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Cited by 141Sleep and Wakefulness ResearchNeuroinflammation and Neurodegeneration MechanismsSleep and Work-Related Fatigue

Evidence for Neuroinflammatory and Microglial Changes in the Cerebral Response to Sleep Loss

Open access
Wisor, Jonathan P., Schmidt, Michelle A., Clegern, William C.·2011·Sleep
DOI 10.1093/sleep/34.3.261PMC PMC3041702
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Abstract

STUDY OBJECTIVES: Sleep loss has pro-inflammatory effects, but the roles of specific cell populations in mediating these effects have not been delineated. We assessed the modulation of the electroencephalographic and molecular responses to sleep deprivation (S-DEP) by minocycline, a compound that attenuates microglial activation occurring in association with neuroinflammatory events. DESIGN: Laboratory rodents were subjected to assessment of sleep and wake in baseline and sleep deprived conditions. PARTICIPANTS: Adult male CD-1 mice (30-35 g) subjected to telemetric electroencephalography. INTERVENTIONS: Minocycline was administered daily. Mice were subjected to baseline data collection on the first day of minocycline administration and, on subsequent days, 2 S-DEP sessions, 1 and 3 h in duration, followed by recovery sleep. Following EEG studies, mice were euthanized either at the end of a 3 h S-DEP or as time-of day controls for sampling of brain messenger RNAs. Gene expression was measured by real-time polymerase chain reaction. MEASUREMENTS AND RESULTS: Minocycline-treated mice exhibited a reduction in time spent asleep, relative to saline-treated mice, in the 3-h interval immediately after administration. S-DEP resulted in an increase in EEG slow wave activity relative to baseline in saline-treated mice. This response to S-DEP was abolished in animals subjected to chronic minocycline administration. S-DEP suppressed the expression of the microglial-specific transcript cd11b and the neuroinflammation marker peripheral benzodiazepine receptor, in the brain at the mRNA level. Minocycline attenuated the elevation of c-fos expression by S-DEP. Brain levels of pro-inflammatory cytokine mRNAs interleukin-1β (il-1β), interleukin-6 (il-6), and tumor necrosis factor-α (tnfα) were unaffected by S-DEP, but were elevated in minocycline-treated mice relative to saline-treated mice. CONCLUSIONS: The anti-neuroinflammatory agent minocycline prevents either the buildup or expression of sleep need in rodents. The molecular mechanism underlying this effect is not known, but it is not mediated by suppression of il-1β, il-6, and tnfα at the transcript level.

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  • Black individuals at higher risk of obstructive sleep apnoea demonstrate more dysfunctional beliefs and attitudes about sleep.

    “These data are consistent with other studies that show that black individuals who are at higher risk of obstructive sleep apnoea demonstrate more dysfunctional beliefs and attitudes about sleep (Pandey et al., 2011).”

    From Addressing sleep disturbances: an opportunity to prevent cardiometabolic disease? (2014) · cites this paper as Pandey et al., 2011

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Research works printed but not linked: 4

  1. Cirelli C, Tononi G. Gene expression in the brain across the sleep-waking cycle. Brain Res 2000;885:303-21.
  2. Mullington JM, Haack M, Toth M, Serrador JM, Meier-Ewert HK. Car- diovascular, inflammatory, and metabolic consequences of sleep depriva- tion. Prog Cardiovasc Dis 2009;51:294-302.
  3. Institute of Laboratory Animal Resources CoLS, National Research Council. Guide for Care and Use of Laboratory Animals. Washington, DC: National Academy Press, 1996.
  4. Veasey SC, Mackiewicz M, Fenik P, Ro M, Ogilvie MD, Pack AI. IL1β knockout mice lack the TNFα response to sleep deprivation but have nor- mal sleep and sleep recovery. Soc Neur Abs 1997;23:792.

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Authors
Wisor, J. P., Schmidt, M. A., & Clegern, W. C.
Affiliations
Washington State University Spokane (US)
Corresponding author
Wisor, Jonathan P.
ORCID
Venue
Sleep
Publisher
Oxford University Press (OUP)
Published
2011-03
Volume
34
Issue
3
Pages
261-272
ISSN
  • 0161-8105 (ISSN-L)
  • 1550-9109
DOI
10.1093/sleep/34.3.261
PMC
PMC3041702
OpenAlex
W1419855764
Cited by
141
References
84
Citations by year
2026: 7 · 2025: 8 · 2024: 9 · 2023: 12 · 2022: 6 · 2021: 12 · 2020: 10 · 2019: 10 · 2018: 9 · 2017: 8 · 2016: 7 · 2015: 12 · 2014: 8 · 2013: 13 · 2012: 6
FWCI
4.87
Type
journal article
Language
en
Open access
Locations
  • SLEEP (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
sleep deprivation, neuroinflammation, microglial activation, minocycline, sleep need, EEG slow-wave activity, CD11b, translocator protein (TSPO), c-fos, inflammatory cytokines, IL-1β, interleukin-6, TNF-α, brain gene expression, mice
MeSH terms
Animals, Anti-Inflammatory Agents, Brain, Brain Chemistry, Electroencephalography, Gene Expression Regulation, Male, Minocycline, Sleep, Sleep Deprivation, Tumor Necrosis Factor-alpha, Interleukin-6, Microglia, Gene Expression Profiling, Mice, Interleukin-1beta

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