ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016
The Dual Hypocretin Receptor Antagonist Almorexant is Permissive for Activation of Wake-Promoting Systems.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Trial
- First-in-human study with ACT-539313, a novel selective orexin-1 receptor antagonist.British journal of clinical pharmacology · 2020Trial
- Emerging and upcoming therapies in insomnia.Translational and clinical pharmacology · 2024Article
- Establishment of a chronic insomnia rat model of sleep fragmentation using unstable platforms surrounded by water.Experimental and therapeutic medicine · 2023Article
- Translatome profiling in fatal familial insomnia implicates TOR signaling in somatostatin neurons.Life science alliance · 2022Article
- Distinct translatome changes in specific neural populations precede electroencephalographic changes in prion-infected mice.PLoS pathogens · 2022Article
- Nonclinical pharmacology of daridorexant: a new dual orexin receptor antagonist for the treatment of insomnia.Psychopharmacology · 2021Review
- Orexin Receptor Antagonists as Emerging Treatments for Psychiatric Disorders.Neuroscience bulletin · 2020Review
- Seasonal decrease in thermogenesis and increase in vasoconstriction explain seasonal response to NJournal of neurochemistry · 2019Article
- The natural Disc1-deletion present in several inbred mouse strains does not affect sleep.Scientific reports · 2017Article
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The dual hypocretin receptor (HcrtR) antagonist almorexant (ALM) may promote sleep through selective disfacilitation of wake-promoting systems, whereas benzodiazepine receptor agonists (BzRAs) such as zolpidem (ZOL) induce sleep through general inhibition of neural activity. Previous studies have indicated that HcrtR antagonists cause less-functional impairment than BzRAs. To gain insight into the mechanisms underlying these differential profiles, we compared the effects of ALM and ZOL on functional activation of wake-promoting systems at doses equipotent for sleep induction. Sprague-Dawley rats, implanted for EEG/EMG recording, were orally administered vehicle (VEH), 100 mg/kg ALM, or 100 mg/kg ZOL during their active phase and either left undisturbed or kept awake for 90 min after which their brains were collected. ZOL-treated rats required more stimulation to maintain wakefulness than VEH- or ALM-treated rats. We measured Fos co-expression with markers for wake-promoting cell groups in the lateral hypothalamus (Hcrt), tuberomammillary nuclei (histamine; HA), basal forebrain (acetylcholine; ACh), dorsal raphe (serotonin; 5HT), and singly labeled Fos(+) cells in the locus coeruleus (LC). Following SD, Fos co-expression in Hcrt, HA, and ACh neurons (but not in 5HT neurons) was consistently elevated in VEH- and ALM-treated rats, whereas Fos expression in these neuronal groups was unaffected by SD in ZOL-treated rats. Surprisingly, Fos expression in the LC was elevated in ZOL- but not in VEH- or ALM-treated SD animals. These results indicate that Hcrt signaling is unnecessary for the activation of Hcrt, HA, or ACh wake-active neurons, which may underlie the milder cognitive impairment produced by HcrtR antagonists compared to ZOL.
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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.