Honors & Awards
Graduate Research Fellowship, National Science Foundation (2021)
Trainee Professional Development Award, Society for Neuroscience (2018)
Undergraduate Research Conference Travel Award, University of Washington (2018)
Husky 100, University of Washington (2018)
Washington Research Foundation Fellowship, Washington Research Foundation (2017)
Rex J. and Ruth C. Robinson Scholarship Fund in Chemistry, University of Washington (2017)
Mary Gates Research Scholarship, University of Washington (2017)
Summer Research Program Scholarship, ThinkSwiss (2017)
Education & Certifications
B.S., University of Washington, Neurobiology and Biochemistry (2018)
Current Research and Scholarly Interests
I am interested in using and developing systems neuroscience approaches to improve understanding and treatment of psychiatric illnesses. My current work is focused on developing translatable, noninvasive deep brain neuromodulation through targeted delivery of psychotropic drugs via ultrasound-sensitive nanoparticles.
Chronic Gq signaling in AgRP neurons does not cause obesity.
Proceedings of the National Academy of Sciences of the United States of America
Maintaining energy homeostasis requires coordinating physiology and behavior both on an acute timescale to adapt to rapid fluctuations in caloric intake and on a chronic timescale to regulate body composition. Hypothalamic agouti-related peptide (AgRP)-expressing neurons are acutely activated by caloric need, and this acute activation promotes increased food intake and decreased energy expenditure. On a longer timescale, AgRP neurons exhibit chronic hyperactivity under conditions of obesity and high dietary fat consumption, likely due to leptin resistance; however, the behavioral and metabolic effects of chronic AgRP neuronal hyperactivity remain unexplored. Here, we use chemogenetics to manipulate Gq signaling in AgRP neurons in mice to explore the hypothesis that chronic activation of AgRP neurons promotes obesity. Inducing chronic Gq signaling in AgRP neurons initially increased food intake and caused dramatic weight gain, in agreement with published data; however, food intake returned to baseline levels within 1 wk, and body weight returned to baseline levels within 60 d. Additionally, we found that, when mice had elevated body weight due to chronic Gq signaling in AgRP neurons, energy expenditure was not altered but adiposity and lipid metabolism were both increased, even under caloric restriction. These findings reveal that the metabolic and behavioral effects of chronic Gq signaling in AgRP neurons are distinct from the previously reported effects of acute Gq signaling and also of leptin insensitivity.
View details for DOI 10.1073/pnas.2004941117
View details for PubMedID 32764144