The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Humoral regulation of physiological sleep: cytokines and GHRH
Abstract
Interleukin‐1, tumour necrosis factor, and growth hormone releasing hormone form part of the humoral mechanisms regulating physiological sleep. Their injection enhances non‐rapid‐eye‐movement sleep whereas their inhibition reduces spontaneous sleep and sleep rebound after sleep deprivation. Changes in their mRNA levels and changes in their protein levels in the brain are consistent within their proposed role in sleep regulation. Furthermore, results from transgenic and mutant animals also are suggestive of their role in sleep regulation. The sites responsible for the growth hormone releasing hormone somnogenic activity seem to reside in the anterior hypothalamus/basal forebrain. Somnogenic sites for interleukin‐1 and tumour necrosis factor likely include the anterior hypothalamus, but also may extend beyond that area. These substances elicit non‐rapid‐eye‐movement sleep via a biochemical cascade that includes other known sleep regulatory substances.
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In the citing paper
“the infection-driven NREM sleep response is independent from the fever response (303).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [303]
In the citing paper
“They can activate the immune system through binding to respective PRRs, which likely leads to systemic increases of sleep regulatory substances, such as TNF and IL-1 (303, 305).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [303]
Citations
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“In fact, peaks in Th1 cytokine activity and, more generally, in proinflammatory cytokine activity during the rest period were mainly detected during the early SWS-dominated portion of sleep, in humans as well as in animals in different tissues including the brain (487, 671) and lymph nodes (359), but also in blood and…”
BackgroundThe Sleep-Immune Crosstalk in Health and Disease
Besedovsky, L., Lange, T., & Haack, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00010.2018 · Cited by 1,479
“In addition, SWS-dependent processes might actively counteract inflammation in the brain (64, 65, 302).”
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Maquet, P. (2001) · Science · doi:10.1126/science.1062856 · Cited by 1,177
Besedovsky, L., Lange, T., & Born, J. (2012) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-011-1044-0 · Cited by 1,153
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Metadata
- Authors
- Krueger, Obál, Jr., & Fang
- Affiliations
- Washington State University (US)
- Corresponding author
- Krueger
- Venue
- Journal of Sleep Research
- Publisher
- Wiley
- Published
- 1999-03
- Volume
- 8
- Issue
- S1
- Pages
- 53-59
- ISSN
- 0962-1105 (ISSN-L)
- 1365-2869
- OpenAlex
- W1990291441
- Cited by
- 112
- References
- 38
- Citations by year
- 2025: 1 · 2021: 1 · 2019: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 4 · 2012: 5
- FWCI
- 9.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Sleep Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS-27250, NS-31453, NS-25378, R01NS031453, R01NS027250, R01NS025378)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Keywords
- sleep regulation, cytokines, interleukin-1, TNF-α, growth hormone-releasing hormone, NREM sleep, sleep deprivation, sleep rebound, anterior hypothalamus, basal forebrain
- MeSH terms
- Animals, Circadian Rhythm, Hypothalamus, Interleukin-1, Prostaglandins, RNA, Messenger, Sleep, REM, Somatostatin, Growth Hormone-Releasing Hormone, Tumor Necrosis Factor-alpha, Rats
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