ArticleScience advances2025
Brainstem circuit for sickness-induced sleep.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Evolution and Reorganization of the Hierarchical Brain-wide Neuronal Network Through Anesthesia.Neuroscience bulletin · 2026Article
- A molecular integrator of sleep duration and interruption.bioRxiv : the preprint server for biology · 2026Article
- HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.Journal of neuroinflammation · 2026Review
- Brain Structures, Circuits, and Networks Involved in Immune Regulation, Periodontal Health, and Disease.Life (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased sleep induced by immune activation plays a crucial role in facilitating recovery from illness. However, the neural mechanisms underlying sickness-induced sleep remain poorly understood. Here, we identify a brainstem circuit originating in the nucleus of the solitary tract (NST) that mediates sickness-induced nonrapid eye movement (NREM) sleep. Using activity-dependent genetic labeling, we tagged NST neurons activated by lipopolysaccharide (LPS) injection and showed that their chemogenetic activation strongly promotes NREM sleep. These NST neurons project extensively to the parabrachial nucleus (PB), where LPS-activated neurons also promote NREM sleep. Fiber photometry recording of several wake-promoting neuromodulators using their biosensors showed that evoked norepinephrine release from locus coeruleus neurons is markedly reduced by either LPS injection or direct activation of NST or PB sickness neurons. These results suggest that sickness-induced NREM sleep is mediated in part by a brainstem circuit that regulates neuromodulator signaling.
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Registered trials
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