Mouse research reveals how the ‘social bonding hormone’ activates neurons that promote cataplexy during rewarding social experiences, offering new clues to the biology of narcolepsy. Previous studies had also identified oxytocin-sensitive neurons in the amygdala, a brain region already implicated in regulating muscle tone. “By blocking oxytocin, we could prevent the increase in cataplexy,” Mahoney says. Administering the agonist increased both the amount of time the mice spent in cataplexy and the number of cataplexy bouts compared to a saline control. The team’s circuit mapping showed that these oxytocin-sensitive neurons shut down brainstem neurons that normally suppress muscle atonia.