Figure 5.

Schematic representation of circuits involved in the development of cataplexy. Inappropriate activation of the REM sleep atonia circuitry during wakefulness is thought to produce cataplexy. Glutamatergic REM-active SLD neurons trigger the paralysis of REM sleep via stimulation of the GABAergic/glycinergic cells in the MM. These MM neurons send inhibitory projections to skeletal motor neurons. Under normal conditions, strong positive emotions are processed via GABAergic neurons of the CeA, which then inhibit cells in the LC and vlPAG. However, in the absence of the LH hypocretinergic neurons in cataplexy, this inhibition fails, so the REM sleep atonia circuit is released from inhibition and triggers muscle paralysis while the individual remains conscious. The inhibition of LC neurons during cataplexy removes noradrenergic inputs to motoneurons, thereby enhancing the muscle paralysis of cataplexy. CeA, central nucleus of the amygdala; GABA, γ-aminobutyric acid; LC, locus coeruleus; LH, lateral hypothalamus; MM, ventral medial medulla; SubC, subcoeruleus; vlPAG, ventrolateral periaqueductal gray; MNs, motoneurons.