Professor, Department of Psychological and Brain Sciences
My laboratory is interested in the behavioral and neural mechanisms of associative learning, the simple learning of relations between environmental stimuli and the outcomes they predict (Pavlovian learning), and between motor actions and the outcomes they produce (Instrumental learning). These simple learned associations guide our behavioral response to the environmental stimuli that continually surround us. Associative learning also provides a means whereby stimuli in the environment come to regulate our emotional responses and to strongly bias our decision-making. Thus we seek to define the behavioral and neural mechanisms for the acquisition of reward-based associations. In addition, we are interested in the neural systems that control expression of stimulus-guided behavior after learning. Because associative learning mechanisms contribute to pathological behaviors such as drug and alcohol addiction and overeating, an additional focus of our work is translational. In these studies, we apply our findings on associative learning to understand better how drug- and alcohol-associated stimuli contribute to relapse. To realize our basic and translational goals, we use well-defined animal models of learning and addiction in concert with in vivo electrophysiological measurement and optogenetic manipulation of neuronal populations in specific brain regions and circuits.
Some current research goals are:
To determine the principles of cue and outcome encoding in the amygdala, and their subcircuit dependence. Our goal is to understand how this region contributes to behavior triggered by cues associated with positive outcomes, such as natural and drug reward, and cues associated with negative outcomes, such as fearful or painful events, with a focus on basal amygdala function.
To determine the functions of dopamine in reward-related behavior. Dopamine plays a crucial role in reward learning and performance. We are leveraging the power of optogenetics to probe the function of ventral tegmental area (VTA) dopamine neurons using TH::cre rodents to allow selective expression of opsins in dopamine neurons to investigate their behavioral role.
To determine the behavioral and neural mechanisms that underlie drug relapse triggered by environmental cues. Currently we are focused upon a model in which the nucleus accumbens and its glutamatergic input from the basal amygdala and its dopaminergic input from the ventral tegmental area are required for relapse to alcohol-predictive cues when encountered in alcohol-associated contexts.