A single unit recording study done in narcoleptic dogs found that, during cataplexy, some amygdala neurons become activated ( Gulyani et al., 2002). In fact, there is some evidence pointing to the involvement of the amygdala as part of the narcolepsy circuit, whereas the exact circuitry involved and the specific abnormalities in the amygdala are still unknown.

An important clue to unraveling the brain circuit of narcolepsy comes from the fact that cataplexy is usually triggered by strong emotions ( Dauvilliers et al., 2014 Morawska et al., 2011).

Cataplexy is cardinal among these symptoms and characterized by a sudden loss of skeletal muscle tone during waking.Įven though it is known that the loss of the neuropeptide orexin (hypocretin, HCRT) system causes narcolepsy with cataplexy ( Lin et al., 1999 Nishino et al., 2000a), the entire brain circuitry responsible for the presentation of all narcoleptic symptoms is not fully understood. Narcolepsy is a chronic sleep disorder characterized by excessive daytime sleepiness, cataplexy, sleep fragmentation, and hypnogogic/hypnopompic hallucinations. We suggest that the abnormal activation and synchronization of CeA GABAergic neurons may trigger emotion-induced cataplexy. Furthermore, we found that CeA GABAergic neurons became highly synchronized during predator odor-induced cataplexy. Majority in the latter group were inactive during regular sleep/wake cycles but were specifically activated by predator odor and continued their intense activities into succeeding cataplexy bouts. Two distinct GABAergic neuronal groups involved in cataplexy were identified: spontaneous cataplexy-ON and predator odor-induced cataplexy-ON neurons. We used a deep brain calcium imaging tool to image the intrinsic calcium transient as a marker of neuronal activity changes in the narcoleptic VGAT-Cre mice by expressing the calcium sensor GCaMP6 into genetically defined CeA GABAergic neurons. However, there is still no direct evidence on CeA GABAergic neurons’ real-time dynamic during cataplexy. Recent studies showed activation of the GABAergic neurons in the central nucleus of the amygdala (CeA) triggered cataplexy of sleep disorder narcolepsy.

Cataplexy attack