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<p>People with narcolepsy have intrusive episodes of muscle weakness known as cataplexy, which are usually triggered by strong, positive emotions. As cataplexy occurs almost exclusively during social interactions, we examined whether it is promoted by the prosocial neuropeptide oxytocin. In a mouse model of narcolepsy, social reunification triggered cataplexy, and an oxytocin antagonist blocked socially induced cataplexy episodes. Oxytocin tone and the activity of oxytocin receptor-expressing neurons in the central amygdala both increased just before cataplexy triggered by social stimuli. Chemo- and optogenetic manipulations demonstrated that oxytocin-responsive neurons in the central amygdala drive cataplexy by inhibiting brainstem neurons that suppress muscle atonia. In addition, chocolate, a rewarding stimulus associated with strong, positive emotions, also engages this oxytocin–amygdala pathway and triggers cataplexy in narcoleptic mice. Together, these findings show that oxytocin acts through the amygdala to promote cataplexy triggered by social and other rewarding stimuli, offering new opportunities for treating cataplexy.</p>

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Oxytocin promotes socially triggered cataplexy

  • 期刊论文

  • 发表日期：

    2026年7月14日

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  • Carrie E. Mahoney,
  • Roberto De Luca,
  • Adam A. Joyal,
  • Caroline Woods,
  • Wenling Zhao,
  • Alissa A. Coffey,
  • Emi Kurimoto,
  • Daniel Kroeger,
  • Lin Zhu,
  • Henning Fenselau,
  • Valery Grinevich,
  • Christian R. Burgess,
  • Elda Arrigoni,
  • Thomas E. Scammell

摘要

People with narcolepsy have intrusive episodes of muscle weakness known as cataplexy, which are usually triggered by strong, positive emotions. As cataplexy occurs almost exclusively during social interactions, we examined whether it is promoted by the prosocial neuropeptide oxytocin. In a mouse model of narcolepsy, social reunification triggered cataplexy, and an oxytocin antagonist blocked socially induced cataplexy episodes. Oxytocin tone and the activity of oxytocin receptor-expressing neurons in the central amygdala both increased just before cataplexy triggered by social stimuli. Chemo- and optogenetic manipulations demonstrated that oxytocin-responsive neurons in the central amygdala drive cataplexy by inhibiting brainstem neurons that suppress muscle atonia. In addition, chocolate, a rewarding stimulus associated with strong, positive emotions, also engages this oxytocin–amygdala pathway and triggers cataplexy in narcoleptic mice. Together, these findings show that oxytocin acts through the amygdala to promote cataplexy triggered by social and other rewarding stimuli, offering new opportunities for treating cataplexy.