PROJECT ABSTRACT Active huddling is a cooperative group behavior that is displayed throughout development and is thought to serve a variety of functions, including energy conservation, thermoregulation, and social reward. However, the genetic basis and neural circuity that regulates huddling behavior in adult mice is not known. Dr. Nelson’s laboratory will investigate the mechanistic basis of adult huddling behavior on two levels. First, Dr. Nelson has observed that a disruption of group huddling is caused by mutation of Shank3b—a gene associated with autism spectrum disorder (ASD) in the human population. His lab will test the hypothesis that this disruption is linked to hypothalamic neural circuits regulating sleep, social reward, and thermoregulation. The Nelson lab will use neural activity and circuit mapping to identify huddling-associated circuits, and functional studies to test the precise role of those circuits on parameters of huddling behavior. Second, while the neuromodulator oxytocin (OT) has been predicted to play a role in adult group huddling, the precise role of cell-type specific oxytocinergic circuits on huddling is unknown. The Nelson lab will use in vivo calcium recordings of hypothalamic OT neurons, along with circuit tracing and functional manipulations, to identify the relationship between OT neural activity and huddling according to group size, sex, and Shank3b mutation. This project is expected to establish a new social behavior paradigm that reveals variation in huddling according to sex and ASD mutation state, and will elucidate how aspects of huddling are regulated by neural circuits.