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Hypocretinergic interactions with the serotonergic system regulate REM sleep and cataplexy
Ali Seifinejad1, Sha Li1, Marie-Laure Possovre1
1Department of Biomedical Sciences, Faculty of Biology and Medicine, University of Lausanne, 1005, Lausanne, Switzerland.
Nature Communications
|November 28, 2020
Summary
Cataplexy, a narcolepsy symptom, was suppressed in mice by altering serotonin transporters. This research reveals distinct mechanisms regulate cataplexy, REM sleep, and sleep need, all influenced by hypocretin input to serotonin neurons.
Area of Science:
- Neuroscience
- Sleep Medicine
- Molecular Biology
Background:
- Cataplexy, the hallmark of narcolepsy, is linked to hypocretin deficiency and often treated with serotonin reuptake inhibitors.
- It's traditionally viewed as an abnormal REM sleep state.
Purpose of the Study:
- To investigate the role of serotonin transporters in hypocretin deficiency-related cataplexy.
- To explore the regulatory mechanisms of cataplexy, REM sleep, and sleep need.
Main Methods:
- Genetic manipulation of serotonin transporters and hypocretin receptors in mice.
- Electrophysiological recordings (EEG) to analyze sleep states and brain activity.
Main Results:
- Deleting the serotonin transporter in hypocretin knockout mice abolished cataplexy and increased REM sleep.
- Mice lacking both showed impaired sleep need accumulation.
- Altering serotonin transporter alleles modulated EEG theta and gamma power during REM sleep and wakefulness.
- Deleting hypocretin receptors on dorsal raphe neurons consolidated REM sleep without inducing cataplexy.
Conclusions:
- Cataplexy and REM sleep are regulated by distinct mechanisms, challenging traditional views.
- Hypocretinergic input to serotonin neurons plays a crucial role in regulating both sleep states and the buildup of sleep need.
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