Assistant Professor My over-arching scientific goal is to understand how distinct neural circuits contribute to motivated behaviors. As a graduate student at the University of North Carolina at Chapel Hill, I utilized rodent models of cocaine self-administration to investigate maladaptations in nucleus accumbens astroglial signaling associated with motivation to seek drugs of abuse. My postdoctoral work at NIH employed a multidisciplinary approach to examine the role of ventral pallidal (VP) cholinergic neurons in innate motivated behaviors. A key finding was the discovery of two distinct and non-overlapping subpopulations of cholinergic neurons in the VP which differentially encode motivation to approach or avoid stimuli. Combined, these findings indicate both astroglial and cholinergic signaling are important mediators of motivation. Research Research Interests: Bidirectional communication between neurons and astrocytes is critical for the development, maintenance and function of neural circuits. Disruptions in neuron-astrocyte communication are associated with neurodegenerative and neuropsychiatric disorders. Our goal is to develop a mechanistic and functional understanding of the interactions between neurons and astrocytes, and how the coordinated activity of neurons and astrocyte influence behavioral outputs. We investigate these questions using an interdisciplinary approach, with an emphasis on circuit manipulation, in-vivo imaging with high spatiotemporal resolution, and large-scale data analysis of neuron-astrocyte interactions. We examine neuron-astrocyte interactions in the context of motivated behaviors. Proper motivational drive ensures appropriate behavioral responses to stimuli, such as avoiding harmful stimuli and seeking reward. Neuropsychiatric disorders are characterized by improper motivational balance. For example, drug addiction is defined as hyper-motivation to seek drugs despite adverse consequences. In contrast, amotivation, a reduction in motivation toward goal-directed behavior, is a hallmark of mood and anxiety disorders. Accordingly, we will examine how changes in neuron-astrocyte interactions lead to the development of neuropsychiatric disorders. We focus on the interaction between astroglial and cholinergic signaling. Alterations in cholinergic signaling are associated with a variety of behaviors including motivated behaviors. Changes to the structure and function of astrocytes have also been associated with alterations in motivation. While astrocytes express cholinergic receptors and exhibit elevated calcium in response to acetylcholine, it is unclear how cholinergic signaling mediates astrocyte activity (and vice versa), and how these interactions mediate motivation. Our goal is to fundamentally advance the understanding of how astrocytes and neurons interact to mediate behavioral outcomes.
