Prosocial Behavior Lab
Our research aims to understand the neural basis of prosociality–the ability to perceive others’ needs and take actions that improve their conditions. Our previous work has developed various paradigms of prosocial behaviors in laboratory mice. Using these models, our current research focuses on the neural circuit and molecular mechanisms underlying these behaviors, their long-term regulation by prior experiences, and their disruption in neuropsychiatric disorders such as autism.
Neural circuit mechanisms underlying prosocial behaviors and their long-term modulation by prior experiences
The expression of prosocial behaviors requires the perception of others’ affective states and the integration of self- and other-regarding information to guide behavioral decisions. Using in vivo calcium imaging, we examine how affective states of self and others, as well as prosocial decisions, are represented across different brain regions. We further apply functional manipulations to identify neural circuits that causally control prosocial behaviors. Real-world prosocial interactions often involve repeated, bidirectional exchanges within social groups. We develop new behavioral paradigms to investigate how prior experiences shape future prosocial decisions and to uncover the underlying neural mechanisms.
Molecular underpinnings of prosocial interaction
​The molecular basis of prosocial behavior remains poorly understood. Using single-cell RNA sequencing of brain regions implicated in prosociality, we examine acute and long-term transcriptomic changes induced by prosocial interactions. Our goal is to identify specific molecular pathways and cell types engaged during prosocial behavior and to determine their functional roles through genetic perturbations and cell-type–specific manipulations.
Neural mechanisms underlying deficits in empathy and prosocial behavior in neuropsychiatric disorders
Impairments in social affective processing and social interaction are hallmarks of a range of neuropsychiatric disorders, including autism spectrum disorders (ASD), personality disorders, and affective and anxiety disorders. However, how empathic and prosocial capacities are altered in these conditions, and the neural mechanisms underlying these deficits, remain largely unexplored. We aim to investigate how empathic and prosocial processes are disrupted in mouse models of ASD and other psychiatric conditions at behavioral, circuit, and molecular levels, with the ultimate goal of guiding the development of effective interventions to improve social functioning in these conditions.
