ArticleNature neuroscience2015
Neuronal ensembles sufficient for recovery sleep and the sedative actions of α2 adrenergic agonists.
Article in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 264 citations in OpenAlex.
- Effect of dexmedetomidine on postoperative systemic inflammation and recovery in patients undergoing digest tract cancer surgery: A meta-analysis of randomized controlled trials.Frontiers in oncology · 2022Pooled it
- Efficacy and safety of preoperative intranasal dexmedetomidine in adults: a systematic review and meta-analysis of randomized controlled trials.Brazilian journal of anesthesiology (Elsevier)Pooled it
- Dexmedetomidine versus remifentanil in sedation, analgesia, and vital signs in stereotactic brain biopsy: A randomized, single-blind, active-controlled clinical trial.The Journal of international medical research · 2026Trial
- Effects of different administration routes of dexmedetomidine on sleep quality in patients undergoing total knee arthroplasty.Scientific reports · 2026Trial
- Oral Dexmedetomidine Promotes Non-rapid Eye Movement Stage 2 Sleep in Humans.Anesthesiology · 2020Trial
- Anesthesia unconsciousness recruits dynamic parabrachial activity within a distributed brain-wide ensemble.bioRxiv : the preprint server for biology · 2026Article
- A male-biased hypothalamic circuit modulates postmating sleep suppression in mice.Science advances · 2026Article
- The Central Medial Thalamus Serves as a Critical Hub for Preserved Arousability During Dexmedetomidine Sedation.Neuroscience bulletin · 2026Article
- Article
- Sleep circuit modulation: from animal models to human translation.Brain : a journal of neurology · 2026Review
- Catecholamine modulation of frontal cortical ignition during wakefulness, sleep and anesthesia.National science review · 2026Article
- Article
- Lateral septum GABAergic neurons mediate the effects of dexmedetomidine on allodynia and sleep in a male mouse model of neuropathic pain.Nature communications · 2026Article
- Role of Preoptic Area γ-Aminobutyric Acid-mediated Neurons in Distinctly Regulating Sleep and Rousability during Dexmedetomidine Sedation in Mice.Anesthesiology · 2026Article
- Acsl4-mediated Lipid Homeostasis Orchestrates Synaptic and Cognitive Plasticity.Research square · 2026Article
- Edinger-Westphal Neurons Contribute to Emergence from Desflurane and Sevoflurane Anesthesia in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Disrupted temperature-sleep coupling mechanism in a Dravet syndrome mouse model.Nature communications · 2026Article
- Article
- Dexmedetomidine produces more sleep-like brain activity compared with propofol in human participants.British journal of anaesthesia · 2026Article
- Neurophysiological differences between dexmedetomidine sedation and natural sleep across the rodent lifespan: implications for aging and perioperative brain health.Anesthesiology and perioperative science · 2026Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
Abstract
Do sedatives engage natural sleep pathways? It is usually assumed that anesthetic-induced sedation and loss of righting reflex (LORR) arise by influencing the same circuitry to lesser or greater extents. For the α2 adrenergic receptor agonist dexmedetomidine, we found that sedation and LORR were in fact distinct states, requiring different brain areas: the preoptic hypothalamic area and locus coeruleus (LC), respectively. Selective knockdown of α2A adrenergic receptors from the LC abolished dexmedetomidine-induced LORR, but not sedation. Instead, we found that dexmedetomidine-induced sedation resembled the deep recovery sleep that follows sleep deprivation. We used TetTag pharmacogenetics in mice to functionally mark neurons activated in the preoptic hypothalamus during dexmedetomidine-induced sedation or recovery sleep. The neuronal ensembles could then be selectively reactivated. In both cases, non-rapid eye movement sleep, with the accompanying drop in body temperature, was recapitulated. Thus, α2 adrenergic receptor-induced sedation and recovery sleep share hypothalamic circuitry sufficient for producing these behavioral states.
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Registered trials
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.