ArticleProceedings of the National Academy of Sciences of the United States of America2017
Serotonin neurons in the dorsal raphe mediate the anticataplectic action of orexin neurons by reducing amygdala activity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 102 citations in OpenAlex.
- Therapeutic Prospects of Ketamine for Cataplexy in Narcolepsy Type 1: Evidence from a Human Case and a Murine Model.Annals of neurology · 2026Article
- Oxytocin promotes socially triggered cataplexy.Nature neuroscience · 2026Article
- A GABAergic network from AVP- to VIP-neurons in the suprachiasmatic nucleus sets the timing of circadian behavior rhythms.PLoS biology · 2026Article
- Narcolepsy and rapid eye movement sleep.Journal of sleep research · 2025Review
- Hypocretin: a promising target for the regulation of homeostasis.Frontiers in neuroscience · 2025Review
- Individual and environmental risk factors for post-traumatic stress among hospital nurses after the 2024 Noto Peninsula earthquake in Japan.Frontiers in psychiatry · 2025Article
- Impact of Circadian Rhythm and Sleep Architecture Changes on Prognosis in Patients with Acute Hemorrhagic Stroke.Nature and science of sleep · 2025Article
- Gain control of sensory input across polysynaptic circuitries in mouse visual cortex by a single G protein-coupled receptor type (5-HTNature communications · 2024Article
- Orexin Receptor Antagonists as Adjunct Drugs for the Treatment of Depression: A Mini Meta-Analysis.Noro psikiyatri arsivi · 2024Review
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- Multi-Region Microdialysis Imaging Platform Revealed Dorsal Raphe Nucleus Calcium Signaling and Serotonin Dynamics during Nociceptive Pain.International journal of molecular sciences · 2023Article
- Activation of the rostral nucleus accumbens shell by optogenetics induces cataplexy-like behavior in orexin neuron-ablated mice.Scientific reports · 2023Article
- Amygdala neurocircuitry at the interface between emotional regulation and narcolepsy with cataplexy.Frontiers in neuroscience · 2023Review
- Optogenetic induction of hibernation-like state with modified human Opsin4 in mice.Cell reports methods · 2022Article
- Neural serotonergic circuits for controlling long-term voluntary alcohol consumption in mice.Molecular psychiatry · 2022Article
- Paraventricular hypothalamic vasopressin neurons induce self-grooming in mice.Molecular brain · 2022Article
- Activity of putative orexin neurons during cataplexy.Molecular brain · 2022Article
- Chemogenetics as a neuromodulatory approach to treating neuropsychiatric diseases and disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Review
- What evidence is there for implicating the brain orexin system in neuropsychiatric symptoms in dementia?Frontiers in psychiatry · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Narcolepsy is a sleep disorder caused by the loss of orexin (hypocretin)-producing neurons and marked by excessive daytime sleepiness and a sudden weakening of muscle tone, or cataplexy, often triggered by strong emotions. In a mouse model for narcolepsy, we previously demonstrated that serotonin neurons of the dorsal raphe nucleus (DRN) mediate the suppression of cataplexy-like episodes (CLEs) by orexin neurons. Using an optogenetic tool, in this paper we show that the acute activation of DRN serotonin neuron terminals in the amygdala, but not in nuclei involved in regulating rapid eye-movement sleep and atonia, suppressed CLEs. Not only did stimulating serotonin nerve terminals reduce amygdala activity, but the chemogenetic inhibition of the amygdala using designer receptors exclusively activated by designer drugs also drastically decreased CLEs, whereas chemogenetic activation increased them. Moreover, the optogenetic inhibition of serotonin nerve terminals in the amygdala blocked the anticataplectic effects of orexin signaling in DRN serotonin neurons. Taken together, the results suggest that DRN serotonin neurons, as a downstream target of orexin neurons, inhibit cataplexy by reducing the activity of amygdala as a center for emotional processing.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.