for psychiatric disorders, with a focus on stress hormones. These glucocorticoids (GCs) have been shown to alter gene expression pattern and to induce long-lasting epigenetic changes in specific loci through binding of the glucocorticoid receptor (GR) to glucocorticoid responsive elements (GREs).


The talk will first highlight data from a human hippocampal cell line that identify long lasting epigenetic changes in DNA methylation in response to GCs. These lasting epigenetic changes are located in brain development- and disease-relevant gene enhancer regions and lead to increased transcriptional sensitivity to future stress exposure. Data from human brain organoids and single cell sequencing will then delineate whether specific subtypes of cells show differential sensitivity to early GC exposure during brain development .The second focus will be on common genetic variants in long-range enhancer elements that can modulate the transcriptional and epigenetic response to GR activation and early life adversity. These functional genetic variants associate with increased risk for psychiatric phenotypes and differences in neural correlated of stress processing and are in turn enriched among the loci showing lasting DNA methylation changes with GC in the hippocampal cell line described above.

Overall, the presentation will outline how stress-exposure can have lasting effects on cell and tissue function and how this relates to risk or resilience to stress-related disorders in the context of common genetic variation.

Martin P. Paulus, MD
Thursday, April 19, 2018
11:00am – 12:00pm



Computational Dysfunctions In Anxiety: Failure To Differentiate Signal From Noise

Differentiating whether an action leads to an outcome by chance or by an underlying statistical regularity that signals environmental change profoundly affects adaptive behavior.  Prior studies have shown that anxious individuals may not appropriately differentiate between these situations. This investigation aims to precisely quantify the process deficit in anxious individuals and determine the degree to which these process dysfunctions are specific to anxiety. 122 subjects recruited as part of an ongoing large clinical population study completed a change point detection task. Reinforcement learning models were used to explicate observed behavioral differences in Low Anxiety (OASIS<=8) and High Anxiety (OASIS>=9) groups. High anxious individuals used a sub-optimal decision strategy characterized by a higher lose-shift rate. Computational models and simulations revealed that this difference was due to a higher base-learning rate.  These findings are better explained in a context-dependent reinforcement-learning model. Anxious subjects’ exaggerated response to uncertainty leads to a sub-optimal decision strategy that makes it difficult for these individuals to determine whether an action is associated with an outcome by chance or by some statistical regularity.  These findings have important implications for developing new behavioral intervention strategies utilizing learning models.


Kristen Brennand, PhD
Thursday, April 19, 2018
2:30 – 3:30pm



Modelling Predisposition to Schizophrenia Using Stem Cells


Schizophrenia (SZ) is a debilitating psychiatric disorder for which the molecular mechanisms underlying the disease state remain unclear. To address this, we reprogrammed fibroblasts from SZ patients into human induced pluripotent stem cells (hiPSCs) and subsequently differentiated these disorder-specific hiPSCs into neural progenitor cells (NPCs) and neurons. Our hiPSC neural cells, from controls and patients with SZ, better resemble fetal rather than adult brain tissue, indicating that hiPSC-based models may be best suited for studies of disease predisposition. At the cellular level, we have previously reported aberrant migration, increased oxidative stress, abnormal WNT signaling and elevated global protein synthesis in SZ hiPSC NPCs, together with diminished neuronal connectivity and impaired synaptic function in SZ hiPSC neurons. Early network-based analyses identified microRNA-9 (miR-9) to be significantly downregulated in a subset of SZ NPCs, a finding that was corroborated by a replication NPC cohort derived from childhood-onset-SZ (COS) patients and further validated by an independent gene-set enrichment analysis of the largest SZ genome-wide association study (GWAS) to date. Overall, this has demonstrated a remarkable convergence of independent hiPSC- and genetics-based discovery approaches. We have now conducted more comprehensive network-based evaluations of both our original SZ and our replication COS hiPSCs cohorts, in an attempt to better understand the genetic risk factors contributing to SZ. We have identified both activity-dependent and disease-specific changes of the transcriptome, finding that the effect of activity-dependent changes of gene expression in SZ neurons was attenuated compared with control neurons. Our overall objective is to understand the cell-type specific contributions of these risk genes to disease predisposition.


Frances A. Champagne, PhD
Friday, April 20, 2018
8:00 – 9:00am



Dynamic Epigenetic Pathways in Development

Experiences occurring during the prenatal and postnatal period set the stage for later life physical and emotional health.  Advances in the methodologies available to examine these developmental effects from a cellular and molecular perspective indicate that dynamic epigenetic variation is ongoing throughout development and in response to environmental signals.  This epigenetic variation serves as a form of developmental plasticity that may have detrimental effects on health when there is a mismatch in the quality of the experiences occurring in early life and the physical and emotional context/challenges of later life.  This plasticity may also occur in offspring in response to the experiences of parents – leading to a multigenerational impact of adverse environmental conditions.  Critical to consider within this epigenetic framework is the cascade of events and individual differences that contribute to divergent developmental trajectories and the complex mechanisms which can lead to continuity or discontinuity in biobehavioral outcomes across generations.

Kevin S. LaBar, Ph.D.
Friday, April 20, 2018
10:45 – 11:45am



Fear Generalization and Contextualization

Fear learning is highly beneficial to individuals as a means to identify potential sources of threat in the environment. However, fears that are overgeneralized to innocuous stimuli or those expressed in safe contexts can promote maladaptive avoidant behaviors. While much research has identified brain mechanisms for the initial acquisition of fear, the circuits responsible for fear generalization and contextualization are relatively unknown. We recently discovered two ways by which learned fears generalize across stimuli in the environment. First, we found that aversive conditioning to a moderately fearful face generalizes to faces that express higher fear intensity as a form of perceptual generalization. Second, we found that aversive conditioning to a few objects from a given semantic category generalizes to other exemplars from the same category as a form of conceptual generalization. In the first part of this talk, I will detail the neural bases of these novel generalization effects and their translational potential to understand the pathophysiology of posttraumatic stress disorder. Next, I will describe our pioneering application of immersive 3-D virtual reality technology to investigate contextual influences over fear learning. I will show how shifts in virtual environmental contexts shape the expression of acquired fears and alter prefrontal cortex engagement to promote the recovery of extinguished fears. Finally, I will demonstrate how to harness the power of generalization to de-contextualize extinction learning and potentially prevent the return of fear.