Upcoming Events!




Please note the location change to the Knight Campus Beetham Family Seminar Room and earlier pre-seminar reception start time of 3:30pm for this week's seminar.
From the sky bridge cross to Knight Campus and take either the stairs of elevator to the first floor (street level). The seminar room will be to the left, and the reception will be just outside of the room.
My lab aims to understand the molecular mechanisms underlying the sensations of itch, touch, and pain. Humans rely on these senses for a broad range of essential behaviors. For example, acute pain acts as a warning signal that alerts us to noxious mechanical, chemical, and thermal stimuli, which can potentially damage tissue. Likewise, itch sensations trigger reflexes that may protect us from disease-carrying insects. Despite these essential protective functions, itch and pain can outlast their usefulness and become chronic diseases. We use cellular physiology, molecular biology, molecular genetics, and behavioral studies to elucidate the mechanisms underlying itch and pain transduction under normal and pathophysiological conditions. This talk will highlight the interactions between the nervous system and immune system that promote chronic itch, pain and inflammation.


Past Events


Abstract: Mammals learn a large repertoire of novel actions by refining variable movements into...
Abstract: Mammals learn a large repertoire of novel actions by refining variable movements into precise skills. The brain achieves this by assigning credit to movements that led to desired outcomes. Even for simple actions such as reaching to a spatial target, the brain could assign credit to the direction, endpoint target location, speed, etc. As such, different movement strategies may emerge across individuals, depending on what is assigned with credit.My goal is to dissect the sensorimotor areas controlling different aspects of these movements, and probe what determines the learning of different reach strategies.I developed a behavior task in which head-fixed mice generate exploratory forelimb trajectories with a joystick and are rewarded when they hit a covert target in the workspace. As mice learn, they refine their reaches which become less variable in direction, tortuosity, speed, and targeting precision. We show that different aspects of the reach such as direction or speed are learned and controlled through distinct cortical and thalamic networks. For instance, sensorimotor cortex is required to generate reaches with high directional variability across different positions of the workspace, while a specific nucleus of thalamus is required to refine the overall reach direction.
But what reach strategies are mice learning? By relocating the start position in a small number of probe trials I discovered that some animals learned a direction-based strategy (move in the same initial direction from new starts), while others learned an endpoint-based strategy (guide the joystick into the target from new starts, adjusting their direction). Which strategy an individual animal learned correlated with the degree of spatial directional variability during exploration, the aspect of the reach controlled by cortex. We find that when we train reinforcement learning model agents in a similar task they also show this relationship between exploration and endpoint- vs. direction-learning bias. Overall, these findings suggest that the sensorimotor system learns different control strategies by exploring and reinforcing certain movement aspects during learning, and these aspects are likely generated by distinct circuits.


This is an ectopic seminar hosted by the Zebrafish Groupie & is open to the UO community
Abstract...
This is an ectopic seminar hosted by the Zebrafish Groupie & is open to the UO community
Abstract: Social behavior ranges from simple pairwise interactions to thousands of individuals coordinating goal-directed movements across animal species. Regardless of the scale, these interactions are governed by multimodal sensory input that requires animals to actively attend to cues and respond appropriately for the context. We leveraged the zebrafish, a highly social and experimentally tractable model organism, to study naturalistic pairwise interactions early in development. We identified stereotyped positions and coordinated movements in interacting pairs, and generated a model to automatically classify states of active interaction. We then manipulated visual and mechanosensory cues to test the contributions of these distinct sensory inputs to behavioral states and corresponding brain activity. Whole-brain immunolabeling for recently active neurons revealed neuronal populations in the forebrain and habenula are selectively active in social contexts and predict sociality of individual pairs. Altogether, we find coordinated social interactions are reliably elicited in juvenile zebrafish early in development, and that specific social behaviors rely on different sensory modalities and distinct brain circuits.





Social interactions play a major a major role in different functional domains relevant for Darwinian fitness, such as finding food, choosing mates, or avoiding predators. Therefore, at the proximate level social interactions are a key mortality risk factor with health implications and at the ultimate level, sociality impacts ecological and evolutionary processes. Our lab studies social behavior at both levels, combining the study of proximate causes (genes, hormones, neural circuits, cognitive processes) and ultimate effects (evolutionary consequences). For this purpose, we have been using two model organisms in the lab - zebrafish and fruit flies - to study the neural circuits and the genetic architecture of social behavior. In this talk, I will provide some examples of the work done in our lab in both model organisms. First, I will show how oxytocin plays a critical role in the development of sociality in zebrafish and how it interacts with the developmental environment to shape the emergence of different aspects of adult social behavior. I will then, show how oxytocin is necessary and sufficient for complex social behavior in adult zebrafish, including social contagion of fear and emotion recognition. Finally, I will address the evolvability of sociality in zebrafish illustrated by an artificial selection experiment (currently in the F7). In the second part of my talk, I will present results on a study that investigates the genetic architecture of social cognition in Drosophila. We specifically address the question of social learning being a domain-specific or a general-domain cognitive process. For this purpose, we have phenotyped social and asocial learning in the core lines of the DGRP panel. We show that there is no phenotypic correlation between the two learning types and that the GWAS revealed different genetic variants located in different genes associated with social and asocial learning. Finally, we show that most social learning-associated genes are expressed in the Drosophila mushroom bodies and functionally confirmed their involvement in learning using RNAi lines. Together these results highlight the potential of each model organism to address question related to the mechanisms underlying sociality.
