Furthermore, the effect of orexin neurons inhibiting cataplexy was found to be abolished when serotonin release was inhibited selectively in the amygdala.Ĭataplexy takes place, triggered by a sudden emotional excitement of positive valence such as a big laughter. When the amygdala activity was artificially reduced in a direct manner, cataplexy was inhibited, while artificially augmented, frequency of cataplexy attack increased. In addition, the team found that serotonin release reduced the amygdala activity. The same experimental operation in the other brain region that controls REM sleep did not inhibit cataplexy. In this study, with an optogenetic*6 tool, the team has discovered that catalepsy was almost completely inhibited by artificial augmentation of serotonin release induced by selectively stimulating serotonin nerve terminals in the amygdala in the narcolepsy model mice*7. Serotonin neurons in the dorsal raphe nucleus extend projections throughout the brain and send information. In this study, the international research team led by the researchers of Kanazawa University has discovered that serotonin neurons in the dorsal raphe nucleus inhibits catalepsy by reducing activities of the amygdala*5 that controls emotion. The one is noradrenaline neurons in the locus coeruleus of the brain, suppressing strong sleepiness, and the other is serotonin*4 neurons in the dorsal raphe nucleus of the brain, inhibiting cataplexy. The research team previously found two types of neurons preventing narcolepsy by receiving orexin from orexin neurons. Cataplexy attack is thought that atonia, a characteristics of REM sleep, takes place while one is awoken. Dreams are dreamt usually during REM sleep, where most of the muscles are controlled to be relaxed (called atonia) in order to prevent the dreamer to make real actions.
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