ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Sleep deprivation triggers inducible nitric oxide-dependent nitric oxide production in wake-active basal forebrain neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Sleep deprivation and oxidative stress in animal models: a systematic review.Oxidative medicine and cellular longevity · 2015Pooled it
- Effects of β-alanine supplementation on physical performance, cognition, endocrine function, and inflammation during a 24 h simulated military operation.Physiological reports · 2018Trial
- Transcranial photobiomodulation to enhance sleep by elevating adenosine signaling: a translational study.Molecular psychiatry · 2026Article
- Adenosine ABiomolecules & therapeutics · 2026Review
- Insomnia: the gut microbiome connection, prospects for probiotic and postbiotic therapies, and future directions.Journal of advanced research · 2026Review
- Effect of chronic sleep restriction on ethanol preference and cortical structural plasticity.Neurobiology of sleep and circadian rhythms · 2025Article
- Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection.Neurobiology of sleep and circadian rhythms · 2025Article
- Reproductive hormones and sex chromosomes drive sex differences in the sleep-wake cycle.Frontiers in neuroscience · 2024Review
- Photoperiod-driven concurrent changes in hypothalamic and brainstem transcription of sleep and immune genes in migratory redheaded bunting.Proceedings. Biological sciences · 2023Article
- Translational approaches to influence sleep and arousal.Brain research bulletin · 2022Review
- Sleep, Narcolepsy, and Sodium Oxybate.Current neuropharmacology · 2022Article
- Neuroinflammation, Sleep, and Circadian Rhythms.Frontiers in cellular and infection microbiology · 2022Review
- Cellular Effects of Rhynchophylline and Relevance to Sleep Regulation.Clocks & sleep · 2021Review
- Effect of memantine, an anti-Alzheimer's drug, on rodent microglial cells in vitro.Scientific reports · 2021Article
- Sleep loss mediates the effect of stress on nitrergic signaling in female mice.Neuroscience letters · 2021Article
- Sleep deprivation and stress: a reciprocal relationship.Interface focus · 2020Review
- Sleep and Cellular Stress.Current opinion in physiology · 2020Article
- Acute and Chronic Sleep Deprivation-Related Changes in N-methyl-D-aspartate Receptor-Nitric Oxide Signalling in the Rat Cerebral Cortex with Reference to Aging and Brain Lateralization.International journal of molecular sciences · 2019Article
- The Temperature Dependence of Sleep.Frontiers in neuroscience · 2019Review
- Donepezil suppresses intracellular CaJournal of neuroinflammation · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Sleep loss negatively impacts performance, mood, memory, and immune function, but the homeostatic factors that impel sleep after sleep loss are imperfectly understood. Pharmacological studies had implicated the basal forebrain (BF) inducible nitric oxide (NO) synthase (iNOS)-dependent NO as a key homeostatic factor, but its cellular source was obscure. To obtain direct evidence about the cellular source of iNOS-generated NO during sleep deprivation (SD), we used intracerebroventricular perfusion in rats of the cell membrane-permeable dye diaminofluorescein-2/diacetate (DAF-2/DA) that, once intracellular, bound NO and fluoresced. To circumvent the effects of neuronal NOS (nNOS), DAF-2/DA was perfused in the presence of an nNOS inhibitor. SD led to DAF-positive fluorescence only in the BF neurons, not glia. SD increased expression of iNOS, which colocalized with NO in neurons and, more specifically, in prolonged wakefulness-active neurons labeled by Fos. SD-induced iNOS expression in wakefulness-active neurons positively correlated with sleep pressure, as measured by the number of attempts to enter sleep. Importantly, SD did not induce Fos or iNOS in stress-responsive central amygdala and paraventricular hypothalamic neurons, nor did SD elevate corticosterone, suggesting that the SD protocol did not provoke iNOS expression through stress. We conclude that iNOS-produced neuronal NO is an important homeostatic factor promoting recovery sleep after SD.
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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.