GABA Cells in the Central Nucleus of the Amygdala Control Cataplexy

Cataplexy is a hallmark of narcolepsy characterized by the sudden onset of muscle weakness or paralysis during wakefulness. It can occur spontaneously but is typically triggered by positive emotions like laughter. Although cataplexy was identified over 130 years ago, its neural mechanism remains unclear. Here, we show that a newly identified GABA circuit within the central nucleus of the amygdala (CeA) may play a causal role in promoting cataplexy. We found that, in narcoleptic mice, chemogenetic activation of GABA cells within the CeA triggered a 253% increase in the number of cataplexy attacks without affecting their duration. We also show that GABA cell activation only promotes cataplexy attacks associated with emotionally rewarding stimuli such as wheel running, without impacting spontaneous attacks. Our results indicate that the CeA plays a pivotal role in controlling cataplexy onset, and that emotionally rewarding stimuli may trigger cataplexy by activating GABA cells in the CeA.