By Ingrid Fadelli
Credit: Unsplash/CC0 Public Domain
Narcolepsy is a chronic neurological condition characterized by disruptions in the regulation of sleep-wake cycles. People with this condition often experience extreme sleepiness during the day and, in some cases, a sudden but temporary loss of muscle strength while conscious, called cataplexy.
Past studies suggest that cataplexy often occurs when people with narcolepsy experience positive emotions, such as excitement, amusement or joy. The neurophysiological processes that prompt this sudden loss of muscle strength during social interactions, however, remain poorly understood.
Researchers at Harvard Medical School recently carried out a study aimed at better understanding why people with narcolepsy often experience cataplexy during pleasant social interactions. Their findings, published in Nature Neuroscience, suggest that oxytocin, a hormone released by nerve cells during social bonding and joyful exchanges, could contribute to the emergence of cataplexy in pleasant moments.
"For many years, people with narcolepsy have reported that cataplexy is often triggered during social interactions, especially when laughing or spending time with friends and family," Carrie E. Mahoney, first author of the paper, told Medical Xpress.
"Despite these consistent reports, we didn't understand why social situations were such powerful triggers. As oxytocin is a neuropeptide involved in social behavior and bonding, we wondered whether it might contribute to these episodes."
Investigating why social interactions can prompt cataplexy
The main objective of the recent work by Mahoney and her colleagues was to determine whether oxytocin plays a role in socially triggered cataplexy and identify the brain circuits through which it may act. To do this, they started by studying a well-established mouse model of narcolepsy—more specifically, mice that lack orexin, a small protein-like chemical messenger (i.e., peptide) produced by neurons in the hypothalamus.
Mice that lack this peptide exhibit behaviors and symptoms that resemble those observed in human patients with narcolepsy. The researchers observed the mice as they interacted with some of their peers. They also administered a compound that prevents oxytocin from binding to its receptors in the mouse brain to determine whether the hormone played a role in socially triggered cataplexy.
"We gave the mice an oxytocin receptor agonist and determined that cataplexy was increased, and if we blocked the oxytocin receptor before treatment with the agonist, this increase in cataplexy was blocked," Mahoney explained.
"This global approach at least supported the fact that oxytocin had a role in promoting cataplexy. We then set out to determine if there was a specific brain circuit that could explain where and how oxytocin could influence the onset of cataplexy."
Subsequently, the researchers also manipulated the activity of neurons in the mouse brain that produced oxytocin and neurons that responded to it. This allowed them to determine their contribution to a neuronal circuit that has previously been linked to the onset of cataplexy.
"Our findings demonstrate that oxytocin contributes to socially triggered cataplexy and that a neuronal circuit underlying socially triggered cataplexy overlaps with reward-triggered cataplexy in a mouse model of narcolepsy," Mahoney said. "Together, these results suggest that different positive emotional experiences may converge on a common neural network that ultimately triggers cataplexy."
Toward a better understanding of cataplexy
The findings gathered by Mahoney and her colleagues indicate that oxytocin plays a role in the onset of cataplexy during pleasant social interactions. As their study focused on a mouse model of narcolepsy, further research will be needed to determine whether the same or similar processes also occur in the human brain.
The researchers' efforts could eventually shed light on why social bonding and positive emotions provoke cataplexy in many individuals with narcolepsy. In the future, their work could potentially help identify new therapeutic targets for socially induced cataplexy.
"Our next goal will be to better understand the oxytocin-sensitive neurons within the central amygdala by characterizing their gene expression profiles," Mahoney added.
"We also want to determine whether oxytocin promotes cataplexy by reducing stress or anxiety, thereby allowing emotionally positive experiences to more readily trigger cataplexy. Ultimately, we hope these studies will provide a more complete understanding of how emotional and social signals influence the brain in narcolepsy."
More information: Carrie E. Mahoney et al, Oxytocin promotes socially triggered cataplexy, Nature Neuroscience (2026). DOI: 10.1038/s41593-026-02352-7.
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