Kate's research interests are centered around serotonergic modulation of the neural circuits underlying social and emotional behavior. Two behaviors that she is currently studying are aggression and impulsivity. These behaviors can both be modulated through serotonin signaling at the 5-HT1B receptor. However, the sensitive periods and neural systems mediating these effects are dissociable.
Using mouse models of inducible and tissue-specific knockdown of the 5-HT1B receptor, Kate has shown that there is a developmental sensitive period for the generation of aggressive behavior. Understanding these developmentally "programmed" circuits is important for the determination of neural targets to treat aggression in adulthood.
Impulsive behaviors are characterized generally as lacking in lack self-control. The ability to delay gratification and suppress responses are both facets of a multi-dimensional construct of impulsivity. Dysregulated impulsive behavior is a key component in a number of psychiatric disorders including ADHD, binge eating, substance use disorders, and behavioral addictions like gambling disorder. Serotonin signaling through the 5-HT1B receptor affects impulsivity.
The serotonergic hypothesis of depression has dominated the field for over 5 decades. Kate's research has addressed this theory in a number of different projects. Past work has focused on how the immune system can influence depressive-related behaviors through its contributions of serotonin to the hippocampus. Other work has used tissue-specific genetic mouse models to delineate the role of specific serotonin receptor populations in depressive behavior and also the response to antidepressants. Finally, since over a third of depressed patients don't respond to current serotonin acting antidepressants, an additional project is currently investigating the role of the mu opioid receptor in antidepressant treatments.